[X] Close
You are about to erase all the values you have customized, search history, page format, etc.
Click here to RESET all values       Click here to GO BACK without resetting any value
Items 1 to 100 of about 2067
1. Andrade FH, Figueiroa FC, Bersano PR, Bissacot DZ, Rocha NS: Malignant mammary tumor in female dogs: environmental contaminants. Diagn Pathol; 2010;5:45
COS Scholar Universe. author profiles.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Malignant mammary tumor in female dogs: environmental contaminants.
  • Mammary tumors of female dogs have greatly increased in recent years, thus demanding rapid diagnosis and effective treatment in order to determine the animal survival.
  • There is considerable scientific interest in the possible role of environmental contaminants in the etiology of mammary tumors, specifically in relation to synthetic chemical substances released into the environment to which living beings are either directly or indirectly exposed.
  • In this study, the presence of pyrethroid insecticide was observed in adjacent adipose tissue of canine mammary tumor.
  • High Precision Liquid Chromatography - HPLC was adapted to detect and identify environmental contaminants in adipose tissue adjacent to malignant mammary tumor in nine female dogs, without predilection for breed or age.
  • Five grams of adipose tissue adjacent to the tumor were collected to detect of environmental contaminants.
  • From these tumors, seven (77.8%) presented aggressiveness degree III and two (22.2%) degree I.
  • Five tumors were positive for estrogen receptors in immunohistochemical analysis.
  • The contamination level was observed in more aggressive tumors.
  • This was the first report in which the level of environmental contaminants could be detected in adipose tissue of female dogs with malignant mammary tumor, by HPLC.
  • Results suggest the possible involvement of pyrethroid in the canine mammary tumor carcinogenesis.
  • Hence, the dog may be used as a sentinel animal for human breast cancer, since human beings share the same environment and basically have the same eating habits.
  • [MeSH-major] Carcinogens, Environmental / adverse effects. Carcinoma / chemically induced. Dog Diseases / chemically induced. Insecticides / adverse effects. Mammary Glands, Animal / drug effects. Mammary Neoplasms, Animal / chemically induced. Pyrethrins / adverse effects

  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [Cites] Carcinogenesis. 2000 Mar;21(3):427-33 [10688862.001]
  • [Cites] Prev Vet Med. 2000 Nov 16;47(3):187-204 [11058779.001]
  • [Cites] Cancer Lett. 2002 Jul 26;181(2):179-86 [12175533.001]
  • [Cites] J Natl Cancer Inst. 1969 Dec;43(6):1249-61 [4319248.001]
  • [Cites] Bull World Health Organ. 1971;44(1-3):11-22 [5315342.001]
  • [Cites] Biochem Biophys Res Commun. 1998 Oct 29;251(3):855-9 [9790999.001]
  • [Cites] J Comp Pathol. 1989 Nov;101(4):389-97 [2558128.001]
  • [Cites] J Reprod Fertil Suppl. 1993;47:483-7 [8229967.001]
  • [Cites] Diagn Cytopathol. 1995 Nov;13(4):347-51 [8599924.001]
  • [Cites] J Anal Toxicol. 1997 Sep;21(5):397-402 [9288595.001]
  • [Cites] Vet Pathol. 1983 Mar;20(2):127-42 [6836870.001]
  • (PMID = 20587072.001).
  • [ISSN] 1746-1596
  • [Journal-full-title] Diagnostic pathology
  • [ISO-abbreviation] Diagn Pathol
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Carcinogens, Environmental; 0 / Insecticides; 0 / Pyrethrins
  • [Other-IDs] NLM/ PMC2909155
  •  go-up   go-down


2. Moody SE, Perez D, Pan TC, Sarkisian CJ, Portocarrero CP, Sterner CJ, Notorfrancesco KL, Cardiff RD, Chodosh LA: The transcriptional repressor Snail promotes mammary tumor recurrence. Cancer Cell; 2005 Sep;8(3):197-209
The Lens. Cited by Patents in .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] The transcriptional repressor Snail promotes mammary tumor recurrence.
  • Breast cancer recurrence is a fundamental clinical manifestation of tumor progression and represents the principal cause of death from this disease.
  • Using a conditional transgenic mouse model for the recurrence of HER2/neu-induced mammary tumors, we demonstrate that the transcriptional repressor Snail is spontaneously upregulated in recurrent tumors in vivo and that recurrence is accompanied by epithelial-to-mesenchymal transition (EMT).
  • Consistent with a causal role for Snail in these processes, we show that Snail is sufficient to induce EMT in primary tumor cells, that Snail is sufficient to promote mammary tumor recurrence in vivo, and that high levels of Snail predict decreased relapse-free survival in women with breast cancer.
  • [MeSH-major] Mammary Neoplasms, Experimental / genetics. Neoplasm Recurrence, Local / genetics. Transcription Factors / genetics
  • [MeSH-minor] Animals. Breast Neoplasms / genetics. Epithelial Cells / pathology. Female. Gene Expression Regulation, Neoplastic. Humans. Mesoderm / pathology. Mice. Mice, Transgenic. Receptor, ErbB-2 / genetics


3. Lin T, Meng L, Li Y, Tsai RY: Tumor-initiating function of nucleostemin-enriched mammary tumor cells. Cancer Res; 2010 Nov 15;70(22):9444-52
NCI CPTC Antibody Characterization Program. NCI CPTC Antibody Characterization Program .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Tumor-initiating function of nucleostemin-enriched mammary tumor cells.
  • Nucleostemin (NS) is highly expressed in normal stem cells and tumors and is upregulated by estradiol in MCF7 breast cancer cells.
  • To investigate the role of NS in mammary tumorigenesis, we established first that NS is expressed at higher levels in the basal cell type than in the luminal cell type in mouse mammary tumors and human breast cancer cells.
  • NS expression was also increased during progression of mammary tumors in MMTV-Wnt1 and MMTV-PyMT transgenic mice and by the tumor sphere culture.
  • To determine the function of NS-enriched tumor cells, we generated a bacterial artificial chromosome transgenic mouse line expressing green fluorescent protein (GFP) from the NS promoter and bred it to MMTV-Wnt1 mice, so that NS-expressing cells can be prospectively isolated based on their GFP levels.
  • Notably, NS-enriched mammary tumor cells exhibited stronger in vitro and in vivo tumorigenic activities and expressed higher levels of K5, CD133, Oct4, telomerase reverse transcriptase, and C-X-C chemokine ligand 12 compared with NS-deficient mammary tumor cells.
  • Our findings establish the tumor-initiating and molecular features of NS-enriched mammary tumor cells, suggesting that NS may offer a valuable therapeutic target.

  • COS Scholar Universe. author profiles.
  • KOMP Repository. gene/protein/disease-specific - KOMP Repository (subscription/membership/fee required).
  • Mouse Genome Informatics (MGI). Mouse Genome Informatics (MGI) .
  • NCI CPTAC Assay Portal. NCI CPTAC Assay Portal .
  • NCI CPTAC Assay Portal. NCI CPTAC Assay Portal .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [Copyright] Copyright © 2010 AACR.
  • [Cites] Nat Cell Biol. 2001 Sep;3(9):793-801 [11533658.001]
  • [Cites] Science. 2009 Jun 26;324(5935):1670-3 [19556499.001]
  • [Cites] Dev Biol. 2002 May 1;245(1):42-56 [11969254.001]
  • [Cites] Am J Pathol. 2002 Sep;161(3):1087-97 [12213737.001]
  • [Cites] Genes Dev. 2002 Dec 1;16(23):2991-3003 [12464630.001]
  • [Cites] Int J Oncol. 2003 Jan;22(1):209-12 [12469206.001]
  • [Cites] Proc Natl Acad Sci U S A. 2003 Apr 1;100(7):3983-8 [12629218.001]
  • [Cites] J Cell Biochem. 2003 Aug 15;89(6):1235-49 [12898521.001]
  • [Cites] Cancer Res. 2003 Sep 15;63(18):5821-8 [14522905.001]
  • [Cites] Am J Pathol. 2003 Nov;163(5):2113-26 [14578209.001]
  • [Cites] Proc Natl Acad Sci U S A. 2003 Dec 23;100(26):15853-8 [14668450.001]
  • [Cites] Proc Natl Acad Sci U S A. 2004 Mar 23;101(12):4158-63 [15020770.001]
  • [Cites] Neoplasia. 2004 Jan-Feb;6(1):7-14 [15068666.001]
  • [Cites] World J Gastroenterol. 2004 May 1;10(9):1246-9 [15112336.001]
  • [Cites] Nature. 1994 Feb 17;367(6464):645-8 [7509044.001]
  • [Cites] Oncogene. 1997 Mar 13;14(10):1249-53 [9121776.001]
  • [Cites] Nat Med. 1997 Jul;3(7):730-7 [9212098.001]
  • [Cites] Cancer Cell. 2004 Nov;6(5):497-506 [15542433.001]
  • [Cites] Cell. 2005 Jun 17;121(6):823-35 [15960971.001]
  • [Cites] Cancer. 2005 Nov 15;104(10):2255-65 [16228988.001]
  • [Cites] Cancer Res. 2005 Dec 1;65(23):10946-51 [16322242.001]
  • [Cites] Nature. 2006 Jan 5;439(7072):84-8 [16397499.001]
  • [Cites] Nature. 2006 Feb 23;439(7079):993-7 [16395311.001]
  • [Cites] Dev Biol. 2006 May 15;293(2):414-25 [16545360.001]
  • [Cites] J Natl Cancer Inst. 2006 Dec 20;98(24):1777-85 [17179479.001]
  • [Cites] J Cell Biol. 2007 Jan 1;176(1):19-26 [17190790.001]
  • [Cites] Oncogene. 2000 Feb 21;19(8):1002-9 [10713683.001]
  • [Cites] Proc Natl Acad Sci U S A. 2000 Apr 11;97(8):4262-6 [10759547.001]
  • [Cites] Am J Pathol. 2000 Jun;156(6):1997-2005 [10854222.001]
  • [Cites] Cancer Res. 2000 Nov 1;60(21):5977-83 [11085516.001]
  • [Cites] Nature. 2007 Jan 4;445(7123):106-10 [17122772.001]
  • [Cites] Breast Cancer Res. 2006;8(5):R59 [17062128.001]
  • [Cites] Nat Rev Cancer. 2007 Oct;7(10):791-9 [17851544.001]
  • [Cites] Genesis. 2007 Oct;45(10):647-52 [17941047.001]
  • [Cites] Nature. 2008 Jan 17;451(7176):345-9 [18202660.001]
  • [Cites] Stem Cells. 2008 Feb;26(2):364-71 [17975224.001]
  • [Cites] Cell Stem Cell. 2007 Sep 13;1(3):313-23 [18371365.001]
  • [Cites] Breast Cancer Res. 2008;10(1):R10 [18241344.001]
  • [Cites] Cancer Res. 2008 May 1;68(9):3243-50 [18451150.001]
  • [Cites] Cancer Res. 2008 Jun 15;68(12):4674-82 [18559513.001]
  • [Cites] Cell Stem Cell. 2008 Jul 3;3(1):109-18 [18593563.001]
  • [Cites] Cancer Biol Ther. 2008 Feb;7(2):268-74 [18059186.001]
  • [Cites] Curr Biol. 2008 Jul 22;18(14):1094-9 [18635350.001]
  • [Cites] Cancer Res. 2008 Oct 1;68(19):7711-7 [18829523.001]
  • [Cites] Cell Stem Cell. 2007 Nov;1(5):555-67 [18371393.001]
  • [Cites] Stem Cells. 2008 Dec;26(12):3237-46 [18802033.001]
  • [Cites] Genes Dev. 2002 Mar 15;16(6):693-706 [11914275.001]
  • (PMID = 21045149.001).
  • [ISSN] 1538-7445
  • [Journal-full-title] Cancer research
  • [ISO-abbreviation] Cancer Res.
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / CA113750-05; United States / NCI NIH HHS / CA / R01 CA113750; United States / NCI NIH HHS / CA / R01 CA124820; United States / NCI NIH HHS / CA / R01 CA113750-05
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / AC133 antigen; 0 / Antigens, CD; 0 / Carrier Proteins; 0 / GNL3 protein, human; 0 / Glycoproteins; 0 / Nuclear Proteins; 0 / Octamer Transcription Factor-3; 0 / Peptides; 0 / Pou5f1 protein, mouse; 0 / nucleostemin protein, mouse; 147336-22-9 / Green Fluorescent Proteins; EC 3.6.1.- / GTP-Binding Proteins
  • [Other-IDs] NLM/ NIHMS238554; NLM/ PMC2982898
  •  go-up   go-down


Advertisement
4. Izumchenko E, Singh MK, Plotnikova OV, Tikhmyanova N, Little JL, Serebriiskii IG, Seo S, Kurokawa M, Egleston BL, Klein-Szanto A, Pugacheva EN, Hardy RR, Wolfson M, Connolly DC, Golemis EA: NEDD9 promotes oncogenic signaling in mammary tumor development. Cancer Res; 2009 Sep 15;69(18):7198-206
The Lens. Cited by Patents in .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] NEDD9 promotes oncogenic signaling in mammary tumor development.
  • However, whereas some studies have identified elevated NEDD9 expression as prometastatic, other work has suggested a negative role in tumor progression.
  • We here show that the Nedd9-null genetic background significantly limits mammary tumor initiation in the MMTV-polyoma virus middle T genetic model.
  • Action of NEDD9 is tumor cell intrinsic, with immune cell infiltration, stroma, and angiogenesis unaffected.
  • The majority of the late-appearing mammary tumors of MMTV-polyoma virus middle T;Nedd9(-/-) mice are characterized by depressed activation of proteins including AKT, Src, FAK, and extracellular signal-regulated kinase, emphasizing an important role of NEDD9 as a scaffolding protein for these prooncogenic proteins.
  • Analysis of cells derived from primary Nedd9(+/+) and Nedd9(-/-) tumors showed persistently reduced FAK activation, attachment, and migration, consistent with a role for NEDD9 activation of FAK in promoting tumor aggressiveness.
  • This study provides the first in vivo evidence of a role for NEDD9 in breast cancer progression and suggests that NEDD9 expression may provide a biomarker for tumor aggressiveness.

  • COS Scholar Universe. author profiles.
  • KOMP Repository. gene/protein/disease-specific - KOMP Repository (subscription/membership/fee required).
  • Mouse Genome Informatics (MGI). Mouse Genome Informatics (MGI) .
  • NCI CPTAC Assay Portal. NCI CPTAC Assay Portal .
  • NCI CPTAC Assay Portal. NCI CPTAC Assay Portal .
  • NCI CPTAC Assay Portal. NCI CPTAC Assay Portal .
  • NCI CPTC Antibody Characterization Program. NCI CPTC Antibody Characterization Program .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [Cites] Trends Cell Biol. 2000 Mar;10(3):111-9 [10675905.001]
  • [Cites] Cancer Genomics Proteomics. 2008 May-Aug;5(3-4):161-8 [18820370.001]
  • [Cites] Mol Cell Biol. 2000 Jul;20(14):5184-95 [10866674.001]
  • [Cites] Nature. 2000 Aug 17;406(6797):747-52 [10963602.001]
  • [Cites] Mol Cell Biol. 2000 Dec;20(23):9018-27 [11074000.001]
  • [Cites] EMBO J. 2000 Dec 15;19(24):6759-69 [11118211.001]
  • [Cites] Mol Cell Biol. 2001 Aug;21(15):5094-108 [11438665.001]
  • [Cites] Eur J Immunol. 2001 May;31(5):1417-27 [11465098.001]
  • [Cites] J Cell Sci. 2002 Jan 1;115(Pt 1):99-111 [11801728.001]
  • [Cites] J Biol Chem. 2002 Feb 15;277(7):5441-7 [11739395.001]
  • [Cites] Proc Natl Acad Sci U S A. 2002 May 14;99(10):6967-72 [12011455.001]
  • [Cites] Nat Rev Cancer. 2002 Dec;2(12):951-6 [12459733.001]
  • [Cites] Am J Pathol. 2003 Nov;163(5):2113-26 [14578209.001]
  • [Cites] Annu Rev Cell Dev Biol. 2004;20:337-66 [15473844.001]
  • [Cites] Mol Cell Biol. 1992 Mar;12(3):954-61 [1312220.001]
  • [Cites] Oncogene. 1995 Dec 7;11(11):2331-8 [8570184.001]
  • [Cites] Mol Cell Biol. 1996 Jul;16(7):3327-37 [8668148.001]
  • [Cites] J Exp Med. 1996 Oct 1;184(4):1365-75 [8879209.001]
  • [Cites] J Biol Chem. 1997 Aug 8;272(32):19719-24 [9242628.001]
  • [Cites] Mol Cell Biol. 1998 Jun;18(6):3540-51 [9584194.001]
  • [Cites] Nat Genet. 1998 Aug;19(4):361-5 [9697697.001]
  • [Cites] Exp Cell Res. 1999 Oct 10;252(1):224-35 [10502414.001]
  • [Cites] Nature. 2005 Jul 28;436(7050):518-24 [16049480.001]
  • [Cites] Cancer Res. 2005 Aug 1;65(15):6755-63 [16061657.001]
  • [Cites] J Immunol. 2005 Sep 15;175(6):3492-501 [16148091.001]
  • [Cites] Nat Cell Biol. 2005 Oct;7(10):937-46 [16184168.001]
  • [Cites] Cell Cycle. 2006 Feb;5(4):384-91 [16479169.001]
  • [Cites] Oncogene. 2006 Mar 16;25(12):1721-32 [16288224.001]
  • [Cites] Cancer Res. 2006 May 1;66(9):4672-80 [16651418.001]
  • [Cites] Cell. 2006 Jun 30;125(7):1269-81 [16814714.001]
  • [Cites] Cell. 2006 Aug 11;126(3):489-502 [16901783.001]
  • [Cites] Oncogene. 2006 Aug 17;25(36):4998-5010 [16568086.001]
  • [Cites] Cancer Res. 2007 Jan 1;67(1):167-77 [17210696.001]
  • [Cites] Cell. 2007 Jan 26;128(2):225-31 [17254958.001]
  • [Cites] Nature. 2007 Aug 16;448(7155):807-10 [17676035.001]
  • [Cites] Cell Biochem Biophys. 2007;48(1):54-72 [17703068.001]
  • [Cites] Cancer Res. 2007 Oct 1;67(19):8975-9 [17908996.001]
  • [Cites] Proc Natl Acad Sci U S A. 2007 Dec 18;104(51):20302-7 [18056629.001]
  • [Cites] Breast. 2008 Jan;17 Suppl 1:S3-8 [18279764.001]
  • [Cites] EMBO J. 2008 Mar 19;27(6):910-20 [18273058.001]
  • [Cites] Cell. 2008 Oct 31;135(3):510-23 [18984162.001]
  • [Cites] Nat Cell Biol. 2008 Sep;10(9):1027-38 [19160483.001]
  • [Cites] J Clin Invest. 2009 Feb;119(2):252-66 [19147981.001]
  • [Cites] J Cell Biochem. 2008 Sep 1;105(1):121-8 [18465784.001]
  • [Cites] Mol Biol Cell. 2008 Apr;19(4):1627-36 [18256281.001]
  • [Cites] Cancer Res. 2008 Sep 1;68(17):7219-27 [18757438.001]
  • [Cites] J Biol Chem. 2000 Mar 24;275(12):8271-4 [10722653.001]
  • (PMID = 19738060.001).
  • [ISSN] 1538-7445
  • [Journal-full-title] Cancer research
  • [ISO-abbreviation] Cancer Res.
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / R01 CA63366; United States / NCI NIH HHS / CA / R01 CA063366-14A1; United States / NCI NIH HHS / CA / CA083638-10; United States / NCI NIH HHS / CA / CA113342-02; United States / NCI NIH HHS / CA / T32 CA009035-34; United States / NCI NIH HHS / CA / PA50 CA-083638; United States / NCI NIH HHS / CA / R01 CA063366; United States / NCI NIH HHS / CA / R01 CA148671; United States / NIAID NIH HHS / AI / R01 AI026782; United States / NCI NIH HHS / CA / R01 CA113342; United States / NCI NIH HHS / CA / CA009035-34; United States / NCI NIH HHS / CA / CA113342; United States / NCI NIH HHS / CA / R01 CA136596; United States / NCI NIH HHS / CA / P50 CA083638-10; United States / NCI NIH HHS / CA / R01 CA113342-02; United States / NCI NIH HHS / CA / P50 CA083638; United States / NCI NIH HHS / CA / T32 CA-009035; United States / NCI NIH HHS / CA / P30 CA006927-47; United States / NCI NIH HHS / CA / CA063366-14A1; United States / NCI NIH HHS / CA / P30 CA006927; United States / NCI NIH HHS / CA / CA006927-47; United States / NCI NIH HHS / CA / CA-06927; United States / NCI NIH HHS / CA / T32 CA009035
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't; Research Support, U.S. Gov't, Non-P.H.S.
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Adaptor Proteins, Signal Transducing; 0 / NEDD9 protein, mouse; 0 / Proteins; EC 2.7.10.2 / Focal Adhesion Kinase 1; EC 2.7.10.2 / Ptk2 protein, mouse
  • [Other-IDs] NLM/ NIHMS135664; NLM/ PMC2758619
  •  go-up   go-down


5. Coelingh Bennink HJT, Singer C, Simoncini T, Genazzani AR, Holinka CF, Kubista E: Estetrol, a pregnancy-specific human steroid, prevents and suppresses mammary tumor growth in a rat model. Climacteric; 2008;11(sup1):29

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Estetrol, a pregnancy-specific human steroid, prevents and suppresses mammary tumor growth in a rat model.
  • We report that E<sub>4</sub>, dose-dependently, prevents the growth of chemically induced (7,12-dimethylbenz(a)anthracene, DMBA) mammary tumors in female Sprague-Dawley rats and that E<sub>4</sub> has the potential to reduce the number and size of pre-existing mammary tumors.
  • Rats treated with DMBA develop estrogen-responsive breast tumors.
  • This model has become the standard pharmacological model to investigate the effect of new compounds on breast tumors.
  • When DMBA-induced rats were co-treated with E<sub>4</sub> for 8 weeks, this resulted in a dose-dependent reduction in the number and size of tumors, an effect that appeared equally effective as tamoxifen treatment or ovariectomy and was not seen with ethinylestradiol.
  • When E<sub>4</sub> was administered to rats in which tumors had already developed, a significant decrease in the number and size of tumors was observed after 4 weeks.

  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 28485647.001).
  • [ISSN] 1473-0804
  • [Journal-full-title] Climacteric : the journal of the International Menopause Society
  • [ISO-abbreviation] Climacteric
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] England
  • [Keywords] NOTNLM ; BREAST TUMOR / DMBA / E4 / ESTETROL / PREVENTION / TREATMENT
  •  go-up   go-down


6. Wallach-Dayan SB, Rubinstein AM, Hand C, Breuer R, Naor D: DNA vaccination with CD44 variant isoform reduces mammary tumor local growth and lung metastasis. Mol Cancer Ther; 2008 Jun;7(6):1615-23
NCI CPTC Antibody Characterization Program. NCI CPTC Antibody Characterization Program .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] DNA vaccination with CD44 variant isoform reduces mammary tumor local growth and lung metastasis.
  • Successful cure from mammary tumor requires resolution of local tumor growth and metastases.
  • We have examined whether targeting of CD44 cell surface adhesion molecule by cDNA vaccination plays a role in resolving mammary tumor development.
  • We show here that CD44 cDNA vaccination decreases the tumor mass and metastatic potential in experimental mammary tumor of BALB/c mice.
  • Vaccination of mice, inoculated with the mammary tumors, by cDNA of CD44 variant (CD44v) but not by cDNA of standard CD44, markedly reduced local tumor development and lung metastasis.
  • Concomitantly, transfection of CD44 antisense into a highly metastatic mammary tumor cell line disrupted the CD44 expression of the cells and reduced their ability to establish local tumors as well as metastatic colonies in the lung.
  • Moreover, when CD44v, but not standard CD44 sense cDNA, was transfected into the poorly metastatic cell line, tumor development was markedly enhanced.
  • It is possible therefore that DNA vaccination with a specific CD44v construct could induce an immune resistance to mammary tumor progression.
  • [MeSH-major] Antigens, CD44 / immunology. Lung Neoplasms / secondary. Mammary Neoplasms, Experimental / pathology. Mammary Neoplasms, Experimental / therapy. Vaccination. Vaccines, DNA / therapeutic use
  • [MeSH-minor] Animals. Antibodies, Neoplasm / immunology. Cell Proliferation. Clone Cells. Epitopes. Female. Humans. Lymph Nodes / immunology. Mice. Mice, Inbred BALB C. Phenotype. Protein Isoforms / immunology. Transfection. Tumor Cells, Cultured

  • MedlinePlus Health Information. consumer health - Immunization.
  • MedlinePlus Health Information. consumer health - Lung Cancer.
  • NCI CPTAC Assay Portal. NCI CPTAC Assay Portal .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 18566232.001).
  • [ISSN] 1535-7163
  • [Journal-full-title] Molecular cancer therapeutics
  • [ISO-abbreviation] Mol. Cancer Ther.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antibodies, Neoplasm; 0 / Antigens, CD44; 0 / Epitopes; 0 / Protein Isoforms; 0 / Vaccines, DNA
  •  go-up   go-down


7. Manjili MH, Arnouk H, Knutson KL, Kmieciak M, Disis ML, Subjeck JR, Kazim AL: Erratum to: Emergence of immune escape variant of mammary tumors that has distinct proteomic profile and a reduced ability to induce "danger signals". Breast Cancer Res Treat; 2006 Apr;96(3):243

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Erratum to: Emergence of immune escape variant of mammary tumors that has distinct proteomic profile and a reduced ability to induce "danger signals".

  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [ErratumFor] Breast Cancer Res Treat. 2006 Apr;96(3):233-41 [16211331.001]
  • (PMID = 28303485.001).
  • [ISSN] 1573-7217
  • [Journal-full-title] Breast cancer research and treatment
  • [ISO-abbreviation] Breast Cancer Res. Treat.
  • [Language] eng
  • [Publication-type] Published Erratum
  • [Publication-country] Netherlands
  •  go-up   go-down


8. Evers B, Drost R, Schut E, de Bruin M, van der Burg E, Derksen PW, Holstege H, Liu X, van Drunen E, Beverloo HB, Smith GC, Martin NM, Lau A, O'Connor MJ, Jonkers J: Selective inhibition of BRCA2-deficient mammary tumor cell growth by AZD2281 and cisplatin. Clin Cancer Res; 2008 Jun 15;14(12):3916-25
The Lens. Cited by Patents in .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Selective inhibition of BRCA2-deficient mammary tumor cell growth by AZD2281 and cisplatin.
  • PURPOSE: To assess efficacy of the novel, selective poly(ADP-ribose) polymerase-1 (PARP-1) inhibitor AZD2281 against newly established BRCA2-deficient mouse mammary tumor cell lines and to determine potential synergy between AZD2281 and cisplatin.
  • EXPERIMENTAL DESIGN: We established and thoroughly characterized a panel of clonal cell lines from independent BRCA2-deficient mouse mammary tumors and BRCA2-proficient control tumors.
  • RESULTS: Genetic, transcriptional, and functional analyses confirmed the successful isolation of BRCA2-deficient and BRCA2-proficient mouse mammary tumor cell lines.
  • Treatment of these cell lines with 11 different anticancer drugs or with gamma-irradiation showed that AZD2281, a novel and specific PARP inhibitor, caused the strongest differential growth inhibition of BRCA2-deficient versus BRCA2-proficient mammary tumor cells.
  • Finally, drug combination studies showed synergistic cytotoxicity of AZD2281 and cisplatin against BRCA2-deficient cells but not against BRCA2-proficient control cells.
  • CONCLUSION: We have successfully established the first set of BRCA2-deficient mammary tumor cell lines, which form an important addition to the existing preclinical models for BRCA-mutated breast cancer.
  • [MeSH-major] BRCA2 Protein / genetics. Cell Proliferation / drug effects. Cisplatin / administration & dosage. Mammary Neoplasms, Animal / drug therapy. Phthalazines / administration & dosage. Piperazines / administration & dosage
  • [MeSH-minor] Animals. Antineoplastic Agents / administration & dosage. Cell Line, Tumor. DNA Damage. Drug Evaluation, Preclinical. Drug Resistance, Neoplasm / drug effects. Drug Resistance, Neoplasm / genetics. Enzyme Inhibitors / pharmacology. Female. Mice. Mice, Transgenic. Neoplastic Stem Cells / radiation effects. Poly(ADP-ribose) Polymerase Inhibitors. Rad51 Recombinase / genetics

  • Hazardous Substances Data Bank. CIS-DIAMINEDICHLOROPLATINUM .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 18559613.001).
  • [ISSN] 1078-0432
  • [Journal-full-title] Clinical cancer research : an official journal of the American Association for Cancer Research
  • [ISO-abbreviation] Clin. Cancer Res.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / BRCA2 Protein; 0 / Enzyme Inhibitors; 0 / Phthalazines; 0 / Piperazines; 0 / Poly(ADP-ribose) Polymerase Inhibitors; EC 2.7.7.- / Rad51 Recombinase; Q20Q21Q62J / Cisplatin; WOH1JD9AR8 / olaparib
  •  go-up   go-down


9. Stratmann N, Failing K, Richter A, Wehrend A: Mammary tumor recurrence in bitches after regional mastectomy. Vet Surg; 2008 Jan;37(1):82-6

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Mammary tumor recurrence in bitches after regional mastectomy.
  • OBJECTIVES: To investigate the histologic diagnosis and incidence of new mammary tumor growth in the remaining mammary chain tissue after regional mastectomy.
  • ANIMALS: Female dogs (n=99) that had excision of a single mammary tumor.
  • METHODS: Female dogs that had regional mastectomy to remove a single tumor were followed for >or=1 year postoperatively.
  • Data regarding tumor type, tumor recurrence, and development of metastasis were recorded.
  • RESULTS: Fifty-seven (58%) dogs developed a new tumor in the ipsilateral mammary chain after the 1st surgery; 77% had repeat surgery.
  • There was no significant correlation between the time to new tumor development and the histologic diagnosis for the 1st and 2nd tumor types.
  • In 31 dogs, the histologic diagnosis for initial and subsequent tumors was identical and there was a significant correlation such that dogs with an initial malignant tumor are likely to develop another malignant tumor (P=.0089).
  • The histologic classification of the new tumor was likely to be malignant if it was located close to the side where the initial tumor had been removed (P=.026).
  • CONCLUSIONS: Our results show that 58% of dogs developed a new tumor in the remaining mammary glands of the ipsilateral chain after regional mastectomy for removal of a single tumor.
  • CLINICAL RELEVANCE: This should be taken into account when deciding on the surgical management (radical or regional mastectomy) in dogs with single mammary tumors.
  • [MeSH-major] Dog Diseases / surgery. Mammary Neoplasms, Animal / surgery. Mastectomy, Segmental / veterinary. Neoplasm Recurrence, Local / veterinary. Reoperation / veterinary
  • [MeSH-minor] Animals. Disease-Free Survival. Dogs. Female. Follow-Up Studies. Incidence. Mastectomy, Radical / adverse effects. Mastectomy, Radical / methods. Mastectomy, Radical / veterinary. Prospective Studies. Time Factors. Treatment Outcome

  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 18199060.001).
  • [ISSN] 1532-950X
  • [Journal-full-title] Veterinary surgery : VS
  • [ISO-abbreviation] Vet Surg
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  •  go-up   go-down


10. Rajkumar L, Balasubramanian K, Arunakaran J, Govindarajulu P, Srinivasan N: Influence of estradiol on mammary tumor collagen solubility in DMBA-induced rat mammary tumors. Cell Biol Int; 2006 Feb;30(2):164-8
Hazardous Substances Data Bank. 7,12-DIMETHYLBENZ(A)ANTHRACENE .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Influence of estradiol on mammary tumor collagen solubility in DMBA-induced rat mammary tumors.
  • Estradiol plays a vital role in the growth and development of mammary glands.
  • A critical factor in determining mammary glandular morphology is the stroma.
  • The present investigation explored the influence of estradiol on collagen solubility and metabolism in mammary tumors during tumor progression and regression.
  • With the appearance of the first palpable mammary tumor, the rats were treated with 0.5 microg estradiol or 50 microg tamoxifen daily for 30 days.
  • Estradiol appears to stimulate the synthesis of new collagens and thus contributes to the enlargement of the mammary tumors.
  • This might have created a potential microenvironment by increasing the synthesis of suitable matrix that sustains the growth of the mammary tumors.
  • In short, the present findings emphasize a definite mediatory role for collagen in estradiol promoted mammary tumor growth.
  • [MeSH-major] 9,10-Dimethyl-1,2-benzanthracene / pharmacology. Collagen / metabolism. Estradiol / pharmacology. Mammary Neoplasms, Experimental / chemically induced. Mammary Neoplasms, Experimental / metabolism

  • Hazardous Substances Data Bank. Sodium ascorbate .
  • Hazardous Substances Data Bank. LACTIC ACID .
  • Hazardous Substances Data Bank. ESTRADIOL .
  • Hazardous Substances Data Bank. L-Ascorbic Acid .
  • Hazardous Substances Data Bank. PROGESTERONE .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 16388971.001).
  • [ISSN] 1065-6995
  • [Journal-full-title] Cell biology international
  • [ISO-abbreviation] Cell Biol. Int.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] England
  • [Chemical-registry-number] 33X04XA5AT / Lactic Acid; 4G7DS2Q64Y / Progesterone; 4TI98Z838E / Estradiol; 57-97-6 / 9,10-Dimethyl-1,2-benzanthracene; 9002-62-4 / Prolactin; 9007-34-5 / Collagen; PQ6CK8PD0R / Ascorbic Acid
  •  go-up   go-down


11. Bromley E, Owczarczak B, Keltner L, Wang S, Gollnick SO: Characterization of an antitumor immune response after light-activated drug therapy using talaporfin sodium in a spontaneously metastasizing mammary tumor model. J Clin Oncol; 2009 May 20;27(15_suppl):3052

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Characterization of an antitumor immune response after light-activated drug therapy using talaporfin sodium in a spontaneously metastasizing mammary tumor model.
  • Tumor destruction involves direct and indirect tumor kill through apoptosis, vascular occlusion, and potentially antitumor immunologic effects.
  • To provide evidence for the potential antitumor immunologic effects, we have used the therapy to treat primary tumors and examine prevention of metastases in the 4T1 tumor model, an aggressive, spontaneously metastasizing murine mammary tumor model that mirrors human breast cancer.
  • When grown in the mammary fat pad of BALB/c mice, untreated 4T1 tumors rapidly metastasize to lung, liver, lymph nodes, and brain.
  • METHODS: To confirm tumor kill by this therapy, the primary 4T1 tumors grown in mice were treated and animal survival was followed.
  • Recipients were challenged with a tumorigenic dose of 4T1 cells 3 days after adoptive transfer and primary and secondary tumor growth in the recipients was examined.
  • RESULTS: Treatment of primary tumors significantly increased survival (p≤0.01) when compared to animals treated with either light or drug alone.
  • LN cells isolated from treated mice, but not control mice, significantly inhibited primary tumor growth in recipients (p≤0.0001) and dramatically reduced the number of lung metastases present 40d after tumor challenge (p≤0.02).
  • The ability to inhibit primary and secondary tumor growth in recipients depended on the presence of CD8<sup>+</sup> T cells; depletion of CD8<sup>+</sup> T cells from the LN abolished the effect.
  • Preliminary evidence for such effect on untreated tumors has been observed in human trials of this therapy.
  • CONCLUSIONS: These results indicated that this light-activated drug therapy not only destroyed the treated tumors directly but also controlled growth of untreated tumors through induction of a specific host antitumor immune response mediated by CD8<sup>+</sup> T cells.

  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 27962000.001).
  • [ISSN] 1527-7755
  • [Journal-full-title] Journal of clinical oncology : official journal of the American Society of Clinical Oncology
  • [ISO-abbreviation] J. Clin. Oncol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  •  go-up   go-down


12. Weng S, Wu E, Kulp SK, Wang D, Chen C, Yee LD: The antitumor effects of OSU-HDAC42, a novel histone deacetylase inhibitor, in HER-2-positive breast cancer. J Clin Oncol; 2009 May 20;27(15_suppl):e14587

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • : e14587 Background: Elevated HER-2/neu expression in primary breast tumors is associated with frequent relapse and poor prognosis.
  • Tumor growth was assessed in an orthotopic HER2+ mammary tumor model, using diets ± OSU-HDAC42.
  • In vivo administration of OSU-HDAC42 resulted in reductions of 76% and 82% in NT5 (HER2+,ER-) tumor mass and volume, respectively, concomitant with tubulin hyperacetylation, increased PARP cleavage, and decreased HER2 levels in OSU-HDAC42 treated mouse tumors.

  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 27963744.001).
  • [ISSN] 1527-7755
  • [Journal-full-title] Journal of clinical oncology : official journal of the American Society of Clinical Oncology
  • [ISO-abbreviation] J. Clin. Oncol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  •  go-up   go-down


13. Marana HC, Benevides L, Tiezzi DG, Andrade JM, Brito LG, Schiavon VF, da Silva JS: Intra tumoral CD8-mediated type 1 anti-tumor responses and differentiated triple negative (TN) and HER-2 advanced breast cancer under neoadjuvant chemotherapy. J Clin Oncol; 2009 May 20;27(15_suppl):e22106

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Intra tumoral CD8-mediated type 1 anti-tumor responses and differentiated triple negative (TN) and HER-2 advanced breast cancer under neoadjuvant chemotherapy.
  • : e22106 Background: To determine the predictive value of CD8 T cells tumor infiltrated lymphocytes (TIL) for treatment response in locally advanced breast cancer (LABC) primarily submitted to neoadjuvant chemotherapy.
  • RESULTS: Univariate analysis showed that CD8 T cell, FoxP3 and production of IFN-γ are more pronounced in Triple Negative (TN) tumor (39±4.1%, 44,15±11.2% and 17.66±9.18% respectivilly) than HER-2 tumor (30.2±3.4%; 31,7±2.62% and 9.69±6.07%) and this difference was not significantly changed by the neoadjuvant chemotherapy.
  • CONCLUSIONS: The results suggest that mammary tumor growth and progression were dependent, in part, on effector cell-derived IFN-γ.
  • Here we postulated that this condition was associated to response to neoadjuvante chemotherapy and was distinct expressed by different gene type of tumor breast.
  • This suggested that CD8-mediated type 1 antitumor responses cannot only promote accumulation of distinct endogenous CD8 T cell subpopulations, but also facilitate and preferentially modulate their localization kinetics, persistence, states of activation/differentiation, and function within the primary tumor environment of tumor response/regression.
  • The TN tumor was more chemo-sensitive and had high IFN-γ production.
  • The action way could be done by CD44 high, FoxP3 and TGFβ<sub>1</sub> and the activatioin of Treg in TIL that help in the tumor progression.
  • The chemotherapy breaks this and facilitated the tumor regression.

  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 27963503.001).
  • [ISSN] 1527-7755
  • [Journal-full-title] Journal of clinical oncology : official journal of the American Society of Clinical Oncology
  • [ISO-abbreviation] J. Clin. Oncol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  •  go-up   go-down


14. Song Y, Aglipay JA, Bernstein JD, Goswami S, Stanley P: The bisecting GlcNAc on N-glycans inhibits growth factor signaling and retards mammary tumor progression. Cancer Res; 2010 Apr 15;70(8):3361-71
Mouse Genome Informatics (MGI). Mouse Genome Informatics (MGI) .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] The bisecting GlcNAc on N-glycans inhibits growth factor signaling and retards mammary tumor progression.
  • The branching of complex N-glycans attached to growth factor receptors promotes tumor progression by prolonging growth factor signaling.
  • The Mgat3 gene is not expressed in virgin mammary gland but is upregulated during lactation and is expressed in mouse mammary tumor virus (MMTV)/PyMT tumors.
  • Mice lacking Mgat3 that cannot transfer the bisecting GlcNAc to N-glycans acquire PyMT-induced mammary tumors more rapidly and have an increased tumor burden, increased migration of tumor cells, and increased early metastasis to lung.
  • Tumors and tumor-derived cells lacking Mgat3 exhibit enhanced signaling through the Ras pathway and reduced amounts of functionally glycosylated alpha-dystroglycan.
  • Constitutive overexpression of an MMTV/Mgat3 transgene inhibits early mammary tumor development and tumor cell migration.
  • Thus, the addition of the bisecting GlcNAc to complex N-glycans of mammary tumor cell glycoprotein receptors is a cell autonomous mechanism serving to retard tumor progression by reducing growth factor signaling.

  • KOMP Repository. gene/protein/disease-specific - KOMP Repository (subscription/membership/fee required).
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [Copyright] (c) 2010 AACR.
  • [Cites] Nat Med. 2000 Mar;6(3):306-12 [10700233.001]
  • [Cites] J Biol Chem. 2010 Feb 19;285(8):5759-75 [19951948.001]
  • [Cites] Cancer Res. 2000 Jun 15;60(12):3313-9 [10866326.001]
  • [Cites] Cancer Res. 2000 Oct 1;60(19):5401-4 [11034079.001]
  • [Cites] J Biol Chem. 2001 Apr 13;276(15):11956-62 [11134020.001]
  • [Cites] J Biol Chem. 2002 Jul 19;277(29):26300-9 [11986323.001]
  • [Cites] Breast Cancer. 2002;9(3):208-15 [12185331.001]
  • [Cites] Free Radic Res. 2002 Aug;36(8):827-33 [12420740.001]
  • [Cites] Nat Rev Cancer. 2002 Dec;2(12):951-6 [12459733.001]
  • [Cites] Cancer Res. 2003 May 1;63(9):2179-87 [12727837.001]
  • [Cites] Am J Pathol. 2003 Nov;163(5):2113-26 [14578209.001]
  • [Cites] Cancer Res. 2003 Nov 15;63(22):7753-9 [14633700.001]
  • [Cites] J Biol Chem. 2004 May 7;279(19):19747-54 [14998999.001]
  • [Cites] Cancer Res. 2004 Sep 1;64(17):5973-81 [15342376.001]
  • [Cites] Science. 2004 Oct 1;306(5693):120-4 [15459394.001]
  • [Cites] Cancer Res. 2004 Oct 1;64(19):7022-9 [15466195.001]
  • [Cites] J Biol Chem. 1982 Sep 10;257(17):10235-42 [6213618.001]
  • [Cites] J Biol Chem. 1984 Nov 10;259(21):13370-8 [6238035.001]
  • [Cites] Mol Cell Biol. 1992 Mar;12(3):954-61 [1312220.001]
  • [Cites] Proc Natl Acad Sci U S A. 1995 Sep 12;92(19):8754-8 [7568011.001]
  • [Cites] Cancer Res. 1996 Jan 15;56(2):412-8 [8542600.001]
  • [Cites] J Biol Chem. 1996 Jun 7;271(23):13811-5 [8662832.001]
  • [Cites] Glycobiology. 1997 Feb;7(1):45-56 [9061364.001]
  • [Cites] Genes Chromosomes Cancer. 1998 Feb;21(2):108-12 [9491321.001]
  • [Cites] Glycobiology. 2005 Jan;15(1):43-53 [15329358.001]
  • [Cites] J Mol Med (Berl). 2005 May;83(5):362-76 [15662539.001]
  • [Cites] J Biol Chem. 2005 May 27;280(21):20851-9 [15788414.001]
  • [Cites] Oncogene. 2005 Aug 4;24(33):5173-90 [15897883.001]
  • [Cites] Glycobiology. 2006 Apr;16(4):305-17 [16319083.001]
  • [Cites] J Biol Chem. 2006 May 12;281(19):13038-46 [16537539.001]
  • [Cites] J Clin Invest. 2006 Jun;116(6):1561-70 [16741576.001]
  • [Cites] Methods Enzymol. 2006;416:159-82 [17113866.001]
  • [Cites] Curr Med Chem. 2007;14(7):735-43 [17346159.001]
  • [Cites] Transgenic Res. 2007 Apr;16(2):193-201 [17206489.001]
  • [Cites] Cell. 2007 Apr 6;129(1):123-34 [17418791.001]
  • [Cites] J Pathol. 2007 Jul;212(3):306-15 [17534844.001]
  • [Cites] BMC Genomics. 2007;8:183 [17584498.001]
  • [Cites] FEBS J. 2008 May;275(9):1939-48 [18384383.001]
  • [Cites] Proteomics. 2008 Aug;8(16):3210-20 [18690643.001]
  • [Cites] Proteomics. 2008 Aug;8(16):3221-8 [18690644.001]
  • [Cites] Glycobiology. 2009 Jan;19(1):68-75 [18849326.001]
  • [Cites] Glycobiology. 2009 May;19(5):547-59 [19225046.001]
  • [Cites] Curr Opin Cell Biol. 2009 Apr;21(2):177-84 [19208461.001]
  • [Cites] J Biol Chem. 2009 Apr 24;284(17):11279-84 [19244252.001]
  • [Cites] J Cell Biol. 2009 May 4;185(3):381-5 [19398762.001]
  • [Cites] Proc Natl Acad Sci U S A. 2009 Jul 21;106(29):12109-14 [19587235.001]
  • [Cites] Carbohydr Res. 2009 Aug 17;344(12):1387-90 [19508951.001]
  • [Cites] Traffic. 2009 Nov;10(11):1569-78 [19761541.001]
  • [Cites] FEBS Lett. 2000 Mar 31;470(3):263-8 [10745079.001]
  • (PMID = 20395209.001).
  • [ISSN] 1538-7445
  • [Journal-full-title] Cancer research
  • [ISO-abbreviation] Cancer Res.
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / P30CA013330; United States / NCI NIH HHS / CA / CA030645-25A1; United States / NCI NIH HHS / CA / CA030645-28; United States / NCI NIH HHS / CA / R01 CA030645-27; United States / NCI NIH HHS / CA / CA030645-27; United States / NCI NIH HHS / CA / R01 CA030645-29; United States / PHS HHS / / R0136434; United States / NCI NIH HHS / CA / R01 CA030645; United States / NCI NIH HHS / CA / CA030645-29; United States / NCI NIH HHS / CA / CA030645-26; United States / NCI NIH HHS / CA / R01 CA030645-28; United States / NCI NIH HHS / CA / R01 CA030645-25A1; United States / NCI NIH HHS / CA / P30 CA013330; United States / NCI NIH HHS / CA / R01 CA030645-26; United States / PHS HHS / / R0130645
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Intercellular Signaling Peptides and Proteins; 0 / Polysaccharides; 146888-27-9 / Dystroglycans; EC 2.4.1.- / N-Acetylglucosaminyltransferases; EC 2.4.1.144 / beta-1,4-mannosyl-glycoprotein beta-1,4-N-acetylglucosaminyltransferase; V956696549 / Acetylglucosamine
  • [Other-IDs] NLM/ NIHMS176591; NLM/ PMC2856092
  • [Keywords] NOTNLM ; LEC10 / MMTV/PyMT mammary tumors / Mgat3 / bisecting GlcNAc / invasion / metastasis
  •  go-up   go-down


15. Hubbard NE, Lim D, Erickson KL: Beef tallow increases the potency of conjugated linoleic acid in the reduction of mouse mammary tumor metastasis. J Nutr; 2006 Jan;136(1):88-93
The Lens. Cited by Patents in .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Beef tallow increases the potency of conjugated linoleic acid in the reduction of mouse mammary tumor metastasis.
  • Animal studies consistently show that dietary conjugated linoleic acid (CLA) reduces mammary tumorigenesis including metastasis.
  • We reasoned that the concentration of CLA required to effectively alter mammary tumor metastasis may be dependent on the type of dietary fat because select fatty acids can enhance or suppress normal or malignant cell growth and metastasis.
  • For this study, the diets (a total of 12 different groups) differed in fatty acid composition but not in energy from fat (40%).
  • In experiments involving spontaneous metastasis, mice were fed for 11 wk; in experiments in which mice were injected i.v. with tumor cells, they were fed for 7 wk.
  • Mice were then assessed for the effect of CLA concentration on mammary tumorigenesis.
  • Mammary tumor growth was not altered, but metastasis was significantly decreased when beef tallow (BT) replaced half of a defined vegetable fat blend (VFB).
  • In addition, that same VFB:BT diet lowered the concentration of CLA required to significantly decrease mammary tumor metastasis from 0.1% of the diet to 0.05%.
  • A diet in which corn oil replaced half of the VFB did not lower the threshold from 0.1 to 0.05%.
  • In vitro, the main fatty acid in vegetable oil, linoleic acid, reduced the efficacy of CLA toxicity on mammary tumor cells in culture.
  • Alternatively, fatty acids normally found in BT, such as oleic, stearic, and palmitic acids, either did not change or enhanced the cytolytic effects of CLA isomers on mouse mammary tumor cells in culture.
  • These data provide evidence that dietary BT, itself with negligible levels of CLA, may increase the efficacy of dietary CLA in reducing mammary tumorigenesis.
  • [MeSH-major] Dietary Fats / therapeutic use. Fats / pharmacology. Linoleic Acids, Conjugated / therapeutic use. Mammary Neoplasms, Experimental / drug therapy. Neoplasm Metastasis / prevention & control

  • MedlinePlus Health Information. consumer health - Dietary Fats.
  • COS Scholar Universe. author profiles.
  • Hazardous Substances Data Bank. TALLOW .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 16365064.001).
  • [ISSN] 0022-3166
  • [Journal-full-title] The Journal of nutrition
  • [ISO-abbreviation] J. Nutr.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Dietary Fats; 0 / Fats; 0 / Linoleic Acids, Conjugated; 61789-97-7 / tallow
  •  go-up   go-down


16. Singh MK, Izumchenko E, Klein-Szanto AJ, Egleston BL, Wolfson M, Golemis EA: Enhanced genetic instability and dasatinib sensitivity in mammary tumor cells lacking NEDD9. Cancer Res; 2010 Nov 1;70(21):8907-16
NCI CPTC Antibody Characterization Program. NCI CPTC Antibody Characterization Program .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Enhanced genetic instability and dasatinib sensitivity in mammary tumor cells lacking NEDD9.
  • Elevated expression of the NEDD9/HEF1/Cas-L scaffolding protein promotes tumor cell invasion and metastasis in multiple cancer cell types.
  • Conversely, generation of mammary tumors in the mouse mammary tumor virus (MMTV)-polyoma virus middle T (PyVT) genetic model is delayed by a Nedd9(-/-) genotype.
  • These activities arise from the role of NEDD9 in assembling complexes and supporting activity of cancer signaling proteins, including FAK, Src, Shc, and AKT, and would support evaluation of NEDD9 expression as an unambiguous biomarker for tumor aggressiveness.
  • However, we here show that despite the initial delay in tumor growth, cells derived from MMTV-PyVT;Nedd9(-/-) tumors are characteristically hyperaggressive versus MMTV-PyVT;Nedd9(+/+) cells in anchorage-independent growth, in growth on three-dimensional matrix produced by tumor-associated fibroblasts, and in formation of tumors after mammary orthotopic reinjection and of lung metastases after tail vein injection.
  • These studies identify NEDD9 as a complex modulator of different aspects of mammary tumor growth.

  • MedlinePlus Health Information. consumer health - Lung Cancer.
  • COS Scholar Universe. author profiles.
  • KOMP Repository. gene/protein/disease-specific - KOMP Repository (subscription/membership/fee required).
  • Mouse Genome Informatics (MGI). Mouse Genome Informatics (MGI) .
  • NCI CPTAC Assay Portal. NCI CPTAC Assay Portal .
  • NCI CPTAC Assay Portal. NCI CPTAC Assay Portal .
  • NCI CPTAC Assay Portal. NCI CPTAC Assay Portal .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [Copyright] ©2010 AACR.
  • [Cites] Cancer Res. 2010 Mar 15;70(6):2296-306 [20215510.001]
  • [Cites] Oncogene. 2009 Oct 15;28(41):3642-51 [19648964.001]
  • [Cites] EMBO J. 2000 Dec 15;19(24):6759-69 [11118211.001]
  • [Cites] Cell Mol Life Sci. 2010 Apr;67(7):1025-48 [19937461.001]
  • [Cites] Mol Cell Biol. 2001 Aug;21(15):5094-108 [11438665.001]
  • [Cites] Eur J Immunol. 2001 May;31(5):1417-27 [11465098.001]
  • [Cites] J Cell Sci. 2002 Jan 1;115(Pt 1):99-111 [11801728.001]
  • [Cites] Cell. 2003 Sep 5;114(5):585-98 [13678582.001]
  • [Cites] Mol Cell. 2003 Oct;12(4):851-62 [14580337.001]
  • [Cites] J Med Chem. 2004 Dec 30;47(27):6658-61 [15615512.001]
  • [Cites] Nat Rev Cancer. 2005 Jan;5(1):42-50 [15630414.001]
  • [Cites] Am J Pathol. 2005 Aug;167(2):475-88 [16049333.001]
  • [Cites] Nature. 2005 Jul 28;436(7050):518-24 [16049480.001]
  • [Cites] Nat Cell Biol. 2005 Oct;7(10):937-46 [16184168.001]
  • [Cites] Mol Biol Cell. 2006 Mar;17(3):1204-17 [16394104.001]
  • [Cites] Cell Cycle. 2006 Feb;5(4):384-91 [16479169.001]
  • [Cites] Oncogene. 2006 Mar 16;25(12):1721-32 [16288224.001]
  • [Cites] Cell. 2006 Jun 30;125(7):1269-81 [16814714.001]
  • [Cites] Cancer Res. 2007 Mar 1;67(5):2226-38 [17332353.001]
  • [Cites] Mol Cancer Ther. 2007 Mar;6(3):898-906 [17363484.001]
  • [Cites] Cell. 2007 Jun 29;129(7):1351-63 [17604723.001]
  • [Cites] Nature. 2007 Aug 16;448(7155):807-10 [17676035.001]
  • [Cites] Breast Cancer Res Treat. 2007 Nov;105(3):319-26 [17268817.001]
  • [Cites] Cancer Res. 2007 Oct 1;67(19):8975-9 [17908996.001]
  • [Cites] Matrix Biol. 2008 Jul;27(6):573-85 [18411046.001]
  • [Cites] Nat Cell Biol. 2008 Sep;10(9):1027-38 [19160483.001]
  • [Cites] Methods Mol Biol. 2009;522:275-305 [19247611.001]
  • [Cites] Cancer Metastasis Rev. 2009 Jun;28(1-2):185-95 [19189202.001]
  • [Cites] Cancer Res. 2009 Sep 15;69(18):7198-206 [19738060.001]
  • [Cites] Oncogene. 2010 Aug 5;29(31):4449-59 [20498643.001]
  • (PMID = 20940402.001).
  • [ISSN] 1538-7445
  • [Journal-full-title] Cancer research
  • [ISO-abbreviation] Cancer Res.
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / R01 CA063366; United States / NCI NIH HHS / CA / R01 CA113342; United States / NCI NIH HHS / CA / R01-CA63366; United States / NCI NIH HHS / CA / R01-CA113342; United States / NCI NIH HHS / CA / P30 CA006927; United States / NCI NIH HHS / CA / CA-06927
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't; Research Support, U.S. Gov't, Non-P.H.S.
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Adaptor Proteins, Signal Transducing; 0 / NEDD9 protein, mouse; 0 / Protein Kinase Inhibitors; 0 / Pyrimidines; 0 / Thiazoles; EC 2.7.10.1 / Protein-Tyrosine Kinases; EC 2.7.10.2 / src-Family Kinases; EC 2.7.11.1 / Aurora Kinases; EC 2.7.11.1 / Protein-Serine-Threonine Kinases; EC 2.7.11.1 / Proto-Oncogene Proteins c-akt; RBZ1571X5H / Dasatinib
  • [Other-IDs] NLM/ NIHMS236112; NLM/ PMC2970659
  •  go-up   go-down


17. Schoeffner DJ, Matheny SL, Akahane T, Factor V, Berry A, Merlino G, Thorgeirsson UP: VEGF contributes to mammary tumor growth in transgenic mice through paracrine and autocrine mechanisms. Lab Invest; 2005 May;85(5):608-23
The Lens. Cited by Patents in .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] VEGF contributes to mammary tumor growth in transgenic mice through paracrine and autocrine mechanisms.
  • To address its role in mammary carcinogenesis, we used transgenic mice with human VEGF(165) targeted to mammary epithelial cells under the control of the mouse mammary tumor virus (MMTV) promoter.
  • Metastatic mammary carcinomas were induced by mating the MMTV-VEGF mice with MMTV-polyoma virus middle T-antigen (MT) mice to generate VEGF/MT mice.
  • Tumor latency was decreased in the VEGF/MT mice, which developed mammary carcinomas with increased vasodilatation at 4 weeks of age.
  • There was increased incidence, multiplicity, and weight of the mammary tumors in 6- and 8-week-old VEGF/MT mice, compared to their MT-only littermates.
  • Macro- and microscopic lung metastases were detected in the VEGF/MT mice but not the MT mice at 6 and 8 weeks of age.
  • Enhanced tumor growth was attributed to increased microvascular density (MVD), as well as increased tumor cell proliferation and survival.
  • Angiogenesis array analysis showed that 24 of 25 differentially expressed genes were upregulated in the VEGF/MT tumors.
  • In vitro studies revealed increased proliferative activity and upregulation of Flk-1 in the VEGF/MT tumor cells, compared with the MT-only tumor cells.
  • Moreover, there was decreased proliferative activity with downregulation of Flk-1 in tumor cells isolated from conditional knockout (VEGF(-/-)) MT-induced mammary carcinomas.
  • The slow growing VEGF(-/-) tumor cells were accumulated in the G(1)/G(0) phase of the cell cycle and this was associated with stimulation of p16(ink4a) and p21(WAF1).
  • Similarly, p16(ink4a) was stimulated in VEGF(lox/lox)/MT mammary tumor cells following Adeno-cre-mediated VEGF gene inactivation.
  • Collectively, the data from these transgenic models indicate that VEGF contributes to mammary tumor growth through increased neovascularization, as well as autocrine stimulation of growth and inhibition of apoptosis.
  • [MeSH-major] Adenocarcinoma / genetics. Mammary Neoplasms, Animal / genetics. Vascular Endothelial Growth Factor A / genetics
  • [MeSH-minor] Animals. Apoptosis / genetics. Blotting, Northern. Cell Cycle Proteins / genetics. Cell Proliferation. Cyclin-Dependent Kinase Inhibitor p21. Female. Genes, p16. Immunohistochemistry. Lung Neoplasms / genetics. Lung Neoplasms / metabolism. Lung Neoplasms / secondary. Male. Mice. Mice, Knockout. Mice, Transgenic. Oligonucleotide Array Sequence Analysis. RNA, Messenger / metabolism. RNA, Neoplasm / analysis. Reverse Transcriptase Polymerase Chain Reaction. Up-Regulation. Vascular Endothelial Growth Factor Receptor-2 / genetics. Vascular Endothelial Growth Factor Receptor-2 / metabolism

  • COS Scholar Universe. author profiles.
  • KOMP Repository. gene/protein/disease-specific - KOMP Repository (subscription/membership/fee required).
  • Mouse Genome Informatics (MGI). Mouse Genome Informatics (MGI) .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 15765121.001).
  • [ISSN] 0023-6837
  • [Journal-full-title] Laboratory investigation; a journal of technical methods and pathology
  • [ISO-abbreviation] Lab. Invest.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Cdkn1a protein, mouse; 0 / Cell Cycle Proteins; 0 / Cyclin-Dependent Kinase Inhibitor p21; 0 / RNA, Messenger; 0 / RNA, Neoplasm; 0 / Vascular Endothelial Growth Factor A; 0 / vascular endothelial growth factor A, mouse; EC 2.7.10.1 / Vascular Endothelial Growth Factor Receptor-2
  •  go-up   go-down


18. Hammamieh R, Anderson M, Carr K, Tran CN, Yourick DL, Jett M: Students investigating the antiproliferative effects of synthesized drugs on mouse mammary tumor cells. Cell Biol Educ; 2005;4(3):221-34
NCI CPTAC Assay Portal. NCI CPTAC Assay Portal .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Students investigating the antiproliferative effects of synthesized drugs on mouse mammary tumor cells.
  • Personalized cancer treatments based on a tumor's genetic profile are now feasible and can reveal both the cells' susceptibility and resistance to chemotherapeutic agents.
  • Using mouse mammary tumor cell cultures treated with "unknown" drugs historically recommended for breast cancer treatment, students are introduced to common molecular biology techniques from in vitro cell culture to fluorescence microscopy.

  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [Cites] Mol Cancer Ther. 2002 Sep;1(11):929-35 [12481414.001]
  • [Cites] Nature. 2001 May 17;411(6835):342-8 [11357141.001]
  • [Cites] Front Biosci. 2003 May 1;8:s718-21 [12700125.001]
  • [Cites] Integr Cancer Ther. 2002 Mar;1(1):7-37; discussion 37 [14664746.001]
  • [Cites] J Cell Biochem. 2004 Mar 1;91(4):796-807 [14991771.001]
  • [Cites] Toxicon. 2002 Dec;40(12):1701-8 [12457882.001]
  • [Cites] J Exp Clin Cancer Res. 2002 Sep;21(3 Suppl):9-12 [12585647.001]
  • [Cites] Acta Pol Pharm. 2002 Nov-Dec;59(6):473-8 [12669776.001]
  • [Cites] Anticancer Drug Des. 2001 Dec;16(6):261-70 [12375879.001]
  • [Cites] Sci Am. 1999 Feb;280(2):19, 22 [9924811.001]
  • [Cites] Anticancer Drugs. 1997 Jun;8(5):470-81 [9215611.001]
  • [Cites] Arch Intern Med. 1997 Apr 28;157(8):913-9 [9129552.001]
  • [Cites] Oncologist. 2004;9(4):378-84 [15266091.001]
  • [Cites] J Ky Med Assoc. 2004 May;102(5):202-8 [15152445.001]
  • (PMID = 16220143.001).
  • [ISSN] 1536-7509
  • [Journal-full-title] Cell biology education
  • [ISO-abbreviation] Cell Biol Educ
  • [Language] ENG
  • [Grant] United States / NCRR NIH HHS / RR / R25 RR015629; United States / NCRR NIH HHS / RR / R25 RR018619; United States / NCRR NIH HHS / RR / 1R25RR018619-01; United States / NCRR NIH HHS / RR / 5R25RR15629-01
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, U.S. Gov't, P.H.S.
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antineoplastic Agents
  • [Other-IDs] NLM/ PMC1200777
  •  go-up   go-down


19. Cardiff RD, Kenney N: Mouse mammary tumor biology: a short history. Adv Cancer Res; 2007;98:53-116
NCI CPTC Antibody Characterization Program. NCI CPTC Antibody Characterization Program .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Mouse mammary tumor biology: a short history.
  • For over a century, mouse mammary tumor biology and the associated Mouse mammary tumor virus (MMTV) have served as the foundation for experimental cancer research, in general, and, in particular, experimental breast cancer research.
  • Spontaneous mouse mammary tumors were the basis for studies of the natural history of neoplasia, oncogenic viruses, host responses, endocrinology, and neoplastic progression.
  • However, lacking formal proof of a human mammary tumor virus, the preeminence of the mouse model faded in the 1980s.
  • Since the late 1980s, genetically engineered mice (GEM) have proven extremely useful for studying breast cancer and have become the animal model for human breast cancer.
  • Hundreds of mouse models of human breast cancer have been developed since the first demonstration, in 1984, that the mouse mammary gland could be molecularly targeted and used to test the oncogenicity of candidate human genes.
  • The GEM have attracted a new generation of molecular and cellular biologists eager to apply their skills to these surrogates of the human disease.
  • Newcomers often enter the field without an appreciation of the origins of mouse mammary tumor biology and the basis for many of the prevailing concepts.
  • Our purpose in writing this short history of mouse mammary tumor biology is to provide a historical perspective for the benefit of the newcomers.
  • [MeSH-major] Mammary Neoplasms, Experimental / history. Mammary Tumor Virus, Mouse / isolation & purification. Retroviridae Infections / history. Tumor Virus Infections / history
  • [MeSH-minor] Animals. Cell Transformation, Neoplastic. Disease Models, Animal. History, 20th Century. History, 21st Century. Mice

  • COS Scholar Universe. author profiles.
  • Mouse Genome Informatics (MGI). Mouse Genome Informatics (MGI) .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 17433908.001).
  • [ISSN] 0065-230X
  • [Journal-full-title] Advances in cancer research
  • [ISO-abbreviation] Adv. Cancer Res.
  • [Language] eng
  • [Publication-type] Historical Article; Journal Article; Portraits; Review
  • [Publication-country] United States
  • [Number-of-references] 329
  •  go-up   go-down


20. Provenzano PP, Inman DR, Eliceiri KW, Knittel JG, Yan L, Rueden CT, White JG, Keely PJ: Collagen density promotes mammary tumor initiation and progression. BMC Med; 2008 Apr 28;6:11
Mouse Genome Informatics (MGI). Mouse Genome Informatics (MGI) .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Collagen density promotes mammary tumor initiation and progression.
  • Despite the strong clinical correlation, breast density has not been causally linked to tumorigenesis, largely because no animal model has existed for studying breast tissue density.
  • Thus, the influence of the extracellular matrix on breast carcinoma development and the underlying molecular mechanisms are not understood.
  • METHODS: To study the effects of collagen density on mammary tumor formation and progression, we utilized a bi-transgenic tumor model with increased stromal collagen in mouse mammary tissue.
  • Imaging of the tumors and tumor-stromal interface in live tumor tissue was performed with multiphoton laser-scanning microscopy to generate multiphoton excitation and spectrally resolved fluorescent lifetimes of endogenous fluorophores.
  • RESULTS: Herein we demonstrate that increased stromal collagen in mouse mammary tissue significantly increases tumor formation approximately three-fold (p < 0.00001) and results in a significantly more invasive phenotype with approximately three times more lung metastasis (p < 0.05).
  • Furthermore, the increased invasive phenotype of tumor cells that arose within collagen-dense mammary tissues remains after tumor explants are cultured within reconstituted three-dimensional collagen gels.
  • To better understand this behavior we imaged live tumors using nonlinear optical imaging approaches to demonstrate that local invasion is facilitated by stromal collagen re-organization and that this behavior is significantly increased in collagen-dense tissues.
  • CONCLUSION: This study provides the first data causally linking increased stromal collagen to mammary tumor formation and metastasis, and demonstrates that fundamental differences arise and persist in epithelial tumor cells that progressed within collagen-dense microenvironments.

  • COS Scholar Universe. author profiles.
  • KOMP Repository. gene/protein/disease-specific - KOMP Repository (subscription/membership/fee required).
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [Cites] JAMA. 2001 Jan 10;285(2):171-6 [11176809.001]
  • [Cites] Curr Opin Genet Dev. 2001 Feb;11(1):54-9 [11163151.001]
  • [Cites] Curr Oncol Rep. 2001 Jul;3(4):314-21 [11389815.001]
  • [Cites] Endocr Relat Cancer. 2001 Sep;8(3):197-209 [11566611.001]
  • [Cites] Cancer Res. 2001 Oct 1;61(19):7079-90 [11585739.001]
  • [Cites] Biophys J. 2002 May;82(5):2811-25 [11964266.001]
  • [Cites] Proc Natl Acad Sci U S A. 2002 Aug 20;99(17):11014-9 [12177437.001]
  • [Cites] N Engl J Med. 2002 Sep 19;347(12):886-94 [12239257.001]
  • [Cites] Br J Cancer. 2002 Oct 7;87(8):876-82 [12373602.001]
  • [Cites] Cancer Res. 2002 Nov 1;62(21):6278-88 [12414658.001]
  • [Cites] Nat Med. 2003 Jun;9(6):796-800 [12754503.001]
  • [Cites] Breast Cancer Res. 2003;5(3):130-5 [12793893.001]
  • [Cites] Proc Natl Acad Sci U S A. 2003 Jun 10;100(12):7075-80 [12756303.001]
  • [Cites] J Pathol. 2003 Jul;200(4):429-47 [12845611.001]
  • [Cites] J Photochem Photobiol B. 1995 Dec;31(3):101-12 [8583278.001]
  • [Cites] J Biol Chem. 1998 Mar 20;273(12):7162-8 [9507031.001]
  • [Cites] Cancer Epidemiol Biomarkers Prev. 1998 Dec;7(12):1133-44 [9865433.001]
  • [Cites] J Cell Sci. 1999 Mar;112 ( Pt 5):695-706 [9973604.001]
  • [Cites] J Urol. 2005 Jan;173(1):10-20 [15592017.001]
  • [Cites] Biophys J. 2005 Feb;88(2):1377-86 [15533922.001]
  • [Cites] Cancer Epidemiol Biomarkers Prev. 2005 Feb;14(2):343-9 [15734956.001]
  • [Cites] Cancer Epidemiol Biomarkers Prev. 2005 Mar;14(3):662-8 [15767347.001]
  • [Cites] J Clin Invest. 2005 May;115(5):1163-76 [15841211.001]
  • [Cites] Cell. 2005 May 6;121(3):335-48 [15882617.001]
  • [Cites] Breast Cancer Res. 2005;7(5):R605-8 [16168104.001]
  • [Cites] Cancer Cell. 2005 Sep;8(3):241-54 [16169468.001]
  • [Cites] Lancet Oncol. 2005 Oct;6(10):798-808 [16198986.001]
  • [Cites] Annu Rev Cell Dev Biol. 2005;21:695-718 [16212512.001]
  • [Cites] J Cell Biol. 2005 Nov 7;171(3):505-16 [16275754.001]
  • [Cites] Cancer Res. 2006 Jan 15;66(2):794-802 [16424011.001]
  • [Cites] Cancer Res. 2006 May 15;66(10):5216-23 [16707446.001]
  • [Cites] Cancer Epidemiol Biomarkers Prev. 2006 Jun;15(6):1159-69 [16775176.001]
  • [Cites] Breast Cancer Res. 2006;8(2):R24 [16646977.001]
  • [Cites] Breast Cancer Res. 2006;8(3):R30 [16796758.001]
  • [Cites] Biotechniques. 2006 Sep;41(3):249, 251, 253 passim [16989084.001]
  • [Cites] Nat Neurosci. 2006 Nov;9(11):1382-7 [17041593.001]
  • [Cites] BMC Med. 2006;4(1):38 [17190588.001]
  • [Cites] Proc Natl Acad Sci U S A. 2007 Dec 4;104(49):19494-9 [18042710.001]
  • [Cites] J Biomed Opt. 2008 May-Jun;13(3):031220 [18601544.001]
  • [Cites] J Mammary Gland Biol Neoplasia. 2000 Jan;5(1):95-105 [10791772.001]
  • [Cites] Nat Cell Biol. 2000 May;2(5):249-56 [10806474.001]
  • [Cites] Breast Cancer Res. 2003;5(5):R129-35 [12927043.001]
  • [Cites] Am J Pathol. 2003 Nov;163(5):2113-26 [14578209.001]
  • [Cites] J Cell Biol. 2003 Nov 10;163(3):583-95 [14610060.001]
  • [Cites] Clin Cancer Res. 2004 Jan 1;10(1 Pt 1):202-11 [14734471.001]
  • [Cites] Traffic. 2004 Jun;5(6):411-7 [15117315.001]
  • [Cites] Cancer Cell. 2004 Jul;6(1):17-32 [15261139.001]
  • [Cites] Cancer Cell. 2004 Aug;6(2):159-70 [15324699.001]
  • [Cites] Cancer Cell. 2004 Sep;6(3):209-14 [15380511.001]
  • [Cites] J Natl Cancer Inst. 2004 Oct 6;96(19):1467-72 [15467036.001]
  • [Cites] Appl Opt. 2004 Sep 20;43(27):5173-82 [15473237.001]
  • [Cites] J Biochem. 1984 Sep;96(3):683-90 [6548741.001]
  • [Cites] Development. 1989 Feb;105(2):223-35 [2806122.001]
  • [Cites] J Cell Sci. 1995 Feb;108 ( Pt 2):595-607 [7769004.001]
  • [Cites] J Cell Biol. 1995 Jul;130(1):227-37 [7790374.001]
  • [Cites] J Mammary Gland Biol Neoplasia. 1998 Apr;3(2):215-25 [10819529.001]
  • [Cites] Cancer Res. 2000 Jul 15;60(14):3744-8 [10919644.001]
  • [Cites] Genes Dev. 2001 Jan 1;15(1):50-65 [11156605.001]
  • [Cites] Cancer Epidemiol Biomarkers Prev. 2001 Mar;10(3):243-8 [11303594.001]
  • (PMID = 18442412.001).
  • [ISSN] 1741-7015
  • [Journal-full-title] BMC medicine
  • [ISO-abbreviation] BMC Med
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / R01 CA076537; United States / NIBIB NIH HHS / EB / R01 EB000184; United States / NCI NIH HHS / CA / R01-CA076537; United States / NIBIB NIH HHS / EB / R01-EB000184
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't; Research Support, U.S. Gov't, Non-P.H.S.
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Collagen Type I; 0 / collagen type I, alpha 1 chain
  • [Other-IDs] NLM/ PMC2386807
  •  go-up   go-down


21. Hsu WL, Lin HY, Chiou SS, Chang CC, Wang SP, Lin KH, Chulakasian S, Wong ML, Chang SC: Mouse mammary tumor virus-like nucleotide sequences in canine and feline mammary tumors. J Clin Microbiol; 2010 Dec;48(12):4354-62
NCI CPTAC Assay Portal. NCI CPTAC Assay Portal .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Mouse mammary tumor virus-like nucleotide sequences in canine and feline mammary tumors.
  • Mouse mammary tumor virus (MMTV) has been speculated to be involved in human breast cancer.
  • The aim of this study was to detect MMTV-like nucleotide sequences in canine and feline mammary tumors by nested PCR.
  • Results showed that the presence of MMTV-like env and LTR sequences in canine malignant mammary tumors was 3.49% (3/86) and 18.60% (16/86), respectively.
  • For feline malignant mammary tumors, the presence of both env and LTR sequences was found to be 22.22% (2/9).
  • Nevertheless, the MMTV-like LTR and env sequences also were detected in normal mammary glands of dogs and cats.
  • Taken together, our study provides evidence for the existence and expression of MMTV-like sequences in neoplastic and normal mammary glands of dogs and cats.
  • [MeSH-major] Cat Diseases / virology. Dog Diseases / virology. Mammary Glands, Animal / virology. Mammary Neoplasms, Animal / virology. Mammary Tumor Virus, Mouse / isolation & purification. RNA, Viral / isolation & purification

  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [Cites] Nat Genet. 2007 Jun;39(6):759-69 [17468756.001]
  • [Cites] J Gen Virol. 2007 Jun;88(Pt 6):1806-9 [17485542.001]
  • [Cites] J Virol. 2008 Feb;82(4):1808-18 [18077721.001]
  • [Cites] Vet Immunol Immunopathol. 2008 May 15;123(1-2):159-66 [18299153.001]
  • [Cites] J Med Virol. 2008 Aug;80(8):1447-51 [18551605.001]
  • [Cites] Cancer Lett. 2008 Nov 28;271(2):222-30 [18639977.001]
  • [Cites] Vet J. 2009 Apr;180(1):116-23 [18061495.001]
  • [Cites] J Am Vet Med Assoc. 2009 Aug 15;235(4):391-6 [19681719.001]
  • [Cites] Br J Cancer. 2000 Jan;82(2):446-51 [10646903.001]
  • [Cites] Oncogene. 2000 Feb 21;19(8):992-1001 [10713682.001]
  • [Cites] Clin Cancer Res. 2000 Apr;6(4):1273-8 [10778951.001]
  • [Cites] Arch Virol. 2001;146(1):171-80 [11266212.001]
  • [Cites] Int J Oncol. 2001 May;18(5):1041-4 [11295054.001]
  • [Cites] J Virol. 2002 May;76(9):4662-5 [11932434.001]
  • [Cites] Clin Cancer Res. 2003 Mar;9(3):1118-20 [12631616.001]
  • [Cites] Clin Cancer Res. 2004 Jul 1;10(13):4417-9 [15240531.001]
  • [Cites] Int J Cancer. 1980 May 15;25(5):647-54 [6246012.001]
  • [Cites] Mol Biol Evol. 1987 Jul;4(4):406-25 [3447015.001]
  • [Cites] J Virol. 1992 May;66(5):3225-9 [1313927.001]
  • [Cites] Cancer Res. 1995 Nov 15;55(22):5173-9 [7585568.001]
  • [Cites] Mod Pathol. 1998 Feb;11(2):155-68 [9504686.001]
  • [Cites] Microsc Res Tech. 2005 Nov;68(3-4):209-21 [16276510.001]
  • [Cites] Microsc Res Tech. 2005 Nov;68(3-4):197-208 [16276516.001]
  • [Cites] J Am Vet Med Assoc. 2005 Nov 15;227(10):1625-9 [16313041.001]
  • [Cites] Med Hypotheses. 2006;67(1):21-6 [16516398.001]
  • [Cites] Cancer Res. 2007 Sep 15;67(18):8960-5 [17875739.001]
  • (PMID = 20881168.001).
  • [ISSN] 1098-660X
  • [Journal-full-title] Journal of clinical microbiology
  • [ISO-abbreviation] J. Clin. Microbiol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / RNA, Viral; 0 / Viral Envelope Proteins
  • [Other-IDs] NLM/ PMC3008461
  •  go-up   go-down


22. Ursini-Siegel J, Rajput AB, Lu H, Sanguin-Gendreau V, Zuo D, Papavasiliou V, Lavoie C, Turpin J, Cianflone K, Huntsman DG, Muller WJ: Elevated expression of DecR1 impairs ErbB2/Neu-induced mammary tumor development. Mol Cell Biol; 2007 Sep;27(18):6361-71
NCI CPTC Antibody Characterization Program. NCI CPTC Antibody Characterization Program .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Elevated expression of DecR1 impairs ErbB2/Neu-induced mammary tumor development.
  • Tumor cells utilize glucose as a primary energy source and require ongoing lipid biosynthesis for growth.
  • Expression of DecR1, an auxiliary enzyme in the fatty acid beta-oxidation pathway, is significantly diminished in numerous spontaneous mammary tumor models and in primary human breast cancer.
  • Moreover, ectopic expression of DecR1 in ErbB2/Neu-induced mammary tumor cells is sufficient to reduce levels of ErbB2/Neu expression and impair mammary tumor outgrowth.
  • This correlates with a decreased proliferative index and reduced rates of de novo fatty acid synthesis in DecR1-expressing breast cancer cells.
  • Although DecR1 expression does not affect glucose uptake in ErbB2/Neu-transformed cells, sustained expression of DecR1 protects mammary tumor cells from apoptotic cell death following glucose withdrawal.
  • Moreover, expression of catalytically impaired DecR1 mutants in Neu-transformed breast cancer cells restored Neu expression levels and increased mammary tumorigenesis in vivo.
  • These results argue that DecR1 is sufficient to limit breast cancer cell proliferation through its ability to limit the extent of oncogene expression and reduce steady-state levels of de novo fatty acid synthesis.
  • Thus, while downregulation of Neu expression may contribute to DecR1-mediated tumor suppression in certain cell types, this is not an obligate event in all Neu-transformed breast cancer cells.
  • [MeSH-major] Mammary Glands, Animal / pathology. Mammary Neoplasms, Experimental / pathology. Receptor, ErbB-2 / physiology. Receptors, Tumor Necrosis Factor, Member 10c / metabolism
  • [MeSH-minor] Animals. Breast Neoplasms / metabolism. Breast Neoplasms / pathology. Cell Line, Transformed. Cell Line, Tumor. Cell Proliferation. Cell Transformation, Neoplastic. Fatty Acids / biosynthesis. Female. Fluorescent Antibody Technique, Direct. Glucose / metabolism. Humans. Kinetics. Mice. Mice, Nude. Mice, Transgenic. Models, Biological. Mutation. Neoplasm Transplantation. Rats. Transplantation, Homologous

  • COS Scholar Universe. author profiles.
  • Hazardous Substances Data Bank. GLUCOSE .
  • NCI CPTAC Assay Portal. NCI CPTAC Assay Portal .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [Cites] Oncogene. 2005 Nov 14;24(50):7435-42 [16288290.001]
  • [Cites] Mol Cell Proteomics. 2005 Nov;4(11):1686-96 [16048908.001]
  • [Cites] Oncogene. 2006 Jun 1;25(23):3325-34 [16434967.001]
  • [Cites] Cancer Cell. 2006 Jun;9(6):425-34 [16766262.001]
  • [Cites] Proc Natl Acad Sci U S A. 2000 Mar 28;97(7):3444-9 [10716706.001]
  • [Cites] Nutrition. 2000 Mar;16(3):202-8 [10705076.001]
  • [Cites] Curr Opin Clin Nutr Metab Care. 2006 Jul;9(4):358-65 [16778563.001]
  • [Cites] Mol Cell Biol. 2001 Mar;21(5):1540-51 [11238891.001]
  • [Cites] Biochemistry. 2001 Oct 16;40(41):12412-21 [11591162.001]
  • [Cites] Cancer Res. 2003 Jan 1;63(1):132-9 [12517789.001]
  • [Cites] Mod Pathol. 2004 Jun;17(6):690-5 [15044916.001]
  • [Cites] Cancer Res. 2004 Jun 1;64(11):3892-9 [15172999.001]
  • [Cites] Proc Natl Acad Sci U S A. 2004 Jul 20;101(29):10715-20 [15235125.001]
  • [Cites] Cancer Cell. 2004 Aug;6(2):159-70 [15324699.001]
  • [Cites] Clin Cancer Res. 2004 Sep 15;10(18 Pt 1):6143-51 [15448001.001]
  • [Cites] Cancer Res. 1967 Apr;27(4):793-9 [4290628.001]
  • [Cites] Am J Physiol. 1984 Jul;247(1 Pt 2):R146-53 [6742224.001]
  • [Cites] J Clin Invest. 1990 May;85(5):1703-7 [2332510.001]
  • [Cites] J Lipid Res. 1990 Nov;31(11):2045-55 [1964953.001]
  • [Cites] Mol Cell Biol. 1992 Mar;12(3):954-61 [1312220.001]
  • [Cites] Proc Natl Acad Sci U S A. 1994 Jul 5;91(14):6379-83 [8022791.001]
  • [Cites] Cancer Res. 1996 Feb 15;56(4):745-51 [8631008.001]
  • [Cites] Cancer. 1996 Feb 1;77(3):474-82 [8630954.001]
  • [Cites] Cancer Res. 1996 Mar 1;56(5):1164-7 [8640778.001]
  • [Cites] Anticancer Res. 1995 Nov-Dec;15(6B):2895-8 [8669885.001]
  • [Cites] Trends Biochem Sci. 1999 Feb;24(2):68-72 [10098401.001]
  • [Cites] EMBO J. 1999 Apr 15;18(8):2149-64 [10205169.001]
  • [Cites] Science. 1956 Feb 24;123(3191):309-14 [13298683.001]
  • [Cites] Oncogene. 2005 Jan 6;24(1):39-46 [15489885.001]
  • [Cites] J Biol Chem. 2005 Jan 28;280(4):3068-77 [15531764.001]
  • [Cites] Cancer Res. 2005 Feb 1;65(3):698-702 [15705862.001]
  • [Cites] Oncogene. 2005 Jun 16;24(26):4165-73 [15806154.001]
  • [Cites] Oncogene. 2005 Aug 4;24(33):5173-90 [15897883.001]
  • [Cites] Cancer Cell. 2005 Oct;8(4):311-21 [16226706.001]
  • [Cites] Oncogene. 2005 Nov 17;24(51):7599-607 [16170374.001]
  • (PMID = 17636013.001).
  • [ISSN] 0270-7306
  • [Journal-full-title] Molecular and cellular biology
  • [ISO-abbreviation] Mol. Cell. Biol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Fatty Acids; 0 / Receptors, Tumor Necrosis Factor, Member 10c; EC 2.7.10.1 / Receptor, ErbB-2; IY9XDZ35W2 / Glucose
  • [Other-IDs] NLM/ PMC2099621
  •  go-up   go-down


23. Wertheim GB, Yang TW, Pan TC, Ramne A, Liu Z, Gardner HP, Dugan KD, Kristel P, Kreike B, van de Vijver MJ, Cardiff RD, Reynolds C, Chodosh LA: The Snf1-related kinase, Hunk, is essential for mammary tumor metastasis. Proc Natl Acad Sci U S A; 2009 Sep 15;106(37):15855-60
SciCrunch. Marmoset Gene list: Data: Gene Annotation .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] The Snf1-related kinase, Hunk, is essential for mammary tumor metastasis.
  • We previously identified a SNF1/AMPK-related protein kinase, Hunk, from a mammary tumor arising in an MMTV-neu transgenic mouse.
  • Using targeted deletion in mice, we now demonstrate that Hunk is required for the metastasis of c-myc-induced mammary tumors, but is dispensable for normal development.
  • Reconstitution experiments revealed that Hunk is sufficient to restore the metastatic potential of Hunk-deficient tumor cells, as well as defects in migration and invasion, and does so in a manner that requires its kinase activity.
  • In addition, a murine gene expression signature that distinguishes Hunk-wild type from Hunk-deficient mammary tumors predicts clinical outcome in women with breast cancer in a manner consistent with the pro-metastatic function of Hunk in mice.

  • MedlinePlus Health Information. consumer health - Breast Cancer.
  • COS Scholar Universe. author profiles.
  • KOMP Repository. gene/protein/disease-specific - KOMP Repository (subscription/membership/fee required).
  • Mouse Genome Informatics (MGI). Mouse Genome Informatics (MGI) .
  • NCI CPTAC Assay Portal. NCI CPTAC Assay Portal .
  • NCI CPTC Antibody Characterization Program. NCI CPTC Antibody Characterization Program .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [Cites] J Biol Chem. 2004 Jul 23;279(30):31164-70 [15150265.001]
  • [Cites] Nature. 2002 Jan 31;415(6871):530-6 [11823860.001]
  • [Cites] Biochem Biophys Res Commun. 2004 Nov 19;324(3):986-92 [15485651.001]
  • [Cites] Cell. 1984 Oct;38(3):627-37 [6488314.001]
  • [Cites] Cell. 1986 May 23;45(4):485-95 [3011271.001]
  • [Cites] Oncogene Res. 1988;3(1):21-31 [2905033.001]
  • [Cites] Nat Genet. 1995 Sep;11(1):17-26 [7550308.001]
  • [Cites] Dokl Akad Nauk. 1997 Jun;354(4):554-6 [9273061.001]
  • [Cites] Cell Growth Differ. 1998 Mar;9(3):197-208 [9543386.001]
  • [Cites] Annu Rev Biochem. 1998;67:821-55 [9759505.001]
  • [Cites] Proc Natl Acad Sci U S A. 2005 Mar 8;102(10):3738-43 [15701700.001]
  • [Cites] CA Cancer J Clin. 2005 Mar-Apr;55(2):74-108 [15761078.001]
  • [Cites] Biochim Biophys Acta. 2005 Jun 20;1724(1-2):71-85 [15893879.001]
  • [Cites] J Clin Oncol. 2006 Apr 10;24(11):1656-64 [16505416.001]
  • [Cites] Cancer Cell. 2006 Dec;10(6):529-41 [17157792.001]
  • [Cites] Genomics. 2000 Jan 1;63(1):46-59 [10662544.001]
  • [Cites] Dev Biol. 2000 Mar 15;219(2):259-76 [10694421.001]
  • [Cites] Development. 2000 Oct;127(20):4493-509 [11003847.001]
  • [Cites] Br J Cancer. 2000 Dec;83(12):1688-95 [11104567.001]
  • [Cites] Proc Natl Acad Sci U S A. 2000 Dec 5;97(25):13619-24 [11095711.001]
  • [Cites] N Engl J Med. 2001 Apr 5;344(14):1031-7 [11287972.001]
  • [Cites] Biochem J. 2001 Apr 15;355(Pt 2):297-305 [11284715.001]
  • [Cites] Mol Microbiol. 2002 Jul;45(2):453-69 [12123456.001]
  • [Cites] Nature. 2002 Aug 22;418(6900):823 [12192390.001]
  • [Cites] N Engl J Med. 2002 Dec 19;347(25):1999-2009 [12490681.001]
  • [Cites] Nat Rev Cancer. 2003 Jun;3(6):453-8 [12778135.001]
  • [Cites] Oncogene. 2003 Sep 18;22(40):6177-82 [13679856.001]
  • [Cites] Biochem Biophys Res Commun. 2003 Nov 7;311(1):156-61 [14575707.001]
  • [Cites] Proc Natl Acad Sci U S A. 2003 Dec 23;100(26):15901-5 [14665696.001]
  • [Cites] CA Cancer J Clin. 2004 Jan-Feb;54(1):8-29 [14974761.001]
  • [Cites] Am J Pathol. 2004 Mar;164(3):987-95 [14982852.001]
  • [Cites] Mol Cell Biol. 2004 Apr;24(8):3526-35 [15060171.001]
  • [Cites] Science. 2004 Jun 4;304(5676):1497-500 [15118125.001]
  • [Cites] Cancer Cell. 2004 Jun;5(6):607-16 [15193263.001]
  • [Cites] Int J Mol Med. 2002 Feb;9(2):189-96 [11786932.001]
  • [Cites] J Exp Clin Cancer Res. 2004 Jun;23(2):263-8 [15354411.001]
  • (PMID = 19717424.001).
  • [ISSN] 1091-6490
  • [Journal-full-title] Proceedings of the National Academy of Sciences of the United States of America
  • [ISO-abbreviation] Proc. Natl. Acad. Sci. U.S.A.
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / R01 CA127917; United States / NCI NIH HHS / CA / U01 CA105490; United States / NCI NIH HHS / CA / CA105490
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, U.S. Gov't, Non-P.H.S.
  • [Publication-country] United States
  • [Chemical-registry-number] EC 2.7.- / Protein Kinases; EC 2.7.1.- / Hunk protein, mouse; EC 2.7.1.- / SNF1-related protein kinases; EC 2.7.11.1 / Protein-Serine-Threonine Kinases
  •  go-up   go-down


24. Koch JG, Gu X, Han Y, El-Naggar AK, Olson MV, Medina D, Jerry DJ, Blackburn AC, Peltz G, Amos CI, Lozano G: Mammary tumor modifiers in BALB/cJ mice heterozygous for p53. Mamm Genome; 2007 May;18(5):300-9
NCI CPTAC Assay Portal. NCI CPTAC Assay Portal .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Mammary tumor modifiers in BALB/cJ mice heterozygous for p53.
  • BALB/c mice are predisposed to developing spontaneous mammary tumors, which are further increased in a p53 heterozygous state.
  • C57BL/6J mice are resistant to induced mammary tumors and develop less than 1% mammary tumors in both wild-type and p53+/- states.
  • To map modifiers of mammary tumorigenesis, we have established F1 and F2 crosses and backcrosses to BALB/cJ (N2-BALB/cJ) and C57BL/6J (N2-C57BL/6J) strains.
  • All cohorts developed mammary carcinomas in p53+/- females, suggesting that multiple loci dominantly and recessively contributed to mammary tumorigenesis.
  • We mapped two modifiers of mammary tumorigenesis in the BALB/cJ strain.
  • Mtsm1 (mammary tumor susceptibility modifier), a dominant-acting modifier, is located on chromosome 7.
  • Mtsm1 is suggestive for linkage to mammary tumorigenesis (p = 0.001).
  • Mtsm2 is located on chromosome X and is significantly linked to mammary tumorigenesis (p = 1.03 x 10(-7)).
  • [MeSH-major] Genes, p53. Heterozygote. Mammary Neoplasms, Animal / genetics
  • [MeSH-minor] Animals. Crosses, Genetic. Female. Genetic Predisposition to Disease. Male. Mice. Mice, Inbred BALB C. Mice, Inbred C57BL. Rats. Specific Pathogen-Free Organisms

  • COS Scholar Universe. author profiles.
  • KOMP Repository. gene/protein/disease-specific - KOMP Repository (subscription/membership/fee required).
  • Mouse Genome Informatics (MGI). Mouse Genome Informatics (MGI) .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [Cites] Am J Pathol. 2000 Dec;157(6):2151-9 [11106587.001]
  • [Cites] Mol Med Today. 1997 Sep;3(9):390-5 [9302689.001]
  • [Cites] Mol Biol Cell. 2001 Nov;12(11):3340-52 [11694571.001]
  • [Cites] Cancer Res. 2001 Oct 1;61(19):7065-70 [11585737.001]
  • [Cites] Int J Cancer. 1997 Jun 11;71(6):966-71 [9185698.001]
  • [Cites] Genetics. 1998 May;149(1):289-99 [9584103.001]
  • [Cites] Oncogene. 2004 Oct 7;23 (46):7644-50 [15361844.001]
  • [Cites] Cancer. 1998 Mar 15;82(6):1197-207 [9506368.001]
  • [Cites] Nat Genet. 2003 Mar;33 Suppl:238-44 [12610533.001]
  • [Cites] Curr Biol. 1994 Jan 1;4(1):1-7 [7922305.001]
  • [Cites] Cancer Res. 2005 Jul 1;65(13):5481-4 [15994915.001]
  • [Cites] FASEB J. 1993 Jul;7(10):938-43 [8344491.001]
  • [Cites] Hum Genet. 2003 Aug;113(3):238-43 [12802680.001]
  • [Cites] Science. 1990 Nov 30;250(4985):1233-8 [1978757.001]
  • [Cites] Genet Sel Evol. 2005 Jul-Aug;37(4):403-15 [15943919.001]
  • [Cites] Am J Hum Genet. 2003 Oct;73(4):898-925 [14508708.001]
  • [Cites] J Hum Genet. 2002;47(8):381-6 [12181637.001]
  • [Cites] Cancer Res. 2003 May 15;63(10):2364-8 [12750252.001]
  • [Cites] Mol Carcinog. 1995 Sep;14(1):16-22 [7546219.001]
  • [Cites] Cell. 2004 Nov 24;119(5):591-602 [15550242.001]
  • [Cites] Hum Genet. 2005 Dec;118(3-4):489-98 [16284780.001]
  • [Cites] Am J Pathol. 1997 Jan;150(1):1-13 [9006316.001]
  • [Cites] J Cell Physiol. 2000 Nov;185(2):302-9 [11025452.001]
  • [Cites] Nucleic Acids Res. 2005 Jan 1;33(Database issue):D471-5 [15608240.001]
  • [Cites] Proc Natl Acad Sci U S A. 1997 Oct 14;94(21):11472-7 [9326634.001]
  • [Cites] Nat Genet. 1995 Nov;11(3):241-7 [7581446.001]
  • [Cites] Nature. 1992 Mar 19;356(6366):215-21 [1552940.001]
  • [Cites] Int J Cancer. 1971 Jan 15;7(1):141-8 [4322934.001]
  • [Cites] Nature. 1990 Dec 20-27;348(6303):747-9 [2259385.001]
  • [Cites] Am J Hum Genet. 1999 May;64(5):1371-7 [10205268.001]
  • (PMID = 17557176.001).
  • [ISSN] 0938-8990
  • [Journal-full-title] Mammalian genome : official journal of the International Mammalian Genome Society
  • [ISO-abbreviation] Mamm. Genome
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / CA009299; United States / NCI NIH HHS / CA / CA16672; United States / NCI NIH HHS / CA / P01 CA34936; United States / NCI NIH HHS / CA / U01 CA-04-002
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  •  go-up   go-down


25. Bhadra S, Lozano MM, Dudley JP: Conversion of mouse mammary tumor virus to a lymphomagenic virus. J Virol; 2005 Oct;79(19):12592-6
COS Scholar Universe. author profiles.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Conversion of mouse mammary tumor virus to a lymphomagenic virus.
  • Type B leukemogenic virus is a variant of mouse mammary tumor virus (MMTV) that causes thymic lymphomas rather than mammary tumors in mice.

  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [Cites] J Virol. 2000 Mar;74(5):2466-71 [10666282.001]
  • [Cites] Heredity (Edinb). 2005 Jun;94(6):571-6 [15815711.001]
  • [Cites] J Virol. 2000 Oct;74(20):9431-40 [11000212.001]
  • [Cites] J Virol. 2001 Mar;75(5):2174-84 [11160721.001]
  • [Cites] J Virol. 2002 Mar;76(5):2087-99 [11836386.001]
  • [Cites] J Exp Med. 2003 Jan 20;197(2):233-43 [12538662.001]
  • [Cites] J Virol. 2003 Mar;77(6):3866-70 [12610163.001]
  • [Cites] J Virol. 2004 May;78(9):4943-6 [15078980.001]
  • [Cites] Mol Cell Biol. 2004 Jun;24(11):4810-23 [15143175.001]
  • [Cites] J Virol. 1984 Jan;49(1):92-101 [6317898.001]
  • [Cites] Mol Cell Biol. 1985 Apr;5(4):823-30 [2985971.001]
  • [Cites] Virology. 1987 Dec;161(2):357-65 [2825409.001]
  • [Cites] J Virol. 1988 Aug;62(8):2985-93 [2839715.001]
  • [Cites] J Virol. 1988 Dec;62(12):4644-52 [2846876.001]
  • [Cites] Proc Natl Acad Sci U S A. 1988 Dec;85(24):9655-9 [2849114.001]
  • [Cites] J Virol. 1989 Aug;63(8):3466-71 [2545916.001]
  • [Cites] Mol Cell Biol. 1990 Nov;10(11):5822-9 [1700274.001]
  • [Cites] J Biol Chem. 1991 Dec 15;266(35):24101-8 [1660891.001]
  • [Cites] J Virol. 1993 Jan;67(1):112-8 [7677952.001]
  • [Cites] J Exp Med. 1993 Aug 1;178(2):737-41 [7688034.001]
  • [Cites] J Virol. 1995 Dec;69(12):7868-76 [7494299.001]
  • [Cites] Mol Cell Biol. 1997 Sep;17(9):5275-87 [9271405.001]
  • [Cites] Eur J Immunol. 1997 Sep;27(9):2145-51 [9341752.001]
  • [Cites] J Virol. 1998 Jun;72(6):4746-55 [9573239.001]
  • [Cites] J Virol. 2000 Jul;74(14):6348-57 [10864645.001]
  • (PMID = 16160187.001).
  • [ISSN] 0022-538X
  • [Journal-full-title] Journal of virology
  • [ISO-abbreviation] J. Virol.
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / P01 CA077760; United States / NCI NIH HHS / CA / P01 CA77760; United States / NCI NIH HHS / CA / R01 CA34780
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, U.S. Gov't, P.H.S.
  • [Publication-country] United States
  • [Other-IDs] NLM/ PMC1211542
  •  go-up   go-down


26. Hubbard NE, Lim D, Erickson KL: Conjugated linoleic acid alters matrix metalloproteinases of metastatic mouse mammary tumor cells. J Nutr; 2007 Jun;137(6):1423-9
NCI CPTAC Assay Portal. NCI CPTAC Assay Portal .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Conjugated linoleic acid alters matrix metalloproteinases of metastatic mouse mammary tumor cells.
  • Conjugated linoleic acid (CLA) is a group of linoleic acid derivatives that has been implicated in animal studies to reduce a number of components of mammary tumorigenesis.
  • Previously, we showed that CLA could alter the latency and metastasis of the highly metastatic transplantable line 4526 mouse mammary tumor.
  • Several possible mechanisms have been proposed for the actions of CLA, but here we assessed how CLA may act to alter the expression and activity of matrix-modifying proteins within tumors from line 4526.
  • In vitro, highly metastatic mouse mammary tumor cells had significantly decreased invasiveness after treatment with CLA, an indication that matrix-modifying proteins may have been altered.
  • Using these same highly metastatic cells, primary tumors were grown in mice of separate groups fed 0, 0.1, 0.5, and 1% CLA (wt:wt) and evaluated for their levels and activities of matrix-modifying enzymes, enzyme inhibitors, and enzyme activators.
  • The addition of CLA to the diet increased steady-state levels of messenger RNA (mRNA) of the matrix metalloproteinases (MMP) -2 and -9 in primary tumors removed from mice.
  • Suppression of MMP activity, therefore, may be 1 pathway through which CLA reduces tumor invasion and spread.
  • [MeSH-major] Antineoplastic Agents / pharmacology. Linoleic Acids, Conjugated / pharmacology. Mammary Neoplasms, Animal / enzymology. Metalloproteases / antagonists & inhibitors. Tissue Inhibitor of Metalloproteinase-1 / pharmacology. Tissue Inhibitor of Metalloproteinase-2 / pharmacology
  • [MeSH-minor] Animals. Diet. Female. Mice. Mice, Inbred BALB C. Neoplasm Invasiveness

  • COS Scholar Universe. author profiles.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 17513401.001).
  • [ISSN] 0022-3166
  • [Journal-full-title] The Journal of nutrition
  • [ISO-abbreviation] J. Nutr.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, U.S. Gov't, Non-P.H.S.
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / Linoleic Acids, Conjugated; 0 / Tissue Inhibitor of Metalloproteinase-1; 127497-59-0 / Tissue Inhibitor of Metalloproteinase-2; EC 3.4.- / Metalloproteases
  •  go-up   go-down


27. Ilić I, Randelović P, Ilić R, Dordević L, Radojković D: [Granular-cell tumor: a rare variant of mammary tumor]. Vojnosanit Pregl; 2008 Jun;65(6):488-91
NCI CPTC Antibody Characterization Program. NCI CPTC Antibody Characterization Program .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] [Granular-cell tumor: a rare variant of mammary tumor].
  • BACKGROUND: Granular cell tumor (GCT) is a rare variant of mammary tumor beset with diagnostic dilemmas that may be resolved by using numerous, very complex, enzymohistochemical and immunohistochemical methods.
  • CASE REPORTS: We reported three female patients 16, 21 and 65 years old, operated on for mammary tumor at the Surgical Clinic of the School of Medicine in Nis, over the period of thirty years, 1977 to 2007.
  • During this period 14.022 mammary tumors were diagnosed, including these three cases.
  • These tumors had benign characteristics, without associated tumors in other localizations.
  • The tumors were analyzed by sets of histochemical, enzymohistochemical, immunohistochemical methods as well as ultrastructural examination.
  • The ultrastructural analysis confirmed that the tumor cells were enriched by lysosomes and consequential disorganization of cytoplasm.
  • [MeSH-major] Breast Neoplasms / pathology. Granular Cell Tumor / pathology

  • MedlinePlus Health Information. consumer health - Breast Cancer.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 18672708.001).
  • [ISSN] 0042-8450
  • [Journal-full-title] Vojnosanitetski pregled
  • [ISO-abbreviation] Vojnosanit Pregl
  • [Language] srp
  • [Publication-type] Case Reports; English Abstract; Journal Article
  • [Publication-country] Serbia
  •  go-up   go-down


28. Radaelli E, Arnold A, Papanikolaou A, Garcia-Fernandez RA, Mattiello S, Scanziani E, Cardiff RD: Mammary tumor phenotypes in wild-type aging female FVB/N mice with pituitary prolactinomas. Vet Pathol; 2009 Jul;46(4):736-45
Mouse Genome Informatics (MGI). Mouse Genome Informatics (MGI) .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Mammary tumor phenotypes in wild-type aging female FVB/N mice with pituitary prolactinomas.
  • Prolactin-secreting pituitary proliferations play a significant role in mouse mammary tumorigenesis generally producing adenosquamous carcinomas.
  • Since genetically engineered FVB mice are frequently used to study mammary tumor biology, we have examined a cohort of 64 aging wild-type FVB/N females to establish the prevalence and the nature of spontaneous mammary and pituitary tumors.
  • Tissues from mammary and pituitary glands were studied by histopathology and immunohistochemistry.
  • Of the 64 examined mice, 20 had pituitary tumors and 20 had mammary tumors.
  • Mammary and pituitary tumors were associated in 17 mice.
  • All pituitary tumors were prolactin-positive by immunohistochemistry and classified as prolactinomas.
  • Fourteen mammary tumors, including 12 cases with and 2 without concurrent prolactinomas, were adenocarcinomas with different combinations of epithelial growth patterns.
  • Five mice with prolactinomas had mammary tumors characterized by the epithelial-mesenchymal transition (EMT) phenotype.
  • Estrogen receptor alpha (ERalpha)-positivity was observed for 14 of the 18 mammary tumors tested, including both adenocarcinomas with nuclear immunoreactivity and EMT-phenotype tumors with both nuclear and cytoplasmic immunoreactivity.
  • This study confirms that spontaneous prolactinomas and mammary tumors are both common and significantly associated lesions in FVB mice.
  • Parity and age represented risk factors for the development of these tumors.
  • Compared with previous reports, prolactinoma-associated mammary tumors displayed a broader morphologic spectrum, including cases with the EMT phenotype.
  • The elevated number of prolactinoma-associated and ERalpha-positive mammary tumors opens intriguing possibilities concerning the role of ERalpha cytoplasmic localization during EMT tumorigenesis.

  • MedlinePlus Health Information. consumer health - Pituitary Tumors.
  • COS Scholar Universe. author profiles.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 19276050.001).
  • [ISSN] 1544-2217
  • [Journal-full-title] Veterinary pathology
  • [ISO-abbreviation] Vet. Pathol.
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / U01 CA141582; United States / NCI NIH HHS / CA / CA55909
  • [Publication-type] Case Reports; Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  •  go-up   go-down


29. Arumugam G, Shanthi P, Sachdanandam P: Effect of gallium nitrate on tamoxifen induced hypercalcemia in rats bearing mammary tumor. Exp Oncol; 2006 Jun;28(2):141-5
Hazardous Substances Data Bank. CALCIUM, ELEMENTAL .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Effect of gallium nitrate on tamoxifen induced hypercalcemia in rats bearing mammary tumor.
  • AIM: To study the effect of gallium nitrate in the treatment of flare hypercalcemia in rats, bearing mammary tumor with bone metastasis.
  • Animals were divided into 5 groups: normal control; hypercalcemic rats bearing DMBA-induced mammary tumors; flare hypercalcemic animals bearing DMBA-induced mammary tumors (hypercalcemic rats, treated with tamoxifen at the dose of 10 mg/kg); flare hypercalcemic rat bearing DMBA-induced mammary tumors, treated with gallium nitrate at the dose of 2.5 mg/kg; control rats, treated with gallium nitrate at the dose of 2.5 mg/kg.
  • [MeSH-major] Antineoplastic Agents / therapeutic use. Antineoplastic Agents, Hormonal / toxicity. Gallium / therapeutic use. Hypercalcemia / drug therapy. Mammary Neoplasms, Animal / complications. Tamoxifen / toxicity
  • [MeSH-minor] Animals. Bone Neoplasms / drug therapy. Bone Neoplasms / secondary. Calcium / blood. Calcium / urine. Female. Rats. Rats, Sprague-Dawley

  • MedlinePlus Health Information. consumer health - Cancer Chemotherapy.
  • Hazardous Substances Data Bank. TAMOXIFEN .
  • Hazardous Substances Data Bank. GALLIUM .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 16837906.001).
  • [ISSN] 1812-9269
  • [Journal-full-title] Experimental oncology
  • [ISO-abbreviation] Exp. Oncol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Ukraine
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / Antineoplastic Agents, Hormonal; 094ZI81Y45 / Tamoxifen; 13494-90-1 / gallium nitrate; CH46OC8YV4 / Gallium; SY7Q814VUP / Calcium
  •  go-up   go-down


30. Berger T, Cheung CC, Elia AJ, Mak TW: Disruption of the Lcn2 gene in mice suppresses primary mammary tumor formation but does not decrease lung metastasis. Proc Natl Acad Sci U S A; 2010 Feb 16;107(7):2995-3000
NCI CPTAC Assay Portal. NCI CPTAC Assay Portal .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Disruption of the Lcn2 gene in mice suppresses primary mammary tumor formation but does not decrease lung metastasis.
  • Based largely on studies in xenograft models, lipocalin-2 (Lcn2) has been implicated in the progression of multiple types of human tumors, including breast cancer.
  • Here we examine the role of Lcn2 in mammary tumorigenesis and lung metastasis using an in vivo molecular genetics approach.
  • We crossed a well-characterized transgenic mouse model of breast cancer, the MMTV-PyMT (mouse mammary tumor virus-polyoma middle T antigen) mouse, with two independent gene-targeted Lcn2(-/-) mouse strains of the 129/Ola or C57BL/6 genetic background.
  • The onset and progression of mammary tumor development and lung metastasis in the female progeny of these crosses were monitored over a 20-week period.
  • Female Lcn2(-/-)MMTV-PyMT mice of the 129/Ola background (Lcn2(-/-)PyMT(129)) showed delayed onset of mammary tumors, and both Lcn2(-/-)PyMT(129) mice and Lcn2(-/-)MMTV-PyMT mice of the C57BL/6 background (Lcn2(-/-)PyMT(B6)) exhibited significant decreases in multiplicity and tumor burden (approximately 2- to 3-fold), as measured by total tumor weight and volume.
  • At the molecular level, mammary tumors derived from Lcn2(-/-)PyMT(B6) females showed reduced matrix metalloproteinase-9 (MMP-9) activity and a lack of high molecular weight MMP activity.
  • However, although increased MMP-9 activity has been linked to tumor progression, neither Lcn2(-/-)PyMT(B6) nor Lcn2(-/-)PyMT(129) female mice showed a reduction in lung metastases compared to Lcn2(+/+)PyMT controls.
  • Our results demonstrate, using an in vivo animal model approach, that Lcn2 is a potent inducer of mammary tumor growth but not a significant promoter of lung metastasis.

  • MedlinePlus Health Information. consumer health - Lung Cancer.
  • COS Scholar Universe. author profiles.
  • KOMP Repository. gene/protein/disease-specific - KOMP Repository (subscription/membership/fee required).
  • Mouse Genome Informatics (MGI). Mouse Genome Informatics (MGI) .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [Cites] Cancer Res. 2009 Nov 15;69(22):8579-84 [19887608.001]
  • [Cites] Proc Natl Acad Sci U S A. 2009 Mar 10;106(10):3913-8 [19237579.001]
  • [Cites] Oncogene. 2000 Feb 21;19(8):1038-44 [10713687.001]
  • [Cites] Biochim Biophys Acta. 2000 Oct 18;1482(1-2):1-8 [11058742.001]
  • [Cites] Biochim Biophys Acta. 2000 Oct 18;1482(1-2):9-24 [11058743.001]
  • [Cites] J Biol Chem. 2001 Oct 5;276(40):37258-65 [11486009.001]
  • [Cites] Cancer Res. 2001 Nov 15;61(22):8298-305 [11719463.001]
  • [Cites] Oncogene. 2001 Nov 26;20(54):7908-16 [11753673.001]
  • [Cites] Nat Rev Cancer. 2002 Mar;2(3):161-74 [11990853.001]
  • [Cites] Mol Cell. 2002 Nov;10(5):1033-43 [12453412.001]
  • [Cites] Nat Rev Cancer. 2002 Dec;2(12):951-6 [12459733.001]
  • [Cites] Am J Pathol. 2003 Nov;163(5):2113-26 [14578209.001]
  • [Cites] Cancer Res. 2004 Sep 1;64(17):5973-81 [15342376.001]
  • [Cites] Cancer Chemother Pharmacol. 1989;24(3):148-54 [2544306.001]
  • [Cites] Mol Cell Biol. 1992 Mar;12(3):954-61 [1312220.001]
  • [Cites] FEBS Lett. 1992 Dec 21;314(3):386-8 [1281792.001]
  • [Cites] J Biol Chem. 1993 May 15;268(14):10425-32 [7683678.001]
  • [Cites] Genes Dev. 1998 Feb 15;12(4):449-55 [9472013.001]
  • [Cites] Int J Cancer. 1998 Dec 18;79(6):565-72 [9842963.001]
  • [Cites] J Biol Chem. 2004 Dec 3;279(49):51630-46 [15355971.001]
  • [Cites] Clin Cancer Res. 2005 Aug 1;11(15):5390-5 [16061852.001]
  • [Cites] Proc Natl Acad Sci U S A. 2006 Feb 7;103(6):1834-9 [16446425.001]
  • [Cites] Breast Cancer Res. 2006;8(4):212 [16887003.001]
  • [Cites] Eur J Cancer. 2007 Aug;43(12):1869-76 [17604154.001]
  • [Cites] Breast Cancer Res Treat. 2008 Apr;108(3):389-97 [17554627.001]
  • [Cites] Cancer Res. 2008 Aug 1;68(15):6251-9 [18676849.001]
  • [Cites] J Exp Clin Cancer Res. 2008;27:83 [19077278.001]
  • [Cites] Oncogene. 2000 Feb 21;19(8):968-88 [10713680.001]
  • (PMID = 20133630.001).
  • [ISSN] 1091-6490
  • [Journal-full-title] Proceedings of the National Academy of Sciences of the United States of America
  • [ISO-abbreviation] Proc. Natl. Acad. Sci. U.S.A.
  • [Language] ENG
  • [Grant] Canada / Canadian Institutes of Health Research / /
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Acute-Phase Proteins; 0 / Lipocalins; 0 / Oncogene Proteins; 126469-30-5 / Lcn2 protein, mouse; EC 3.4.24.35 / Matrix Metalloproteinase 9
  • [Other-IDs] NLM/ PMC2840296
  •  go-up   go-down


31. Colas S, Germain E, Arab K, Maheo K, Goupille C, Bougnoux P: Alpha-tocopherol suppresses mammary tumor sensitivity to anthracyclines in fish oil-fed rats. Nutr Cancer; 2005;51(2):178-83
Hazardous Substances Data Bank. N-NITROSO-N-METHYLUREA .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Alpha-tocopherol suppresses mammary tumor sensitivity to anthracyclines in fish oil-fed rats.
  • To determine the relevance of this observation in vivo, we examined the effect of the oxidative status of the diet on the activity of epirubicin against N-methylnitrosourea-induced mammary tumors in Sprague-Dawley rats.
  • When the first mammary tumor reached 1 cm2, epirubicin was administrated weekly for 3 wk, and subsequent change in tumor size was documented over time.
  • Two weeks after the end of epirubicin injections, tumor size was increased by 34% in the control group.
  • In the pro-oxidant group, tumor size was decreased by 50%.
  • In contrast, tumor size was increased by 188% in the antioxidant group.
  • Thus, addition of pro-oxidants in a fish oil-enriched diet increased the sensitization of mammary tumors to chemotherapy, whereas addition of alpha-tocopherol suppressed tumor response in vivo, indicating that interaction between components of the diet has to be carefully controlled during chemotherapy.
  • [MeSH-major] Anthracyclines / antagonists & inhibitors. Anthracyclines / pharmacology. Antioxidants / pharmacology. Diet / adverse effects. Drug Resistance, Neoplasm / drug effects. Fish Oils / administration & dosage. Mammary Neoplasms, Experimental / drug therapy. alpha-Tocopherol / pharmacology
  • [MeSH-minor] Adipose Tissue / drug effects. Adipose Tissue / metabolism. Animals. Antibiotics, Antineoplastic / antagonists & inhibitors. Antibiotics, Antineoplastic / pharmacology. Carcinogens. Disease Models, Animal. Drug Antagonism. Epirubicin / antagonists & inhibitors. Epirubicin / pharmacology. Fatty Acids, Unsaturated / pharmacology. Female. Malondialdehyde / metabolism. Methylnitrosourea. Oxidants / administration & dosage. Rats. Rats, Sprague-Dawley. Time Factors

  • MedlinePlus Health Information. consumer health - Antioxidants.
  • Hazardous Substances Data Bank. MALONALDEHYDE .
  • Hazardous Substances Data Bank. EPIRUBICIN .
  • Hazardous Substances Data Bank. VITAMIN E .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 15860440.001).
  • [ISSN] 0163-5581
  • [Journal-full-title] Nutrition and cancer
  • [ISO-abbreviation] Nutr Cancer
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Anthracyclines; 0 / Antibiotics, Antineoplastic; 0 / Antioxidants; 0 / Carcinogens; 0 / Fatty Acids, Unsaturated; 0 / Fish Oils; 0 / Oxidants; 3Z8479ZZ5X / Epirubicin; 4Y8F71G49Q / Malondialdehyde; 684-93-5 / Methylnitrosourea; H4N855PNZ1 / alpha-Tocopherol
  •  go-up   go-down


32. Karayannopoulou M, Polizopoulou ZS, Koutinas AF, Fytianou A, Roubies N, Kaldrymidou E, Tsioli V, Patsikas MN, Constantinidis TC, Koutinas CK: Serum alkaline phosphatase isoenzyme activities in canine malignant mammary neoplasms with and without osseous transformation. Vet Clin Pathol; 2006 Sep;35(3):287-90
MedlinePlus Health Information. consumer health - Bone Cancer.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Serum alkaline phosphatase isoenzyme activities in canine malignant mammary neoplasms with and without osseous transformation.
  • BACKGROUND: Increased serum activity of total alkaline phosphatase (TALP) has been found in dogs with mammary neoplasms, especially malignant mixed tumors.
  • We hypothesized that the bone isoenzyme of alkaline phosphatase (BALP), a specific indicator of osteoblastic activity and bone formation, may contribute to increased TALP in dogs with mammary neoplasms with osseous transformation.
  • OBJECTIVE: The purpose of this study was to compare serum TALP, BALP, and other ALP isoenzyme activities in dogs with mammary malignant neoplasms with and without osseous transformation.
  • METHODS: Twenty-one female dogs with malignant mammary neoplasms were compared with 21 clinically healthy, age-matched female control dogs.
  • Physical, clinicopathologic (including preprandial and postprandial serum bile acids, ACTH stimulation, and low-dose dexamethasone suppression tests), radiographic, and ultrasonographic examinations were performed on all dogs with tumors to assess coexisting conditions.
  • On the basis of histologic examination of excised tumors, dogs were further classified as having epithelial (n = 11) or mesenchymal/mixed (epithelial-mesenchymal) (n = 10) neoplasms, the latter of which had histologic and radiologic evidence of bone formation.
  • RESULTS: Dogs with malignant mammary tumors had significantly higher (P < .05) median serum TALP (170 U/L), BALP (59 U/L), LALP (49 U/L), and CALP (24 U/L) activities, compared with control dogs (81, 32, 37, and 5 U/L, respectively).
  • Significantly higher activities of BALP and LALP were found in dogs with epithelial neoplasms; whereas, only CALP activity was higher in dogs with mesenchymal/mixed neoplasms.
  • CONCLUSION: BALP activity is increased in some dogs with malignant mammary tumors but does not account for the increase in TALP in dogs with neoplasms that have osseous transformation.

  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 16967410.001).
  • [ISSN] 0275-6382
  • [Journal-full-title] Veterinary clinical pathology
  • [ISO-abbreviation] Vet Clin Pathol
  • [Language] ENG
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Biomarkers, Tumor; 0 / Isoenzymes; EC 3.1.3.1 / Alkaline Phosphatase
  •  go-up   go-down


33. Peace BE, Toney-Earley K, Collins MH, Waltz SE: Ron receptor signaling augments mammary tumor formation and metastasis in a murine model of breast cancer. Cancer Res; 2005 Feb 15;65(4):1285-93
The Lens. Cited by Patents in .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Ron receptor signaling augments mammary tumor formation and metastasis in a murine model of breast cancer.
  • Mice with a targeted deletion of the Ron tyrosine kinase signaling domain (TK-/-) were crossed to mice expressing the polyoma virus middle T antigen (pMT) under the control of the mouse mammary tumor virus promoter.
  • Both pMT-expressing wild-type control (pMT+/- TK+/+) and pMT+/- TK-/- mice developed mammary tumors and lung metastases.
  • However, a significant decrease in mammary tumor initiation and growth was found in the pMT+/- TK-/- mice compared with controls.
  • An examination of mammary tumors showed that there was a significant decrease in microvessel density, significantly decreased cellular proliferation, and a significant increase in terminal deoxynucleotidyl transferase-mediated nick end labeling-positive staining in mammary tumor cells from the pMT+/- TK-/- mice compared with the pMT+/- TK+/+ mice.
  • Biochemical analyses on mammary tumor lysates showed that whereas both the pMT-expressing TK+/+ and TK-/- tumors have increased Ron expression compared with normal mammary glands, the pMT-expressing TK-/- tumors have deficits in mitogen-activated protein kinase and AKT activation.
  • These results indicate that Ron signaling synergizes with pMT signaling to induce mammary tumor formation, growth, and metastasis.

  • COS Scholar Universe. author profiles.
  • KOMP Repository. gene/protein/disease-specific - KOMP Repository (subscription/membership/fee required).
  • Mouse Genome Informatics (MGI). Mouse Genome Informatics (MGI) .
  • NCI CPTC Antibody Characterization Program. NCI CPTC Antibody Characterization Program .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 15735014.001).
  • [ISSN] 0008-5472
  • [Journal-full-title] Cancer research
  • [ISO-abbreviation] Cancer Res.
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / R01 CA100002-04; United States / NCI NIH HHS / CA / CA100002-05; United States / NCI NIH HHS / CA / R01 CA100002-05; United States / NCI NIH HHS / CA / CA100002-02; United States / NICHD NIH HHS / HD / HD36888; United States / NCI NIH HHS / CA / CA100002-03; United States / NCI NIH HHS / CA / CA100002-01A1; United States / NCI NIH HHS / CA / R01 CA100002-01A1; United States / NHLBI NIH HHS / HL / T-32-HL07752; United States / NCI NIH HHS / CA / R01 CA100002-03; United States / NCI NIH HHS / CA / CA100002-04; United States / NCI NIH HHS / CA / R01 CA100002; United States / NCI NIH HHS / CA / CA100002; United States / NCI NIH HHS / CA / R01 CA100002-02
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't; Research Support, U.S. Gov't, Non-P.H.S.; Research Support, U.S. Gov't, P.H.S.
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Proto-Oncogene Proteins; EC 2.7.1.- / RON protein; EC 2.7.10.1 / Receptor Protein-Tyrosine Kinases; EC 2.7.11.1 / Protein-Serine-Threonine Kinases; EC 2.7.11.1 / Proto-Oncogene Proteins c-akt
  •  go-up   go-down


34. Nunez NP, Perkins SN, Smith NC, Berrigan D, Berendes DM, Varticovski L, Barrett JC, Hursting SD: Obesity accelerates mouse mammary tumor growth in the absence of ovarian hormones. Nutr Cancer; 2008;60(4):534-41
COS Scholar Universe. author profiles.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Obesity accelerates mouse mammary tumor growth in the absence of ovarian hormones.
  • Suitable animal models are needed to elucidate potential mechanisms for this association.
  • To determine the effects of obesity on mammary tumor growth, nonovariectomized and ovariectomized C57BL/6 mice of various body weights (lean, overweight, and obese) were implanted subcutaneously with mammary tumor cells from syngeneic Wnt-1 transgenic mice.
  • In mice, the lean phenotype was associated with reduced Wnt-1 tumor growth regardless of ovarian hormone status.
  • Ovariectomy delayed Wnt-1 tumor growth consistent with the known hormone responsiveness of these tumors.
  • However, obesity accelerated tumor growth in ovariectomized but not in nonovariectomized animals.
  • Diet-induced obesity in a syngeneic mouse model of breast cancer enhanced tumor growth, specifically in the absence of ovarian hormones.
  • These results support epidemiological evidence that obesity is associated with increased breast cancer incidence and mortality in postmenopausal but not premenopausal women.
  • In contrast, maintaining a lean body weight phenotype was associated with reduced Wnt-1 tumor growth regardless of ovarian hormone status.
  • [MeSH-major] Mammary Neoplasms, Animal / pathology. Obesity / complications. Ovariectomy
  • [MeSH-minor] Animals. Body Mass Index. Disease Models, Animal. Female. Hormones / physiology. Humans. Mice. Mice, Transgenic. Neoplasm Transplantation. Postmenopause. Wnt1 Protein / genetics

  • Genetic Alliance. consumer health - Obesity.
  • MedlinePlus Health Information. consumer health - Obesity.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 18584488.001).
  • [ISSN] 1532-7914
  • [Journal-full-title] Nutrition and cancer
  • [ISO-abbreviation] Nutr Cancer
  • [Language] eng
  • [Grant] United States / Intramural NIH HHS / /
  • [Publication-type] Journal Article; Research Support, N.I.H., Intramural; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Hormones; 0 / Wnt1 Protein; 0 / Wnt1 protein, mouse
  •  go-up   go-down


35. Jacquemart IC, Springs AE, Chen WY: Rassf3 is responsible in part for resistance to mammary tumor development in neu transgenic mice. Int J Oncol; 2009 Feb;34(2):517-28
NCI CPTC Antibody Characterization Program. NCI CPTC Antibody Characterization Program .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Rassf3 is responsible in part for resistance to mammary tumor development in neu transgenic mice.
  • Approximately 80% of these mice develop mammary tumors by 11 months of age, whereas a small percentage appears to have naturally acquired resistance to HER2/neu tumorigenesis.
  • To identify factors responsible for tumor resistance in these transgenic mice, comparative genetic profiling was used to screen alterations in gene expression in the mammary gland.
  • A novel gene, the RAS association domain (RalGDS/AF-6) family 3 (Rassf3), which belongs to a family of RAS effectors and tumor suppressor genes, was identified.
  • Data indicated 1) that Rassf3 is overexpressed in mammary gland of tumor-resistant MMTV/neu mice compared to tumor-susceptible MMTV/neu littermates or non-transgenic mice, and 2) Rassf3 is significantly up-regulated in neu-specific mouse mammary tumors compared to adjacent normal tissues.
  • A novel MMTV/Rassf3-neu bi-transgenic mouse line, overexpressing Rassf3 and neu genes in mammary glands, was established.
  • Mammary tumor incidence in bi-transgenic mice was delayed compared to their MMTV/neu+/- littermates.
  • These data suggest that Rassf3 may influence mammary tumor incidence in MMTV/neu transgenic mice.
  • [MeSH-major] Breast Neoplasms / genetics. Genes, erbB-2. Mammary Neoplasms, Experimental / genetics. Monomeric GTP-Binding Proteins / genetics
  • [MeSH-minor] Animals. Apoptosis. Base Sequence. Cell Survival. DNA Primers. Female. Genes, Tumor Suppressor. Humans. Mice. Mice, Transgenic. Molecular Sequence Data. Rats. Reverse Transcriptase Polymerase Chain Reaction. Transfection


36. Lawson JS, Glenn WK, Salmons B, Ye Y, Heng B, Moody P, Johal H, Rawlinson WD, Delprado W, Lutze-Mann L, Whitaker NJ: Mouse mammary tumor virus-like sequences in human breast cancer. Cancer Res; 2010 May 1;70(9):3576-85
Mouse Genome Informatics (MGI). Mouse Genome Informatics (MGI) .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Mouse mammary tumor virus-like sequences in human breast cancer.
  • Mouse mammary tumor virus (MMTV) sequences have been reported to be present in some human breast cancers, but it is unclear whether they have any causal role.
  • In mice, MMTV promotes tumor formation indirectly by insertional mutagenesis of Wnt oncogenes that lead to their activation.
  • We confirmed the detection of env sequences in the nucleus of human breast cancer specimens that are similar in appearance to mouse mammary tumors expressing MMTV env sequences.
  • Our findings extend the evidence that MMTV sequences found in naturally occurring mouse mammary tumors can be found in some human breast cancers, prompting further evaluation of causal roles in these settings.
  • [MeSH-major] Breast Neoplasms / genetics. Breast Neoplasms / virology. Mammary Tumor Virus, Mouse / genetics
  • [MeSH-minor] Animals. Antigens, Viral, Tumor / genetics. Base Sequence. Carcinoma, Ductal, Breast / genetics. Carcinoma, Ductal, Breast / metabolism. Carcinoma, Ductal, Breast / pathology. Carcinoma, Ductal, Breast / virology. Genes, env. Humans. Immunohistochemistry. Mice. Molecular Sequence Data. Phylogeny. Polymerase Chain Reaction. Sequence Homology, Nucleic Acid. Wnt1 Protein / biosynthesis. Wnt1 Protein / genetics

  • Genetic Alliance. consumer health - Breast Cancer.
  • MedlinePlus Health Information. consumer health - Breast Cancer.
  • COS Scholar Universe. author profiles.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [Copyright] (c)2010 AACR.
  • (PMID = 20388779.001).
  • [ISSN] 1538-7445
  • [Journal-full-title] Cancer research
  • [ISO-abbreviation] Cancer Res.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antigens, Viral, Tumor; 0 / Wnt1 Protein; 0 / glycoprotein 52 antigen, Mouse mammary tumor virus
  •  go-up   go-down


37. Hermes GL, McClintock MK: Isolation and the timing of mammary gland development, gonadarche, and ovarian senescence: implications for mammary tumor burden. Dev Psychobiol; 2008 May;50(4):353-60

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Isolation and the timing of mammary gland development, gonadarche, and ovarian senescence: implications for mammary tumor burden.
  • In this study of Norway rats, we hypothesized that lifelong psychosocial experiences, social isolation or group living, trigger different developmental trajectories in the ovarian system, contributing to predisease pathways for spontaneous mammary tumors.
  • We assessed ovarian function at both points, as well as mammary gland development at puberty and mammary tumor burden in middle age.
  • Social isolation dissociated two components of puberty; it accelerated maturation of ovarian function while it simultaneously delayed mammary tissue development thereby increasing the exposure of developing breast parenchyma to high levels of estrogen.
  • By mid-life, socially isolated rats had greater tumor burden despite having entered estropause prematurely, demonstrating that isolation did not increase tumorigenesis by prolonging ovarian function.
  • [MeSH-major] Cell Aging / physiology. Estrus / physiology. Gonads / pathology. Mammary Glands, Animal / growth & development. Mammary Neoplasms, Animal / pathology. Ovary / pathology. Social Isolation

  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 18393277.001).
  • [ISSN] 1098-2302
  • [Journal-full-title] Developmental psychobiology
  • [ISO-abbreviation] Dev Psychobiol
  • [Language] eng
  • [Grant] United States / NIA NIH HHS / AG / P01 AG18911; United States / NIEHS NIH HHS / ES / P50 ES012382-01; United States / NIMH NIH HHS / MH / R37 MH41788; United States / NICHD NIH HHS / HD / T32 HD007009
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, U.S. Gov't, Non-P.H.S.
  • [Publication-country] United States
  •  go-up   go-down


38. Castillo-Pichardo L, Martínez-Montemayor MM, Martínez JE, Wall KM, Cubano LA, Dharmawardhane S: Inhibition of mammary tumor growth and metastases to bone and liver by dietary grape polyphenols. Clin Exp Metastasis; 2009;26(6):505-16
NCI CPTAC Assay Portal. NCI CPTAC Assay Portal .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Inhibition of mammary tumor growth and metastases to bone and liver by dietary grape polyphenols.
  • We recently reported that combined grape polyphenols at physiologically relevant concentrations are more effective than individual compounds at inhibition of ERalpha(-), ERbeta(+) MDA-MB-231 breast cancer cell proliferation, cell cycle progression, and primary mammary tumor growth (Schlachterman et al., Transl Oncol 1:19-27, 2008).
  • The combined effect of dietary grape polyphenols (5 mg/kg each resveratrol, quercetin, and catechin) was tested on progression of mammary tumors in nude mice created from green fluorescent protein-tagged MDA-MB-435 bone metastatic variant.
  • Fluorescence image analysis of primary tumor growth demonstrated a statistically significant decrease in tumor area by dietary grape polyphenols.
  • Molecular analysis of excised tumors demonstrated that reduced mammary tumor growth may be due to upregulation of FOXO1 (forkhead box O1) and NFKBIA (IkappaBalpha), thus activating apoptosis and potentially inhibiting NfkappaB (nuclear factor kappaB) activity.
  • Overall, these results indicate that combined dietary grape polyphenols are effective at inhibition of mammary tumor growth and site-specific metastasis.
  • [MeSH-major] Bone Neoplasms / secondary. Catechin / therapeutic use. Liver Neoplasms, Experimental / secondary. Mammary Neoplasms, Experimental / drug therapy. Quercetin / therapeutic use. Stilbenes / therapeutic use. Vitis / chemistry
  • [MeSH-minor] Animals. Apoptosis / drug effects. Cell Cycle / drug effects. Cell Line, Tumor. Cell Proliferation / drug effects. Female. Humans. Mice. NF-kappa B / metabolism

  • MedlinePlus Health Information. consumer health - Bone Cancer.
  • Hazardous Substances Data Bank. QUERCETIN .
  • Hazardous Substances Data Bank. RESVERATROL .
  • NCI CPTAC Assay Portal. NCI CPTAC Assay Portal .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [Cites] Anticancer Res. 2006 Mar-Apr;26(2A):1177-81 [16619521.001]
  • [Cites] Cell Mol Biol Lett. 2009;14(2):248-72 [19096763.001]
  • [Cites] Nat Rev Drug Discov. 2006 Jun;5(6):493-506 [16732220.001]
  • [Cites] Cancer Lett. 2006 Jul 18;238(2):202-9 [16129553.001]
  • [Cites] Harvey Lect. 2004-2005;100:103-22 [16970176.001]
  • [Cites] Lasers Surg Med. 2006 Dec;38(10):928-38 [17111410.001]
  • [Cites] Cancer Lett. 2007 Jan 8;245(1-2):144-8 [16466851.001]
  • [Cites] Cancer Metastasis Rev. 2006 Dec;25(4):635-44 [17160709.001]
  • [Cites] Eur J Pharmacol. 2007 Feb 28;557(2-3):221-9 [17184768.001]
  • [Cites] Blood. 2007 Mar 15;109(6):2293-302 [17164350.001]
  • [Cites] Neoplasia. 2007 Feb;9(2):147-58 [17356711.001]
  • [Cites] J Agric Food Chem. 2007 May 30;55(11):4357-65 [17461594.001]
  • [Cites] J Biol Chem. 2007 Jul 6;282(27):19385-98 [17513867.001]
  • [Cites] Cancer Biol Ther. 2007 Jan;6(1):56-61 [17172819.001]
  • [Cites] Endocr Relat Cancer. 1999 Mar;6(1):29-40 [10732784.001]
  • [Cites] J Cell Biochem. 2000 Jun 6;78(3):429-41 [10861841.001]
  • [Cites] Am J Surg. 2000 Nov;180(5):357-61 [11137687.001]
  • [Cites] Cancer Res. 2001 Oct 15;61(20):7456-63 [11606380.001]
  • [Cites] Clin Biochem. 2002 Mar;35(2):119-24 [11983346.001]
  • [Cites] Nat Rev Cancer. 2002 Aug;2(8):584-93 [12154351.001]
  • [Cites] Am J Clin Nutr. 2002 Oct;76(4):865-72 [12324302.001]
  • [Cites] Cancer Metastasis Rev. 2002;21(3-4):231-55 [12549763.001]
  • [Cites] Trends Immunol. 2003 Jul;24(7):358-63 [12860525.001]
  • [Cites] Mol Cell Biochem. 2003 Jul;249(1-2):11-9 [12956393.001]
  • [Cites] Brain Res Mol Brain Res. 2003 Oct 21;118(1-2):72-81 [14559356.001]
  • [Cites] Cancer Epidemiol Biomarkers Prev. 2003 Oct;12(10):953-7 [14578128.001]
  • [Cites] Int J Cancer. 2004 Feb 20;108(5):733-40 [14696100.001]
  • [Cites] Oncol Rep. 2004 Feb;11(2):441-6 [14719081.001]
  • [Cites] J Agric Food Chem. 2004 Jan 28;52(2):255-60 [14733505.001]
  • [Cites] J Agric Food Chem. 2004 Feb 25;52(4):935-42 [14969553.001]
  • [Cites] Int J Cancer. 2005 May 20;115(1):74-84 [15688415.001]
  • [Cites] Neoplasia. 2005 Feb;7(2):128-40 [15802018.001]
  • [Cites] Cancer Res. 2005 Apr 15;65(8):3396-403 [15833874.001]
  • [Cites] J Am Diet Assoc. 2005 Jul;105(7):1053-4 [15983515.001]
  • [Cites] Histol Histopathol. 2005 Oct;20(4):1121-9 [16136495.001]
  • [Cites] J Dairy Res. 2005;72 Spec No:44-50 [16180720.001]
  • [Cites] Cancer Lett. 2006 Jan 8;231(1):113-22 [16356836.001]
  • [Cites] Clin Cancer Res. 2006 Mar 1;12(5):1431-40 [16533765.001]
  • [Cites] Curr Drug Targets. 2006 Apr;7(4):423-42 [16611030.001]
  • [Cites] Breast Cancer Res Treat. 2004 May;85(1):65-79 [15039598.001]
  • [Cites] Cancer Res. 2004 May 15;64(10):3479-85 [15150101.001]
  • [Cites] Cancer Res. 1990 Feb 1;50(3):717-21 [2297709.001]
  • [Cites] Cancer Metastasis Rev. 1990 Feb;8(4):285-97 [2182209.001]
  • [Cites] Am J Clin Nutr. 1998 Aug;68(2):258-65 [9701181.001]
  • [Cites] J Nutr. 2004 Dec;134(12 Suppl):3445S-3452S [15570052.001]
  • [Cites] Am J Clin Nutr. 2005 Jan;81(1 Suppl):230S-242S [15640486.001]
  • [Cites] Biochem J. 2007 Sep 15;406(3):511-8 [17550345.001]
  • [Cites] Invest Ophthalmol Vis Sci. 2007 Nov;48(11):4890-6 [17962435.001]
  • [Cites] Carcinogenesis. 2007 Dec;28(12):2567-74 [17916909.001]
  • [Cites] J Cell Biochem. 2008 Jan 1;103(1):30-41 [17471510.001]
  • [Cites] Clin Cancer Res. 2008 Jan 1;14(1):300-8 [18172282.001]
  • [Cites] CA Cancer J Clin. 2008 Mar-Apr;58(2):71-96 [18287387.001]
  • [Cites] Clin Transl Oncol. 2008 Mar;10(3):143-7 [18321816.001]
  • [Cites] Oncogene. 2008 Apr 7;27(16):2312-9 [18391973.001]
  • [Cites] Prostate. 2008 Jun 1;68(8):820-9 [18324676.001]
  • [Cites] Tumori. 2008 May-Jun;94(3):370-83 [18705406.001]
  • [Cites] J Cell Biochem. 2008 Oct 1;105(2):585-95 [18655187.001]
  • [Cites] Cancer Chemother Pharmacol. 2009 Feb;63(3):567 [18500520.001]
  • [Cites] Biochem Pharmacol. 2006 May 14;71(10):1397-421 [16563357.001]
  • (PMID = 19294520.001).
  • [ISSN] 1573-7276
  • [Journal-full-title] Clinical & experimental metastasis
  • [ISO-abbreviation] Clin. Exp. Metastasis
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / R03 CA109913; United States / NCI NIH HHS / CA / R03 CA109913-01A1; United States / NIMHD NIH HHS / MD / G12 MD007583; United States / NIGMS NIH HHS / GM / R25 GM061838; United States / NICHD NIH HHS / HD / G11 HD052352; United States / NCRR NIH HHS / RR / G12 RR003051; United States / NCRR NIH HHS / RR / 2G12RR003035; United States / NCRR NIH HHS / RR / G12-RR03051; United States / NIMHD NIH HHS / MD / G12 MD007600; United States / NIGMS NIH HHS / GM / S06GM050695; United States / NIGMS NIH HHS / GM / 5R25GM061838-08; United States / NICHD NIH HHS / HD / G11HD052352; United States / NIGMS NIH HHS / GM / S06 GM050695; United States / NCRR NIH HHS / RR / G12 RR003035
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't; Research Support, U.S. Gov't, Non-P.H.S.
  • [Publication-country] Netherlands
  • [Chemical-registry-number] 0 / NF-kappa B; 0 / Stilbenes; 8R1V1STN48 / Catechin; 9IKM0I5T1E / Quercetin; Q369O8926L / resveratrol
  • [Other-IDs] NLM/ NIHMS213825; NLM/ PMC2898569
  •  go-up   go-down


39. Swanson I, Jude BA, Zhang AR, Pucker A, Smith ZE, Golovkina TV: Sequences within the gag gene of mouse mammary tumor virus needed for mammary gland cell transformation. J Virol; 2006 Apr;80(7):3215-24
Mouse Genome Informatics (MGI). Mouse Genome Informatics (MGI) .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Sequences within the gag gene of mouse mammary tumor virus needed for mammary gland cell transformation.
  • Previously, we identified a group of replication-competent exogenous mouse mammary tumor viruses that failed to induce mammary tumors in susceptible mice.
  • Sequence comparison of tumorigenic and tumor-attenuated virus variants has linked the ability of virus to cause high-frequency mammary tumors to the gag gene.
  • To determine the specific sequences within the gag gene that contribute to tumor induction, we constructed five distinct chimeric viruses that have various amino acid coding sequences of gag derived from a tumor-attenuated virus replaced by those of highly tumorigenic virus and tested these viruses for tumorigenic capacities in virus-susceptible C3H/HeN mice.
  • Unlike C3H/HeN mice, BALB/cJ mice develop tumors when infected with all viral variants, irrespective of the gag gene sequences.
  • Using genetic crosses between BALB/cJ and C3H/HeN mice, we were able to determine that the mechanism that confers susceptibility to Gag-independent mammary tumors in BALB/cJ mice is inherited as a dominant trait and is controlled by a single gene, called mammary tumor susceptibility (mts), that maps to chromosome 14.

  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [Cites] Proc Natl Acad Sci U S A. 1989 May;86(10):3862-6 [2542949.001]
  • [Cites] Nature. 2005 Apr 14;434(7035):904-7 [15829964.001]
  • [Cites] Nature. 1991 Feb 7;349(6309):524-6 [1846947.001]
  • [Cites] Nature. 1991 Mar 21;350(6315):203-7 [1706480.001]
  • [Cites] J Virol. 1999 Dec;73(12):10508-13 [10559369.001]
  • [Cites] Science. 1999 Dec 3;286(5446):1965-8 [10583962.001]
  • [Cites] Nature. 1999 Dec 9;402(6762):681-5 [10604476.001]
  • [Cites] Oncogene. 2000 Feb 21;19(8):992-1001 [10713682.001]
  • [Cites] J Virol. 2000 Apr;74(8):3709-14 [10729146.001]
  • [Cites] J Virol. 2000 Oct;74(19):8876-83 [10982330.001]
  • [Cites] Int J Oncol. 2002 Dec;21(6):1269-73 [12429977.001]
  • [Cites] J Exp Med. 2003 Jan 20;197(2):233-43 [12538662.001]
  • [Cites] Nat Immunol. 2003 Jun;4(6):573-8 [12730691.001]
  • [Cites] J Exp Med. 1973 Mar 1;137(3):850-3 [4689339.001]
  • [Cites] Cell. 1977 Jun;11(2):307-19 [196759.001]
  • [Cites] Biochemistry. 1979 Nov 27;18(24):5294-9 [518835.001]
  • [Cites] Cell. 1982 Nov;31(1):99-109 [6297757.001]
  • [Cites] J Virol. 1983 Sep;47(3):495-504 [6312081.001]
  • [Cites] J Virol. 1983 Dec;48(3):685-96 [6313967.001]
  • [Cites] Nature. 1984 Jan 12-18;307(5947):131-6 [6318122.001]
  • [Cites] Nature. 1984 May 17-23;309(5965):273-5 [6325949.001]
  • [Cites] Nature. 1986 Apr 17-23;320(6063):628-31 [3010125.001]
  • [Cites] J Virol. 1987 Jan;61(1):218-20 [3023699.001]
  • [Cites] J Virol. 1987 Feb;61(2):480-90 [3027377.001]
  • [Cites] Cell. 1988 May 20;53(4):531-7 [2836061.001]
  • [Cites] Cell. 1988 Nov 18;55(4):619-25 [3180222.001]
  • [Cites] Proc Natl Acad Sci U S A. 1988 Dec;85(24):9655-9 [2849114.001]
  • [Cites] Nature. 1989 Apr 6;338(6215):505-8 [2538760.001]
  • [Cites] J Virol. 1991 Aug;65(8):4550-4 [1712864.001]
  • [Cites] Genes Dev. 1992 Mar;6(3):345-55 [1372276.001]
  • [Cites] Cell. 1992 May 15;69(4):637-45 [1316806.001]
  • [Cites] Genetics. 1992 Jun;131(2):423-47 [1353738.001]
  • [Cites] Proc Natl Acad Sci U S A. 1993 Jan 15;90(2):740-4 [8380647.001]
  • [Cites] J Exp Med. 1993 Feb 1;177(2):359-66 [8093892.001]
  • [Cites] Cell. 1993 Jun 18;73(6):1067-78 [8513493.001]
  • [Cites] Mamm Genome. 1993;4(6):303-13 [8318734.001]
  • [Cites] Cell. 1993 Aug 13;74(3):529-40 [8394220.001]
  • [Cites] J Exp Med. 1994 Feb 1;179(2):439-46 [8294859.001]
  • [Cites] J Virol. 1994 Aug;68(8):5019-26 [8035502.001]
  • [Cites] Proc Natl Acad Sci U S A. 1995 Mar 14;92(6):2268-72 [7892260.001]
  • [Cites] Immunity. 1995 Jul;3(1):139-46 [7542547.001]
  • [Cites] Cell Growth Differ. 1995 May;6(5):563-77 [7544153.001]
  • [Cites] Nature. 1996 Aug 29;382(6594):826-9 [8752279.001]
  • [Cites] Cell. 1996 Dec 27;87(7):1157-9 [8980222.001]
  • [Cites] J Virol. 1997 Apr;71(4):2615-20 [9060613.001]
  • [Cites] J Virol. 1997 Sep;71(9):6534-40 [9261373.001]
  • [Cites] J Immunol. 1998 Sep 1;161(5):2375-82 [9725233.001]
  • [Cites] Virology. 2004 Dec 20;330(2):398-407 [15567434.001]
  • [Cites] Trends Genet. 1988 Oct;4(10):291-5 [3076290.001]
  • (PMID = 16537589.001).
  • [ISSN] 0022-538X
  • [Journal-full-title] Journal of virology
  • [ISO-abbreviation] J. Virol.
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / P30 CA034196; United States / NCI NIH HHS / CA / R01 CA100383; United States / NCI NIH HHS / CA / CA100383; United States / NCI NIH HHS / CA / CA34196
  • [Publication-type] Comparative Study; Journal Article; Research Support, N.I.H., Extramural
  • [Publication-country] United States
  • [Other-IDs] NLM/ PMC1440402
  •  go-up   go-down


40. Chang CY, Chiou PP, Chen WJ, Li YH, Yiu JC, Cheng YH, Chen SD, Lin CT, Lai YS: Assessment of the tumorigenesis and drug susceptibility of three new canine mammary tumor cell lines. Res Vet Sci; 2010 Apr;88(2):285-93

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Assessment of the tumorigenesis and drug susceptibility of three new canine mammary tumor cell lines.
  • Three canine mammary tumor (CMT) cell lines, namely DE-E, DE-F and DE-SF, have been established from a surgically excised specimen of a malignant mammary tumor.
  • DE-E, DE-F and DE-SF were epithelial, fibroblast and spindle fibroblast in morphology, respectively.
  • Under electron microscope, DE-F and DE-SF cells displayed a higher nucleus/cytoplasm ratio as compared with DE-E.
  • In addition to the morphological characteristics, these cell lines displayed differential patterns of several known mammary tumor cell markers.
  • Following xenotransplantation of the CMT cells into nude mice, DE-F and DE-SF developed tumors within 2 weeks, whereas DE-E failed to develop any visible tumor up to 8 weeks after injection.
  • Lastly, the CMT cell lines exhibited differential chemoresistance to several anti-tumor drugs, including melatonin, cyclosporine A, tamoxifen and indole, suggesting that these cell lines can be used as a comparative experimental model for the tumorigenesis of mammary carcinomas and a valuable tool for anti-cancer drug screening.
  • [MeSH-major] Antineoplastic Agents / pharmacology. Dog Diseases. Mammary Neoplasms, Animal
  • [MeSH-minor] Animals. Biomarkers, Tumor / metabolism. Cell Line, Tumor. Dogs. Female. Gene Expression Regulation, Neoplastic / physiology. Mice. Mice, Nude. Neoplasm Proteins / genetics. Neoplasm Proteins / metabolism. Neoplasms, Experimental

  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [Copyright] Copyright 2009 Elsevier Ltd. All rights reserved.
  • (PMID = 19748110.001).
  • [ISSN] 1532-2661
  • [Journal-full-title] Research in veterinary science
  • [ISO-abbreviation] Res. Vet. Sci.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / Biomarkers, Tumor; 0 / Neoplasm Proteins
  •  go-up   go-down


41. Faschinger A, Rouault F, Sollner J, Lukas A, Salmons B, Günzburg WH, Indik S: Mouse mammary tumor virus integration site selection in human and mouse genomes. J Virol; 2008 Feb;82(3):1360-7
The Lens. Cited by Patents in .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Mouse mammary tumor virus integration site selection in human and mouse genomes.
  • We have previously shown that some human cells sustain mouse mammary tumor virus (MMTV) infection; therefore, we infected a susceptible human breast cell line, Hs578T, and, without introducing a species-specific bias, compared the MMTV integration profile to those of other retroviruses.
  • However, in contrast to ASLV and HTLV, not even a modest tendency in favor of integration within genes was observed.
  • Similarly, repetitive sequences and genes that are frequently tagged by MMTV in mammary tumors were not preferentially targeted in cell culture either in mouse or in human cells; hence, we conclude that MMTV displays the most random dispersion of integration sites among retroviruses determined so far.
  • [MeSH-major] Mammary Tumor Virus, Mouse / physiology. Virus Integration / physiology
  • [MeSH-minor] Animals. Cell Line, Tumor. Humans. Mice. Molecular Sequence Data. Sequence Analysis, DNA

  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [Cites] Cell. 2002 Aug 23;110(4):521-9 [12202041.001]
  • [Cites] J Virol. 2006 Aug;80(15):7316-21 [16840312.001]
  • [Cites] Trends Cell Biol. 2004 May;14(5):261-6 [15130582.001]
  • [Cites] Oncogene. 2004 Aug 12;23(36):6047-55 [15208658.001]
  • [Cites] J Virol. 2004 Sep;78(17):9524-37 [15308744.001]
  • [Cites] PLoS Biol. 2004 Aug;2(8):E234 [15314653.001]
  • [Cites] Science. 2006 Oct 20;314(5798):461-4 [16959972.001]
  • [Cites] J Virol. 2007 Jun;81(12):6731-41 [17409138.001]
  • [Cites] Nat Genet. 2007 Jun;39(6):759-69 [17468756.001]
  • [Cites] J Clin Invest. 2007 Aug;117(8):2083-6 [17671645.001]
  • [Cites] Retrovirology. 2007;4:73 [17931409.001]
  • [Cites] J Virol. 2004 Nov;78(21):11656-63 [15479807.001]
  • [Cites] Nature. 1981 Jan 22;289(5795):253-8 [6256658.001]
  • [Cites] J Virol. 1982 Sep;43(3):819-29 [6292463.001]
  • [Cites] Cell. 1982 Nov;31(1):99-109 [6297757.001]
  • [Cites] Cell. 1983 Jun;33(2):369-77 [6305506.001]
  • [Cites] J Virol. 1984 Jan;49(1):92-101 [6317898.001]
  • [Cites] Mol Cell Biol. 1984 Feb;4(2):375-8 [6321961.001]
  • [Cites] J Virol. 1984 Dec;52(3):784-92 [6092711.001]
  • [Cites] Virology. 1986 Jan 30;148(2):360-8 [3002039.001]
  • [Cites] J Virol. 1987 Jan;61(1):66-74 [3023708.001]
  • [Cites] Virology. 1987 Feb;156(2):229-37 [3027974.001]
  • [Cites] Oncogene. 1992 Mar;7(3):487-92 [1549363.001]
  • [Cites] Proc Natl Acad Sci U S A. 1993 Jan 15;90(2):740-4 [8380647.001]
  • [Cites] Virology. 1993 May;194(1):157-65 [8386870.001]
  • [Cites] Int J Cancer. 1993 Aug 19;55(1):157-63 [8393839.001]
  • [Cites] Proc Natl Acad Sci U S A. 1994 Oct 11;91(21):9823-7 [7937898.001]
  • [Cites] Nucleic Acids Res. 1994 Nov 11;22(22):4673-80 [7984417.001]
  • [Cites] J Virol. 1995 Mar;69(3):1932-8 [7853537.001]
  • [Cites] Proc Natl Acad Sci U S A. 1998 Dec 22;95(26):15270-4 [9860958.001]
  • [Cites] EMBO J. 2004 Nov 24;23(23):4670-8 [15510219.001]
  • [Cites] PLoS Biol. 2004 Dec;2(12):e423 [15550989.001]
  • [Cites] Cancer Res. 2005 Aug 1;65(15):6651-9 [16061645.001]
  • [Cites] J Virol. 2005 Sep;79(18):12035-44 [16140779.001]
  • [Cites] J Virol. 2005 Oct;79(19):12199-204 [16160146.001]
  • [Cites] Nat Med. 2005 Dec;11(12):1287-9 [16311605.001]
  • [Cites] Proc Natl Acad Sci U S A. 2006 Jan 31;103(5):1498-503 [16428288.001]
  • [Cites] Nature. 2006 Jun 1;441(7093):641-5 [16680152.001]
  • [Cites] PLoS Pathog. 2006 Jun;2(6):e60 [16789841.001]
  • [Cites] Science. 2003 Jun 13;300(5626):1749-51 [12805549.001]
  • (PMID = 18032509.001).
  • [ISSN] 1098-5514
  • [Journal-full-title] Journal of virology
  • [ISO-abbreviation] J. Virol.
  • [Language] eng
  • [Databank-accession-numbers] GENBANK/ EU018613/ EU018614/ EU018615/ EU018616/ EU018617/ EU018618/ EU018619/ EU018620/ EU018621/ EU018622/ EU018623/ EU018624/ EU018625/ EU018626/ EU018627/ EU018628/ EU018629/ EU018630/ EU018631/ EU018632/ EU018633/ EU018634/ EU018635/ EU018636/ EU018637/ EU018638/ EU018639/ EU018640/ EU018641/ EU018642/ EU018643/ EU018644/ EU018645/ EU018646/ EU018647/ EU018648/ EU018649/ EU018650/ EU018651/ EU018652/ EU018653/ EU018654/ EU018655/ EU018656/ EU018657/ EU018658/ EU018659/ EU018660/ EU018661/ EU018662/ EU018663/ EU018664/ EU018665/ EU018666/ EU018667/ EU018668/ EU018669/ EU018670/ EU018671/ EU018672/ EU018673/ EU018674/ EU018675/ EU018676/ EU018677/ EU018678/ EU018679/ EU018680/ EU018681/ EU018682/ EU018683/ EU018684/ EU018685/ EU018686/ EU018687/ EU018688/ EU018689/ EU018690/ EU018691/ EU018692/ EU018693/ EU018694/ EU018695/ EU018696/ EU018697/ EU018698/ EU018699/ EU018700/ EU018701/ EU018702/ EU018703/ EU018704/ EU018705/ EU018706/ EU018707/ EU018708/ EU018709/ EU018710/ EU018711/ EU018712/ EU018713/ EU018714/ EU018715/ EU018716/ EU018717/ EU018718/ EU018719/ EU018720/ EU018721/ EU018722/ EU018723/ EU018724/ EU018725/ EU018726/ EU018727/ EU018728/ EU018729/ EU018730/ EU018731/ EU018732/ EU018733/ EU018734/ EU018735/ EU018736/ EU018737/ EU018738/ EU018739/ EU018740/ EU018741/ EU018742/ EU018743/ EU018744/ EU018745/ EU018746/ EU018747/ EU018748/ EU018749/ EU018750/ EU018751/ EU018752/ EU018753/ EU018754/ EU018755/ EU018756/ EU018757/ EU018758/ EU018759/ EU018760/ EU018761/ EU018762/ EU018763/ EU018764/ EU018765/ EU018766/ EU018767/ EU018768/ EU018769/ EU018770/ EU018771/ EU018772/ EU018773/ EU018774/ EU018775/ EU018776/ EU018777/ EU018778/ EU018779/ EU018780/ EU018781/ EU018782/ EU018783/ EU018784/ EU018785/ EU018786/ EU018787/ EU018788/ EU018789/ EU018790/ EU018791/ EU018792/ EU018793/ EU018794/ EU018795/ EU018796/ EU018797/ EU018798/ EU018799/ EU018800/ EU018801/ EU018802/ EU018803/ EU018804/ EU018805/ EU018806/ EU018807/ EU018808/ EU018809/ EU018810/ EU018811/ EU018812/ EU018813/ EU018814/ EU018815/ EU018816/ EU018817/ EU018818/ EU018819/ EU018820/ EU018821/ EU018822/ EU018823/ EU018824/ EU018825/ EU018826/ EU018827/ EU018828/ EU018829/ EU018830/ EU018831/ EU018832/ EU018833/ EU018834/ EU018835/ EU018836/ EU018837/ EU018838/ EU018839/ EU018840/ EU018841/ EU018842/ EU018843/ EU018844/ EU018845/ EU018846/ EU018847/ EU018848/ EU018849/ EU018850/ EU018851/ EU018852/ EU018853/ EU018854/ EU018855/ EU018856/ EU018857/ EU018858/ EU018859/ EU018860/ EU018861/ EU018862/ EU018863/ EU018864/ EU018865/ EU018866/ EU018867/ EU018868/ EU018869/ EU018870/ EU018871/ EU018872/ EU018873/ EU018874/ EU018875/ EU018876/ EU018877/ EU018878/ EU018879/ EU018880/ EU018881/ EU018882/ EU018883/ EU018884/ EU018885/ EU018886/ EU018887/ EU018888/ EU018889/ EU018890/ EU018891/ EU018892/ EU018893/ EU018894/ EU018895/ EU018896/ EU018897/ EU018898/ EU018899/ EU018900/ EU018901/ EU018902/ EU018903/ EU018904/ EU018905/ EU018906/ EU018907/ EU018908/ EU018909/ EU018910/ EU018911/ EU018912/ EU018913/ EU018914/ EU018915/ EU018916/ EU018917/ EU018918/ EU018919/ EU018920/ EU018921/ EU018922/ EU018923/ EU018924/ EU018925/ EU018926/ EU018927/ EU018928/ EU018929/ EU018930/ EU018931/ EU018932/ EU018933/ EU018934/ EU018935/ EU018936/ EU018937/ EU018938/ EU018939/ EU018940/ EU018941/ EU018942/ EU018943/ EU018944/ EU018945/ EU018946/ EU018947/ EU018948/ EU018949/ EU018950/ EU018951/ EU018952/ EU018953/ EU018954/ EU018955/ EU018956/ EU018957/ EU018958/ EU018959/ EU018960/ EU018961/ EU018962/ EU018963/ EU018964/ EU018965/ EU018966/ EU018967/ EU018968/ EU018969/ EU018970/ EU018971/ EU018972/ EU018973/ EU018974/ EU018975/ EU018976/ EU018977/ EU018978/ EU018979/ EU018980/ EU018981/ EU018982/ EU018983/ EU018984/ EU018985/ EU018986/ EU018987/ EU018988/ EU018989/ EU018990/ EU018991/ EU018992/ EU018993/ EU018994/ EU018995/ EU018996/ EU018997/ EU018998/ EU018999/ EU019000/ EU019001/ EU019002/ EU019003/ EU019004/ EU019005/ EU019006/ EU019007/ EU019008/ EU019009/ EU019010/ EU019011/ EU019012/ EU019013/ EU019014/ EU019015/ EU019016/ EU019017/ EU019018/ EU019019/ EU019020/ EU019021/ EU019022/ EU019023/ EU019024/ EU019025/ EU019026/ EU019027/ EU019028/ EU019029/ EU019030/ EU019031/ EU019032/ EU019033/ EU019034/ EU019035/ EU019036/ EU019037/ EU019038/ EU019039/ EU019040/ EU019041/ EU019042/ EU019043/ EU019044/ EU019045/ EU019046/ EU019047/ EU019048/ EU019049/ EU019050/ EU019051/ EU019052/ EU019053/ EU019054/ EU019055/ EU019056/ EU019057/ EU019058/ EU019059/ EU019060/ EU019061/ EU019062/ EU019063/ EU019064/ EU019065/ EU019066/ EU019067/ EU019068/ EU019069/ EU019070/ EU019071/ EU019072/ EU019073/ EU019074/ EU019075/ EU019076/ EU019077/ EU019078/ EU019079/ EU019080
  • [Publication-type] Comparative Study; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Other-IDs] NLM/ PMC2224419
  •  go-up   go-down


42. Du WW, Yang BB, Shatseva TA, Yang BL, Deng Z, Shan SW, Lee DY, Seth A, Yee AJ: Versican G3 promotes mouse mammary tumor cell growth, migration, and metastasis by influencing EGF receptor signaling. PLoS One; 2010;5(11):e13828
The Lens. Cited by Patents in .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Versican G3 promotes mouse mammary tumor cell growth, migration, and metastasis by influencing EGF receptor signaling.
  • Increased versican expression in breast tumors is predictive of relapse and has negative impact on survival rates.
  • The C-terminal G3 domain of versican influences local and systemic tumor invasiveness in pre-clinical murine models.
  • However, the mechanism(s) by which G3 influences breast tumor growth and metastasis is not well characterized.
  • Here we evaluated the expression of versican in mouse mammary tumor cell lines observing that 4T1 cells expressed highest levels while 66c14 cells expressed low levels.
  • Experiments in a syngeneic orthotopic animal model demonstrated that G3 promoted tumor growth and systemic metastasis in vivo.
  • The activity of G3 on mouse mammary tumor cell growth, migration and its effect on spontaneous metastasis to bone in an orthotopic model was modulated by up-regulating the EGFR-mediated signaling pathway.
  • Taken together, EGFR-signaling appears to be an important pathway in versican G3-mediated breast cancer tumor invasiveness and metastasis.
  • [MeSH-major] Cell Movement. Cell Proliferation. Mammary Neoplasms, Experimental / pathology. Receptor, Epidermal Growth Factor / metabolism. Signal Transduction. Versicans / physiology
  • [MeSH-minor] Animals. Binding Sites / genetics. Blotting, Western. Cell Line, Tumor. Cyclin-Dependent Kinase 2 / metabolism. Epidermal Growth Factor / pharmacology. Female. Gene Expression Regulation, Neoplastic / drug effects. Glycogen Synthase Kinase 3 / metabolism. Humans. Mice. Mice, Inbred BALB C. Neoplasm Metastasis. Neoplasm Transplantation. Phosphorylation. Reverse Transcriptase Polymerase Chain Reaction. Serine / metabolism. Transfection

  • COS Scholar Universe. author profiles.
  • Hazardous Substances Data Bank. L-SERINE .
  • NCI CPTAC Assay Portal. NCI CPTAC Assay Portal .
  • NCI CPTAC Assay Portal. NCI CPTAC Assay Portal .
  • NCI CPTC Antibody Characterization Program. NCI CPTC Antibody Characterization Program .
  • NCI CPTC Antibody Characterization Program. NCI CPTC Antibody Characterization Program .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [Cites] Mol Biol Cell. 2001 Apr;12(4):863-79 [11294892.001]
  • [Cites] PLoS One. 2010;5(6):e10993 [20544025.001]
  • [Cites] Biochem J. 2001 Oct 1;359(Pt 1):1-16 [11563964.001]
  • [Cites] Int J Oncol. 2001 Dec;19(6):1333-9 [11713608.001]
  • [Cites] J Biol Chem. 2002 Feb 8;277(6):4565-72 [11726670.001]
  • [Cites] J Biol Chem. 2002 Apr 5;277(14):12294-301 [11805102.001]
  • [Cites] Clin Cancer Res. 2002 Apr;8(4):1054-60 [11948113.001]
  • [Cites] Drug Resist Updat. 2002 Feb;5(1):11-8 [12127860.001]
  • [Cites] Cancer Biol Ther. 2003 Jul-Aug;2(4 Suppl 1):S38-47 [14508079.001]
  • [Cites] FASEB J. 2004 Apr;18(6):754-6 [14766798.001]
  • [Cites] FASEB J. 2004 Apr;18(6):779-81 [14977887.001]
  • [Cites] Clin Cancer Res. 2004 Apr 1;10(7):2491-8 [15073129.001]
  • [Cites] J Cell Sci. 2004 May 1;117(Pt 11):2227-37 [15126624.001]
  • [Cites] Nat Cell Biol. 2004 Oct;6(10):931-40 [15448698.001]
  • [Cites] Cell Mol Life Sci. 2000 Feb;57(2):276-89 [10766023.001]
  • [Cites] J Biol Chem. 2000 Jul 14;275(28):21255-61 [10801813.001]
  • [Cites] Proc Natl Acad Sci U S A. 2000 Sep 26;97(20):11074-9 [10995469.001]
  • [Cites] J Biol Chem. 2000 Nov 10;275(45):35448-56 [10950950.001]
  • [Cites] J Biol Chem. 2000 Dec 15;275(50):38973-80 [10978313.001]
  • [Cites] Exp Cell Res. 2001 Feb 1;263(1):33-42 [11161703.001]
  • [Cites] J Neurochem. 2001 Apr;77(1):94-102 [11279265.001]
  • [Cites] Lancet. 1985 Feb 16;1(8425):364-6 [2857419.001]
  • [Cites] J Biol Chem. 1986 Oct 15;261(29):13526-35 [3759976.001]
  • [Cites] Science. 1987 Jul 10;237(4811):178-82 [2885917.001]
  • [Cites] EMBO J. 1989 Oct;8(10):2975-81 [2583089.001]
  • [Cites] J Biol Chem. 1992 May 15;267(14):10003-10 [1577773.001]
  • [Cites] Neuron. 1992 Sep;9(3):383-91 [1326293.001]
  • [Cites] J Biol Chem. 1993 Jul 5;268(19):14461-9 [8314802.001]
  • [Cites] J Biol Chem. 1994 Jul 22;269(29):19116-22 [8034670.001]
  • [Cites] Biochem J. 1994 Oct 1;303 ( Pt 1):21-6 [7945242.001]
  • [Cites] J Biol Chem. 1994 Dec 30;269(52):32992-8 [7806529.001]
  • [Cites] J Biol Chem. 1994 Dec 30;269(52):32999-3008 [7528742.001]
  • [Cites] J Biol Chem. 1995 Jan 13;270(2):958-65 [7822336.001]
  • [Cites] Recent Prog Horm Res. 1995;50:131-59 [7740155.001]
  • [Cites] Proc Natl Acad Sci U S A. 1995 Nov 7;92(23):10590-4 [7479846.001]
  • [Cites] Endocr Rev. 1995 Oct;16(5):559-89 [8529572.001]
  • [Cites] J Neuropathol Exp Neurol. 1996 May;55(5):528-33 [8627343.001]
  • [Cites] Ginecol Obstet Mex. 1996 May;64:230-5 [8925983.001]
  • [Cites] Histochem J. 1997 Jan;29(1):21-30 [9088942.001]
  • [Cites] J Biol Chem. 1998 Jun 19;273(25):15758-64 [9624174.001]
  • [Cites] Oncogene. 1999 Jan 21;18(3):813-22 [9989833.001]
  • [Cites] J Neuropathol Exp Neurol. 1999 Jun;58(6):597-605 [10374750.001]
  • [Cites] Arterioscler Thromb Vasc Biol. 1999 Jul;19(7):1630-9 [10397680.001]
  • [Cites] J Biol Chem. 1999 Jul 16;274(29):20444-9 [10400671.001]
  • [Cites] Clin Exp Metastasis. 1999 Mar;17(2):163-70 [10411109.001]
  • [Cites] Clin Cancer Res. 2005 Jan 1;11(1):162-5 [15671541.001]
  • [Cites] Mol Biol Cell. 2005 Mar;16(3):1330-40 [15635104.001]
  • [Cites] Cell Res. 2005 Jul;15(7):483-94 [16045811.001]
  • [Cites] Nat Rev Mol Cell Biol. 2005 Nov;6(11):827-37 [16227978.001]
  • [Cites] Carcinogenesis. 2006 Jun;27(6):1134-45 [16474180.001]
  • [Cites] Breast Cancer Res. 2006;8(2):R20 [16608535.001]
  • [Cites] J Biol Chem. 2006 Jul 14;281(28):19358-68 [16648628.001]
  • [Cites] Curr Top Med Chem. 2006;6(11):1071-89 [16842147.001]
  • [Cites] Cancer Res. 2007 May 15;67(10):4742-50 [17510402.001]
  • [Cites] Proc Natl Acad Sci U S A. 2007 Dec 18;104(51):20350-5 [18077375.001]
  • [Cites] Breast Cancer Res. 2007;9(4):R47 [17662123.001]
  • [Cites] Biochim Biophys Acta. 2008 Feb;1780(2):194-202 [17980161.001]
  • [Cites] PLoS One. 2008;3(6):e2420 [18560585.001]
  • [Cites] PLoS One. 2008;3(8):e2881 [18682844.001]
  • [Cites] PLoS One. 2009;4(2):e4527 [19223980.001]
  • [Cites] PLoS One. 2009;4(9):e7181 [19787069.001]
  • [Cites] PLoS One. 2009;4(10):e7535 [19844573.001]
  • [Cites] PLoS One. 2009;4(12):e8461 [20041153.001]
  • [Cites] J Biol Chem. 2001 Apr 27;276(17):14178-86 [11297534.001]
  • (PMID = 21079779.001).
  • [ISSN] 1932-6203
  • [Journal-full-title] PloS one
  • [ISO-abbreviation] PLoS ONE
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Cspg2 protein, mouse; 126968-45-4 / Versicans; 452VLY9402 / Serine; 62229-50-9 / Epidermal Growth Factor; EC 2.7.10.1 / Receptor, Epidermal Growth Factor; EC 2.7.11.1 / glycogen synthase kinase 3 beta; EC 2.7.11.22 / Cdk2 protein, mouse; EC 2.7.11.22 / Cyclin-Dependent Kinase 2; EC 2.7.11.26 / Glycogen Synthase Kinase 3
  • [Other-IDs] NLM/ PMC2974650
  •  go-up   go-down


43. Wang Y, Peng H, Zhong Y, Li D, Tang M, Ding X, Zhang J: Differential gene expression profiling of human epidermal growth factor receptor 2-overexpressing mammary tumor. Acta Biochim Biophys Sin (Shanghai); 2008 May;40(5):397-405
NCI CPTC Antibody Characterization Program. NCI CPTC Antibody Characterization Program .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Differential gene expression profiling of human epidermal growth factor receptor 2-overexpressing mammary tumor.
  • However, the biological function of HER2 signal transduction pathways is not entirely clear.
  • To investigate gene activation within the pathways, we screened differentially expressed genes in HER2-positive mouse mammary tumor using two-directional suppression subtractive hybridization combined with reverse dot-blotting analysis.
  • Forty genes and expressed sequence tags related to transduction, cell proliferation/growth/apoptosis and secreted/extracellular matrix proteins were differentially expressed in HER2-positive mammary tumor tissue.
  • Among these, 19 were already reported to be differentially expressed in mammary tumor, 11 were first identified to be differentially expressed in mammary tumor in this study but were already reported in other tumors, and 10 correlated with other cancers.
  • [MeSH-major] Gene Expression Regulation, Neoplastic. Mammary Neoplasms, Animal / metabolism. Neoplasm Proteins / metabolism. Receptor, ErbB-2 / metabolism
  • [MeSH-minor] Animals. Female. Gene Expression Profiling. Humans. Mice. Transcriptional Activation. Tumor Cells, Cultured. Up-Regulation

  • Mouse Genome Informatics (MGI). Mouse Genome Informatics (MGI) .
  • NCI CPTAC Assay Portal. NCI CPTAC Assay Portal .
  • NCI CPTC Antibody Characterization Program. NCI CPTC Antibody Characterization Program .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 18465025.001).
  • [ISSN] 1745-7270
  • [Journal-full-title] Acta biochimica et biophysica Sinica
  • [ISO-abbreviation] Acta Biochim. Biophys. Sin. (Shanghai)
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] China
  • [Chemical-registry-number] 0 / Neoplasm Proteins; EC 2.7.10.1 / Receptor, ErbB-2
  •  go-up   go-down


44. Goswami S, Philippar U, Sun D, Patsialou A, Avraham J, Wang W, Di Modugno F, Nistico P, Gertler FB, Condeelis JS: Identification of invasion specific splice variants of the cytoskeletal protein Mena present in mammary tumor cells during invasion in vivo. Clin Exp Metastasis; 2009;26(2):153-9
The Lens. Cited by Patents in .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Identification of invasion specific splice variants of the cytoskeletal protein Mena present in mammary tumor cells during invasion in vivo.
  • We have studied the gene expression pattern of invasive primary mammary tumor cells using a unique in vivo invasion assay that isolates the invasive tumor cells by chemotaxis.
  • One of the genes upregulated in the invasive tumor cells is Mena, an actin binding protein involved in the regulation of cell motility.
  • Using the in vivo invasion assay in rats and mice with mammary tumors we observed that two isoforms of Mena, ++ and +++, are upregulated in the invasive tumor cells and one isoform, 11a, is downregulated.

  • MedlinePlus Health Information. consumer health - Breast Cancer.
  • COS Scholar Universe. author profiles.
  • NCI CPTC Antibody Characterization Program. NCI CPTC Antibody Characterization Program .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [Cites] Cancer Res. 2000 Oct 1;60(19):5401-4 [11034079.001]
  • [Cites] Clin Biochem. 2004 Jul;37(7):584-94 [15234240.001]
  • [Cites] Mol Biol Cell. 2002 Jul;13(7):2533-46 [12134088.001]
  • [Cites] Int J Cancer. 2004 May 10;109(6):909-18 [15027125.001]
  • [Cites] Cancer Res. 2004 Oct 1;64(19):7022-9 [15466195.001]
  • [Cites] Cell. 1996 Oct 18;87(2):227-39 [8861907.001]
  • [Cites] Cell. 1999 May 14;97(4):471-80 [10338211.001]
  • [Cites] Cancer Res. 2004 Nov 1;64(21):7664-7 [15520165.001]
  • [Cites] Cancer Res. 2004 Dec 1;64(23):8585-94 [15574765.001]
  • [Cites] Proc Natl Acad Sci U S A. 2004 Dec 7;101(49):17027-32 [15569942.001]
  • [Cites] J Biol Chem. 2005 Aug 5;280(31):28653-62 [15939738.001]
  • [Cites] Annu Rev Cell Dev Biol. 2005;21:695-718 [16212512.001]
  • [Cites] Mol Biol Cell. 2006 Mar;17(3):1085-95 [16371509.001]
  • [Cites] Clin Cancer Res. 2006 Mar 1;12(5):1470-8 [16533770.001]
  • [Cites] Bioessays. 2006 Apr;28(4):378-86 [16547952.001]
  • [Cites] Biochim Biophys Acta. 2006 Jan-Feb;1759(1-2):99-107 [16494957.001]
  • [Cites] J Cell Biol. 2006 May 8;173(3):395-404 [16651380.001]
  • [Cites] Cancer Res. 2007 Mar 15;67(6):2657-65 [17363586.001]
  • [Cites] Cancer Res. 2007 Apr 15;67(8):3505-11 [17440055.001]
  • [Cites] Mol Cell. 2007 Dec 28;28(6):1071-82 [18158903.001]
  • [Cites] Clin Cancer Res. 2008 Aug 1;14(15):4943-50 [18676769.001]
  • [Cites] Dev Cell. 2008 Dec;15(6):813-28 [19081071.001]
  • [Cites] Cell. 2002 May 17;109(4):509-21 [12086607.001]
  • (PMID = 18985426.001).
  • [ISSN] 1573-7276
  • [Journal-full-title] Clinical & experimental metastasis
  • [ISO-abbreviation] Clin. Exp. Metastasis
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / P01 CA100324; United States / NCI NIH HHS / CA / CA113395-04; United States / NCI NIH HHS / CA / 1-U54-CA112967; United States / NCI NIH HHS / CA / CA 100324; United States / NIGMS NIH HHS / GM / GM58801; United States / NCI NIH HHS / CA / CA100324-06; United States / NCI NIH HHS / CA / U54 CA112967; United States / NIGMS NIH HHS / GM / R01 GM058801; United States / NCI NIH HHS / CA / R01 CA113395-04; United States / NCI NIH HHS / CA / R01 CA113395; United States / NCI NIH HHS / CA / CA113395; United States / NCI NIH HHS / CA / P01 CA100324-06; United States / NIGMS NIH HHS / GM / R01 GM058801-10
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
  • [Publication-country] Netherlands
  • [Chemical-registry-number] 0 / Enah protein, human; 0 / Microfilament Proteins; 0 / Protein Isoforms
  • [Other-IDs] NLM/ NIHMS112723; NLM/ PMC3042857
  •  go-up   go-down


45. Hebbard LW, Garlatti M, Young LJ, Cardiff RD, Oshima RG, Ranscht B: T-cadherin supports angiogenesis and adiponectin association with the vasculature in a mouse mammary tumor model. Cancer Res; 2008 Mar 1;68(5):1407-16
The Lens. Cited by Patents in .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] T-cadherin supports angiogenesis and adiponectin association with the vasculature in a mouse mammary tumor model.
  • T-cadherin delineates endothelial, myoepithelial, and ductal epithelial cells in the normal mouse mammary gland, and becomes progressively restricted to the vasculature during mammary tumorigenesis.
  • To test the function of T-cadherin in breast cancer, we inactivated the T-cadherin (Cdh13) gene in mice and evaluated tumor development and pathology after crossing the mutation into the mouse mammary tumor virus (MMTV)-polyoma virus middle T (PyV-mT) transgenic model.
  • We report that T-cadherin deficiency limits mammary tumor vascularization and reduces tumor growth.
  • Tumor transplantation experiments confirm the stromal role of T-cadherin in tumorigenesis.
  • In comparison with wild-type MMTV-PyV-mT controls, T-cadherin-deficient tumors are pathologically advanced and metastasize to the lungs.
  • We discern adiponectin in association with the T-cadherin-positive vasculature in the normal and malignant mammary glands and report that this interaction is lost in the T-cadherin null condition.
  • This work establishes a role for T-cadherin in promoting tumor angiogenesis and raises the possibility that vascular T-cadherin-adiponectin association may contribute to the molecular cross-talk between tumor cells and the stromal compartment in breast cancer.

  • COS Scholar Universe. author profiles.
  • KOMP Repository. gene/protein/disease-specific - KOMP Repository (subscription/membership/fee required).
  • Mouse Genome Informatics (MGI). Mouse Genome Informatics (MGI) .
  • NCI CPTAC Assay Portal. NCI CPTAC Assay Portal .
  • SciCrunch. Marmoset Gene list: Data: Gene Annotation .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [Cites] Proteomics. 2006 Jul;6(13):3862-70 [16767790.001]
  • [Cites] J Clin Invest. 2006 Jul;116(7):1784-92 [16823476.001]
  • [Cites] Angiogenesis. 2007;10(3):183-95 [17486418.001]
  • [Cites] Cancer Res. 2000 Sep 1;60(17):4682-8 [10987267.001]
  • [Cites] Cancer Res. 2001 Jun 1;61(11):4556-60 [11389090.001]
  • [Cites] Cancer Res. 2001 Nov 15;61(22):8298-305 [11719463.001]
  • [Cites] Mol Cell Biol. 2003 Jan;23(2):566-78 [12509455.001]
  • [Cites] Nat Med. 2003 May;9(5):604-13 [12669032.001]
  • [Cites] Int J Cancer. 2003 Aug 10;106(1):1-7 [12794750.001]
  • [Cites] Am J Pathol. 2003 Nov;163(5):2113-26 [14578209.001]
  • [Cites] J Biol Chem. 2004 Jan 9;279(2):1304-9 [14557259.001]
  • [Cites] Cancer Res. 2004 Jan 1;64(1):169-79 [14729621.001]
  • [Cites] Exp Cell Res. 2004 Feb 15;293(2):207-18 [14729458.001]
  • [Cites] Proc Natl Acad Sci U S A. 2004 Feb 24;101(8):2476-81 [14983034.001]
  • [Cites] J Biol Chem. 2004 Mar 26;279(13):12152-62 [14699128.001]
  • [Cites] Cancer Res. 2004 Jun 15;64(12):4180-9 [15205329.001]
  • [Cites] Proc Natl Acad Sci U S A. 2004 Jul 13;101(28):10308-13 [15210937.001]
  • [Cites] Cancer Res. 2004 Aug 1;64(15):5283-90 [15289334.001]
  • [Cites] Cardiovasc Res. 2004 Oct 1;64(1):132-43 [15364621.001]
  • [Cites] Br J Cancer. 2004 Sep 13;91(6):1139-42 [15292927.001]
  • [Cites] Neuron. 1991 Sep;7(3):391-402 [1654948.001]
  • [Cites] Mol Cell Biol. 1992 Mar;12(3):954-61 [1312220.001]
  • [Cites] J Cell Biol. 1992 Oct;119(2):451-61 [1400585.001]
  • [Cites] Biochem Biophys Res Commun. 1992 Dec 15;189(2):824-31 [1281999.001]
  • [Cites] Invest Ophthalmol Vis Sci. 1994 Jan;35(1):101-11 [7507904.001]
  • [Cites] Cancer Res. 1994 Feb 15;54(4):873-7 [8313373.001]
  • [Cites] J Cell Biol. 1994 Oct;127(1):247-56 [7929567.001]
  • [Cites] J Neurosci. 1994 Dec;14(12):7331-46 [7996179.001]
  • [Cites] Science. 1995 Nov 17;270(5239):1203-7 [7502046.001]
  • [Cites] Nat Med. 1996 Jul;2(7):776-82 [8673923.001]
  • [Cites] Development. 1996 Oct;122(10):3163-71 [8898229.001]
  • [Cites] J Cell Biol. 1997 Nov 17;139(4):1025-32 [9362520.001]
  • [Cites] Mol Cell Biol. 1998 Apr;18(4):2344-59 [9528804.001]
  • [Cites] Int J Cancer. 1998 Aug 12;77(4):640-4 [9679770.001]
  • [Cites] Trends Biochem Sci. 1999 Feb;24(2):73-6 [10098402.001]
  • [Cites] Clin Cancer Res. 2005 Jan 1;11(1):166-72 [15671542.001]
  • [Cites] FASEB J. 2005 Apr;19(6):588-90 [15703273.001]
  • [Cites] Cancer Res. 2005 Apr 1;65(7):2761-9 [15805276.001]
  • [Cites] J Biol Chem. 2005 May 6;280(18):18341-7 [15734737.001]
  • [Cites] Int J Cancer. 2005 Sep 20;116(5):734-9 [15849727.001]
  • [Cites] Cancer. 2005 Nov 1;104(9):1825-33 [16177988.001]
  • [Cites] Cancer Res. 2006 Jan 1;66(1):29-33 [16397211.001]
  • [ErratumIn] Cancer Res. 2008 Apr 15;68(8):3076
  • (PMID = 18316604.001).
  • [ISSN] 1538-7445
  • [Journal-full-title] Cancer research
  • [ISO-abbreviation] Cancer Res.
  • [Language] ENG
  • [Grant] United States / NICHD NIH HHS / HD / HD25938; United States / NICHD NIH HHS / HD / HD025938-16A29003; United States / NCI NIH HHS / CA / CA 098778; United States / NICHD NIH HHS / HD / HD025938-179003; United States / NCI NIH HHS / CA / R01 CA089140; United States / NCI NIH HHS / CA / U01 CA105490; United States / NCI NIH HHS / CA / CA089140; United States / NICHD NIH HHS / HD / P01 HD025938; United States / NCI NIH HHS / CA / U01 CA105490-01; United States / NICHD NIH HHS / HD / P01 HD025938-179003; United States / NCI NIH HHS / CA / R01 CA098778; United States / NICHD NIH HHS / HD / P01 HD025938-16A29003
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't; Research Support, U.S. Gov't, Non-P.H.S.
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Adiponectin; 0 / Antigens, CD31; 0 / Cadherins; 0 / H-cadherin
  • [Other-IDs] NLM/ NIHMS109074; NLM/ PMC2676344
  •  go-up   go-down


46. Hulit J, Lee RJ, Li Z, Wang C, Katiyar S, Yang J, Quong AA, Wu K, Albanese C, Russell R, Di Vizio D, Koff A, Thummala S, Zhang H, Harrell J, Sun H, Muller WJ, Inghirami G, Lisanti MP, Pestell RG: p27Kip1 repression of ErbB2-induced mammary tumor growth in transgenic mice involves Skp2 and Wnt/beta-catenin signaling. Cancer Res; 2006 Sep 1;66(17):8529-41
The Lens. Cited by Patents in .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] p27Kip1 repression of ErbB2-induced mammary tumor growth in transgenic mice involves Skp2 and Wnt/beta-catenin signaling.
  • Expression of the cyclin-dependent kinase (Cdk) inhibitor (p27(Kip1)) is frequently reduced in human tumors, often correlating with poor prognosis. p27(Kip1) functions as a haploinsufficient tumor suppressor; however, the mechanism by which one allele of p27(Kip1) regulates oncogenic signaling in vivo is not well understood.
  • We therefore investigated the mechanisms by which p27(Kip1) inhibits mammary tumor onset.
  • Using the common background strain of FVB, p27(Kip1) heterozygosity (p27(+/-)) accelerated ErbB2-induced mammary tumorigenesis.
  • We conducted microarray analyses of mammary tumors developing in mice with genetic haploinsufficiency for p27(Kip1) expressing a mammary-targeted ErbB2 oncogene.
  • Global gene expression profiling and Western blot analysis of ErbB2/p27(+/-) tumors showed that the loss of p27(Kip1) induced genes promoting lymphangiogenesis, cellular proliferation, and collaborative oncogenic signaling (Wnt/beta-catenin/Tcf, Cdc25a, Smad7, and Skp2).
  • The Skp2 component of the SCF(SKP2) complex that degrades p27(Kip1) was increased in ErbB2 tumors correlating with earlier tumor onset.
  • p27(Kip1) is haploinsufficient for ErbB2 mammary tumor suppression in vivo and functions to repress collaborative oncogenic signals including Skp2 and Wnt/beta-catenin signaling.
  • [MeSH-major] Cyclin-Dependent Kinase Inhibitor p27 / physiology. Mammary Neoplasms, Experimental / pathology. beta Catenin / physiology
  • [MeSH-minor] Animals. Cell Nucleus / physiology. Cell Nucleus / ultrastructure. Cyclin-Dependent Kinase Inhibitor p21 / physiology. DNA Primers. Female. Gene Deletion. Mammary Glands, Animal / physiology. Mice. Mice, Inbred Strains. Mice, Knockout. Mice, Transgenic. Polymerase Chain Reaction

  • COS Scholar Universe. author profiles.
  • Gene Ontology. gene/protein/disease-specific - Gene Ontology annotations from this paper .
  • KOMP Repository. gene/protein/disease-specific - KOMP Repository (subscription/membership/fee required).
  • Mouse Genome Informatics (MGI). Mouse Genome Informatics (MGI) .
  • NCI CPTAC Assay Portal. NCI CPTAC Assay Portal .
  • NCI CPTAC Assay Portal. NCI CPTAC Assay Portal .
  • NCI CPTAC Assay Portal. NCI CPTAC Assay Portal .
  • NCI CPTC Antibody Characterization Program. NCI CPTC Antibody Characterization Program .
  • NCI CPTC Antibody Characterization Program. NCI CPTC Antibody Characterization Program .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 16951165.001).
  • [ISSN] 1538-7445
  • [Journal-full-title] Cancer research
  • [ISO-abbreviation] Cancer Res.
  • [Language] eng
  • [Grant] United States / NIA NIH HHS / AG / AG20337C; United States / NCI NIH HHS / CA / CA14462; United States / NCI NIH HHS / CA / CA536340; United States / NCI NIH HHS / CA / CA76642; United States / NCI NIH HHS / CA / P30 CA56036-08; United States / NCI NIH HHS / CA / R01CA70896; United States / NCI NIH HHS / CA / R01CA75503; United States / NCI NIH HHS / CA / R01CA86072; United States / NCI NIH HHS / CA / R01CA93596; United States / NIDDK NIH HHS / DK / T32 DK 07513
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / CTNNB1 protein, mouse; 0 / Cyclin-Dependent Kinase Inhibitor p21; 0 / DNA Primers; 0 / beta Catenin; 147604-94-2 / Cyclin-Dependent Kinase Inhibitor p27
  •  go-up   go-down


47. Yumita N, Okuyama N, Sasaki K, Umemura S: Sonodynamic therapy on chemically induced mammary tumor: pharmacokinetics, tissue distribution and sonodynamically induced antitumor effect of gallium-porphyrin complex ATX-70. Cancer Chemother Pharmacol; 2007 Nov;60(6):891-7
Hazardous Substances Data Bank. 7,12-DIMETHYLBENZ(A)ANTHRACENE .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Sonodynamic therapy on chemically induced mammary tumor: pharmacokinetics, tissue distribution and sonodynamically induced antitumor effect of gallium-porphyrin complex ATX-70.
  • Sonodynamically induced antitumor effect of a gallium porphyrin complex, ATX-70 was evaluated on a chemically induced mammary tumor in Sprague-Dawley rats.
  • The timing of 24 h after the administration of ATX-70 was chosen for ultrasonic exposure, based on pharmacokinetic analysis of ATX-70 concentrations in the tumor, plasma, skin, and muscle.
  • At an ATX-70 dose not less than 2.5 mg/kg and at a free-field ultrasonic intensity not less than 3 W/cm(2), the synergistic effect between ATX-70 administration and ultrasonic exposure on the tumor growth inhibition was significant.
  • These results suggest that ATX-70 is a potential sonosensitizer for sonodynamic treatment of spontaneous mammary tumors.
  • [MeSH-major] Antineoplastic Agents / pharmacology. Mammary Neoplasms, Experimental / therapy. Photosensitizing Agents / pharmacology. Porphyrins / pharmacology. Ultrasonic Therapy

  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 17426974.001).
  • [ISSN] 0344-5704
  • [Journal-full-title] Cancer chemotherapy and pharmacology
  • [ISO-abbreviation] Cancer Chemother. Pharmacol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Germany
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / Photosensitizing Agents; 0 / Porphyrins; 135099-39-7 / ATX 70; 57-97-6 / 9,10-Dimethyl-1,2-benzanthracene
  •  go-up   go-down


48. Wali VB, Bachawal SV, Sylvester PW: Combined treatment of gamma-tocotrienol with statins induce mammary tumor cell cycle arrest in G1. Exp Biol Med (Maywood); 2009 Jun;234(6):639-50
The Lens. Cited by Patents in .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Combined treatment of gamma-tocotrienol with statins induce mammary tumor cell cycle arrest in G1.
  • Previous studies showed that combined statin and gamma-tocotrienol treatment synergistically inhibits growth of highly malignant +SA mammary epithelial cells in culture.
  • To investigate the mechanism mediating this growth inhibition, studies were conducted to determine the effect of combination low dose gamma-tocotrienol and statin treatment on +SA mammary tumor cell cycle progression.
  • These findings demonstrate that combination low dose statin and gamma-tocotrienol treatment induced mammary tumor cell cycle arrest at G1, resulting from an increase in p27 expression, and a corresponding decrease in cyclin D1, CDK2, and hypophosphorylation of Rb protein.
  • [MeSH-major] Chromans / pharmacology. G1 Phase / drug effects. Hydroxymethylglutaryl-CoA Reductase Inhibitors / pharmacology. Mammary Neoplasms, Animal / drug therapy. Vitamin E / analogs & derivatives
  • [MeSH-minor] Animals. Antineoplastic Combined Chemotherapy Protocols / pharmacology. Breast Neoplasms / diet therapy. Breast Neoplasms / metabolism. Breast Neoplasms / pathology. Cell Line, Tumor. Dose-Response Relationship, Drug. Drug Screening Assays, Antitumor. Drug Synergism. Female. Humans. Mice. Neoplasm Proteins / metabolism

  • MedlinePlus Health Information. consumer health - Statins.
  • MedlinePlus Health Information. consumer health - Vitamin E.
  • COS Scholar Universe. author profiles.
  • NCI CPTC Antibody Characterization Program. NCI CPTC Antibody Characterization Program .
  • NCI CPTC Antibody Characterization Program. NCI CPTC Antibody Characterization Program .
  • NCI CPTC Antibody Characterization Program. NCI CPTC Antibody Characterization Program .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 19359655.001).
  • [ISSN] 1535-3702
  • [Journal-full-title] Experimental biology and medicine (Maywood, N.J.)
  • [ISO-abbreviation] Exp. Biol. Med. (Maywood)
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / CA 86833
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Chromans; 0 / Hydroxymethylglutaryl-CoA Reductase Inhibitors; 0 / Neoplasm Proteins; 1406-18-4 / Vitamin E; 4382-43-8 / plastochromanol 8
  •  go-up   go-down


49. Takauji SR, Watanabe M, Uyama R, Nakagawa T, Miyajima N, Mochizuki M, Nishimura R, Sugano S, Sasaki N: Expression and subcellular localization of E-cadherin, alpha-catenin, and beta-catenin in 8 feline mammary tumor cell lines. J Vet Med Sci; 2007 Aug;69(8):831-4
NCI CPTC Antibody Characterization Program. NCI CPTC Antibody Characterization Program .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Expression and subcellular localization of E-cadherin, alpha-catenin, and beta-catenin in 8 feline mammary tumor cell lines.
  • Protein expression and subcellular localization of E-cadherin, alpha-catenin, and beta-catenin in 8 feline mammary tumor cell lines were examined by western blot analysis and fluorescence immunocytochemistry.

  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 17827890.001).
  • [ISSN] 0916-7250
  • [Journal-full-title] The Journal of veterinary medical science
  • [ISO-abbreviation] J. Vet. Med. Sci.
  • [Language] ENG
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Japan
  • [Chemical-registry-number] 0 / Cadherins; 0 / Neoplasm Proteins; 0 / alpha Catenin; 0 / beta Catenin
  •  go-up   go-down


50. Schmitt M, Walker MP, Richards RG, Bocchinfuso WP, Fukuda T, Medina D, Kittrell FS, Korach KS, DiAugustine RP: Expression of heregulin by mouse mammary tumor cells: role in activation of ErbB receptors. Mol Carcinog; 2006 Jul;45(7):490-505
NCI CPTC Antibody Characterization Program. NCI CPTC Antibody Characterization Program .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Expression of heregulin by mouse mammary tumor cells: role in activation of ErbB receptors.
  • The major goal of the present study was to determine whether endogenous HRG causes autocrine/paracrine activation of ErbB-2/ErbB-3 and contributes to the proliferation of mammary epithelial tumor cells.
  • Tyrosine-phosphorylated (activated) ErbB-2 and ErbB-3 receptors were detected in the majority of extracts from tumors that had formed spontaneously or as a result of oncogene expression.
  • HRG-1 transcripts and protein were found in the epithelial cells of most of these mouse mammary tumors.
  • Various mouse mammary cell lines also contained activated ErbB-2/ErbB-3 and HRG transcripts.
  • Addition of an antiserum against HRG to the mammary epithelial tumor cell line TM-6 reduced ErbB-3 Tyr-phosphorylation.
  • The cumulative findings from these experiments show that coexpression of the HRG ligand contributes to activation of ErbB-2/Erb-3 in mouse mammary tumor cells in an autocrine or paracrine fashion.
  • [MeSH-major] Mammary Neoplasms, Experimental / genetics. Neuregulin-1 / genetics. Receptor, ErbB-2 / physiology
  • [MeSH-minor] Amino Acid Sequence. Animals. Cell Line, Tumor. DNA Primers. Female. Gene Expression Regulation, Neoplastic. Humans. Immunohistochemistry. Mice. Peptide Fragments / chemistry. Plasmids. Polymerase Chain Reaction. RNA, Small Interfering / genetics. Recombinant Proteins / metabolism. Transfection

  • COS Scholar Universe. author profiles.
  • NCI CPTAC Assay Portal. NCI CPTAC Assay Portal .
  • NCI CPTC Antibody Characterization Program. NCI CPTC Antibody Characterization Program .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 16482517.001).
  • [ISSN] 0899-1987
  • [Journal-full-title] Molecular carcinogenesis
  • [ISO-abbreviation] Mol. Carcinog.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / DNA Primers; 0 / Neuregulin-1; 0 / Peptide Fragments; 0 / RNA, Small Interfering; 0 / Recombinant Proteins; EC 2.7.10.1 / Receptor, ErbB-2
  •  go-up   go-down


51. Abe F, Dafferner AJ, Donkor M, Westphal SN, Scholar EM, Solheim JC, Singh RK, Hoke TA, Talmadge JE: Myeloid-derived suppressor cells in mammary tumor progression in FVB Neu transgenic mice. Cancer Immunol Immunother; 2010 Jan;59(1):47-62
NCI CPTC Antibody Characterization Program. NCI CPTC Antibody Characterization Program .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Myeloid-derived suppressor cells in mammary tumor progression in FVB Neu transgenic mice.
  • Female mice transgenic for the rat proto-oncogene c-erb-B2, under control of the mouse mammary tumor virus (MMTV) promoter (neuN), spontaneously develop metastatic mammary carcinomas.
  • The development of these mammary tumors is associated with increased number of GR-1(+)CD11b(+) myeloid derived suppressor cells (MDSCs) in the peripheral blood (PB), spleen and tumor.
  • We report a complex relationship between tumor growth, MDSCs and immune regulatory molecules in non-mutated neu transgenic mice on a FVB background (FVB-neuN).
  • The first and second tumors in FVB-neuN mice develop at a median of 265 (147-579) and 329 (161-523) days, respectively, resulting in a median survival time (MST) of 432 (201 to >500) days.
  • During tumor growth, significantly increased number of MDSCs is observed in the PB and spleen, as well as, in infiltrating the mammary tumors.
  • Our results demonstrate a direct correlation between tumor size and the number of MDSCs infiltrating the tumor and an inverse relationship between the frequency of CD4(+) T-cells and MDSCs in the spleen.
  • Quantitative reverse transcription-polymerase chain reaction (qRT-PCR) assessment of enzyme and cytokine transcript levels in the spleen, tumor, tumor-infiltrating non-parenchymal cells (NPCs) and mammary glands revealed a significant increase in transcript levels from grossly normal mammary glands and tumor-infiltrating NPCs during tumor progression.
  • Tumor NPCs, as compared to spleen cells from wild-type (w/t) mice, expressed significantly higher levels of arginase-1 (ARG-1), nitric oxide synthase (NOS-2), vascular endothelial growth factor (VEGF-A) and significantly lower levels of interferon (IFN)-gamma, interleukin (IL)-2 and fms-like tyrosine kinase-3 ligand (Flt3L) transcript levels.
  • Transcript levels in the spleens of tumor-bearing (TB) mice also differed from normal mice, although to a lesser extent than transcript levels from tumor-infiltrating NPCs.
  • Furthermore, both spleen cells and NPCs from TB mice, but not control mice, suppressed alloantigen responses by syngeneic control spleen cells.
  • Correlative studies revealed that the number of MDSCs in the spleen was directly associated with granulocyte colony stimulating factor (G-CSF) transcript levels in the spleen; while the number of MDSCs in the tumors was directly correlated with splenic granulocyte macrophage stimulating factor (GM-CSF) transcript levels, tumor volume and tumor cell number.
  • Together our results support a role for MDSCs in tumor initiation and progressive, T-cell depression and loss of function provide evidence which support multiple mechanisms of MDSC expansion in a site-dependent manner.
  • [MeSH-major] Mammary Neoplasms, Experimental / immunology. Myeloid Cells / physiology

  • COS Scholar Universe. author profiles.
  • NCI CPTAC Assay Portal. NCI CPTAC Assay Portal .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 19449184.001).
  • [ISSN] 1432-0851
  • [Journal-full-title] Cancer immunology, immunotherapy : CII
  • [ISO-abbreviation] Cancer Immunol. Immunother.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Germany
  •  go-up   go-down


52. Lu X, Bennet B, Mu E, Rabinowitz J, Kang Y: Metabolomic changes accompanying transformation and acquisition of metastatic potential in a syngeneic mouse mammary tumor model. J Biol Chem; 2010 Mar 26;285(13):9317-21
COS Scholar Universe. author profiles.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Metabolomic changes accompanying transformation and acquisition of metastatic potential in a syngeneic mouse mammary tumor model.
  • Here, we focus on the systematic alteration of metabolism by using the state of the art metabolomic profiling techniques to investigate the changes of 157 metabolites during the progression of normal mouse mammary epithelial cells to an isogenic series of mammary tumor cell lines with increasing metastatic potentials.
  • Metabolite changes accompanying tumor progression are identified in the intracellular and secreted forms in several pathways, including glycolysis, the tricarboxylic acid cycle, the pentose phosphate pathway, fatty acid and nucleotide biosynthesis, and the GSH-dependent antioxidative pathway.
  • These results suggest possible biomarkers of breast cancer progression as well as opportunities of interrupting tumor progression through the targeting of metabolic pathways.

  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [Cites] Cancer Cell. 2003 Jun;3(6):537-49 [12842083.001]
  • [Cites] FASEB J. 2003 Jan;17(1):64-6 [12424221.001]
  • [Cites] Cell. 2004 Jun 25;117(7):927-39 [15210113.001]
  • [Cites] Nat Rev Cancer. 2004 Jul;4(7):551-61 [15229480.001]
  • [Cites] J Natl Cancer Inst. 1974 Jul;53(1):261-9 [4366196.001]
  • [Cites] J Biol Chem. 1979 Aug 25;254(16):7558-60 [38242.001]
  • [Cites] Cancer Res. 1992 Mar 15;52(6):1399-405 [1540948.001]
  • [Cites] Expert Rev Mol Diagn. 2005 May;5(3):385-95 [15934815.001]
  • [Cites] Nature. 2005 Jul 28;436(7050):518-24 [16049480.001]
  • [Cites] J Chromatogr A. 2006 Aug 25;1125(1):76-88 [16759663.001]
  • [Cites] Cell. 2006 Nov 17;127(4):679-95 [17110329.001]
  • [Cites] J Chromatogr A. 2007 Apr 20;1147(2):153-64 [17376459.001]
  • [Cites] Breast Dis. 2006-2007;26:129-38 [17473371.001]
  • [Cites] PLoS Pathog. 2006 Dec;2(12):e132 [17173481.001]
  • [Cites] J Mammary Gland Biol Neoplasia. 2007 Sep;12(2-3):153-62 [17566854.001]
  • [Cites] CA Cancer J Clin. 2008 Mar-Apr;58(2):71-96 [18287387.001]
  • [Cites] Nature. 2008 Mar 13;452(7184):181-6 [18337815.001]
  • [Cites] Breast Cancer Res Treat. 2008 Jul;110(2):297-307 [17879159.001]
  • [Cites] Cancer Cell. 2008 Jun;13(6):472-82 [18538731.001]
  • [Cites] Nat Biotechnol. 2008 Oct;26(10):1179-86 [18820684.001]
  • [Cites] J Clin Invest. 2008 Dec;118(12):3930-42 [19033663.001]
  • [Cites] Nature. 2009 Feb 12;457(7231):910-4 [19212411.001]
  • [Cites] Genes Dev. 2009 Aug 15;23(16):1882-94 [19608765.001]
  • [Cites] Nutrition. 2000 Mar;16(3):202-8 [10705076.001]
  • [Cites] Nat Rev Cancer. 2002 May;2(5):331-41 [12044009.001]
  • [Cites] Biochem Pharmacol. 2002 Sep;64(5-6):1057-64 [12213605.001]
  • [Cites] Biochem Biophys Res Commun. 2004 Jan 16;313(3):459-65 [14697210.001]
  • (PMID = 20139083.001).
  • [ISSN] 1083-351X
  • [Journal-full-title] The Journal of biological chemistry
  • [ISO-abbreviation] J. Biol. Chem.
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / R01 CA134519; United States / NCI NIH HHS / CA / R21 CA128620; United States / NCI NIH HHS / CA / R01CA134519; United States / NCI NIH HHS / CA / R21CA128620
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't; Research Support, U.S. Gov't, Non-P.H.S.
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Biomarkers, Tumor; 0 / Culture Media, Conditioned; GAN16C9B8O / Glutathione
  • [Other-IDs] NLM/ PMC2843179
  •  go-up   go-down


53. Ma L, Reinhardt F, Pan E, Soutschek J, Bhat B, Marcusson EG, Teruya-Feldstein J, Bell GW, Weinberg RA: Therapeutic silencing of miR-10b inhibits metastasis in a mouse mammary tumor model. Nat Biotechnol; 2010 Apr;28(4):341-7
eagle-i research resources. PMID 20351690 (Special Collections) .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Therapeutic silencing of miR-10b inhibits metastasis in a mouse mammary tumor model.
  • Therefore, the development of effective approaches for sequence-specific inhibition of miRNAs in tumors remains a scientific and clinical challenge.
  • Here we show that systemic treatment of tumor-bearing mice with miR-10b antagomirs-a class of chemically modified anti-miRNA oligonucleotide-suppresses breast cancer metastasis.
  • Administration of miR-10b antagomirs to mice bearing highly metastatic cells does not reduce primary mammary tumor growth but markedly suppresses formation of lung metastases in a sequence-specific manner.


54. Sarkar NH: Mouse mammary tumor virus derived from wild mice does not target Notch-4 protooncogene for the development of mammary tumors in inbred mice. Virology; 2009 May 25;388(1):121-7

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Mouse mammary tumor virus derived from wild mice does not target Notch-4 protooncogene for the development of mammary tumors in inbred mice.
  • The colony of wild mice, named Jyg, has been shown to express an exogenous mouse mammary tumor virus (Jyg-MMTV).
  • This virus induces mammary tumors in its natural host at a high incidence ( approximately 80%) resulting from insertion mutations in Notch-4 (43%), Wnt-1 (26%), and Fgf-3 (13%).
  • Since the activation of Notch-4 is not common in mammary tumors of standard laboratory strains of mice infected with various MMTV strains, we examined the consequences of Jyg-MMTV infection in BALB/c and C57BL/6 mice.
  • The results show that Jyg-MMTV induces mammary tumors in both mouse strains, but the incidence of mammary tumors in BALB/c mice is greater than in C57BL/6 mice.
  • Surprisingly, however, none of the 75 mammary tumors, analyzed both by Southern and Northern hybridizations, showed insertion mutations in or expression of Notch-4.
  • In contrast, both Wnt-1 and Fgf-3 were found to be involved in these tumors.
  • [MeSH-major] Mammary Neoplasms, Experimental / virology. Mammary Tumor Virus, Mouse / metabolism. Proto-Oncogene Proteins / metabolism. Receptors, Notch / metabolism. Retroviridae Infections / metabolism. Tumor Virus Infections / metabolism

  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 19329137.001).
  • [ISSN] 1096-0341
  • [Journal-full-title] Virology
  • [ISO-abbreviation] Virology
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Proto-Oncogene Proteins; 0 / Receptors, Notch; 146991-60-8 / Notch4 protein, mouse
  •  go-up   go-down


55. Huang S, Podsypanina K, Chen Y, Cai W, Tsimelzon A, Hilsenbeck S, Li Y: Wnt-1 is dominant over neu in specifying mammary tumor expression profiles. Technol Cancer Res Treat; 2006 Dec;5(6):565-71
NCI CPTC Antibody Characterization Program. NCI CPTC Antibody Characterization Program .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Wnt-1 is dominant over neu in specifying mammary tumor expression profiles.
  • Wnt-1 and Neu collaborate to induce mammary tumors in bitransgenic mice carrying both MMTV-Wnt-1 and MMTV-Neu.
  • In this report, gene expression profiles were determined for tumors from these bitransgenic mice, and compared with expression profiles of tumors from mice singly transgenic for MMTV-Wnt-1 or MMTV-Neu.
  • While very different from tumors arising in MMTV-Neu transgenic mice, tumors from these bitransgenic mice were found not to have identifiable differences from tumors from MMTV-Wnt-1 transgenic mice, using clustering and multidimensional scaling analyses (unsupervised and supervised), One-way Analysis of Variance (ANOVA), and two sample t test (the later two of which were combined with false discovery rate computation).
  • These observations suggest that Wnt-1 is dominant over Neu in specifying mammary tumor expression profiles.
  • [MeSH-major] Biomarkers, Tumor / metabolism. Breast Neoplasms / genetics. Gene Expression Profiling. Genes, Dominant. Mammary Neoplasms, Animal / genetics. Receptor, ErbB-2 / genetics. Wnt1 Protein / genetics
  • [MeSH-minor] Animals. Female. Gene Expression Regulation, Neoplastic. Humans. Mammary Tumor Virus, Mouse / genetics. Mice. Mice, Transgenic / genetics. Oligonucleotide Array Sequence Analysis

  • MedlinePlus Health Information. consumer health - Breast Cancer.
  • COS Scholar Universe. author profiles.
  • Mouse Genome Informatics (MGI). Mouse Genome Informatics (MGI) .
  • NCI CPTAC Assay Portal. NCI CPTAC Assay Portal .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 17121432.001).
  • [ISSN] 1533-0346
  • [Journal-full-title] Technology in cancer research & treatment
  • [ISO-abbreviation] Technol. Cancer Res. Treat.
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / R01CA113869-01
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Biomarkers, Tumor; 0 / Wnt1 Protein; EC 2.7.10.1 / Receptor, ErbB-2
  •  go-up   go-down


56. Chen H, Lee JS, Liang X, Zhang H, Zhu T, Zhang Z, Taylor ME, Zahnow C, Feigenbaum L, Rein A, Sukumar S: Hoxb7 inhibits transgenic HER-2/neu-induced mouse mammary tumor onset but promotes progression and lung metastasis. Cancer Res; 2008 May 15;68(10):3637-44
NCI CPTC Antibody Characterization Program. NCI CPTC Antibody Characterization Program .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Hoxb7 inhibits transgenic HER-2/neu-induced mouse mammary tumor onset but promotes progression and lung metastasis.
  • Our previous studies have shown that HOXB7 mRNA is overexpressed in approximately 50% of invasive breast carcinomas and promotes tumor progression in breast cancer cells grown as xenografts in mice.
  • In silico analysis of published microarray data showed that high levels of HOXB7 predict a poor outcome in HER-2-positive (P = 0.046), but not in HER-2-negative breast cancers (P = 0.94).
  • To study the function of HOXB7 in vivo in the context of HER-2 overexpression, we generated mouse mammary tumor virus (MMTV)-Hoxb7 transgenic mice, and then crossed them with MMTV-HER-2/neu transgenic mice.
  • In the mice carrying both Hoxb7 and HER-2/neu transgenes, Hoxb7 plays a dual role in mammary tumorigenesis.
  • In double transgenic mice, overexpression of Hoxb7 delayed tumor onset and lowered tumor multiplicity.
  • However, consistent with the clinical data, once the tumors appeared, their growth was faster and metastasis to the lungs occurred at a higher frequency.
  • Our data show, for the first time, that deregulated expression of Hoxb7 in mammary tumor cells can significantly modulate HER-2/neu-oncogene induced tumorigenesis in vivo.

  • MedlinePlus Health Information. consumer health - Lung Cancer.
  • COS Scholar Universe. author profiles.
  • Mouse Genome Informatics (MGI). Mouse Genome Informatics (MGI) .
  • NCI CPTAC Assay Portal. NCI CPTAC Assay Portal .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [Cites] Int J Cancer. 2000 Feb 15;85(4):578-83 [10699933.001]
  • [Cites] Nat Cell Biol. 2007 May;9(5):493-505 [17450133.001]
  • [Cites] Oncogene. 2000 Dec 7;19(52):5982-7 [11146549.001]
  • [Cites] J Mammary Gland Biol Neoplasia. 2000 Apr;5(2):243-4 [11149576.001]
  • [Cites] Proc Natl Acad Sci U S A. 2001 Mar 27;98(7):4060-5 [11274429.001]
  • [Cites] J Cell Physiol. 2001 Aug;188(2):161-9 [11424082.001]
  • [Cites] Cancer Res. 2001 Sep 1;61(17):6532-9 [11522651.001]
  • [Cites] Development. 2002 Mar;129(6):1377-86 [11880347.001]
  • [Cites] Cell. 2002 May 3;109(3):321-34 [12015982.001]
  • [Cites] Nat Rev Cancer. 2002 Oct;2(10):777-85 [12360280.001]
  • [Cites] Oncogene. 2003 Apr 3;22(13):2021-33 [12673207.001]
  • [Cites] Proc Natl Acad Sci U S A. 2003 Jul 8;100(14):8430-5 [12808151.001]
  • [Cites] J Mammary Gland Biol Neoplasia. 2003 Apr;8(2):159-75 [14635792.001]
  • [Cites] Oncogene. 2004 Sep 9;23(41):6980-5 [15286714.001]
  • [Cites] EMBO J. 1988 Jul;7(7):2131-8 [2901346.001]
  • [Cites] Histopathology. 1991 Nov;19(5):403-10 [1757079.001]
  • [Cites] Proc Natl Acad Sci U S A. 1992 Nov 15;89(22):10578-82 [1359541.001]
  • [Cites] Cell Growth Differ. 1993 May;4(5):431-41 [8100147.001]
  • [Cites] Cell. 1994 Jul 29;78(2):191-201 [7913880.001]
  • [Cites] Dev Biol. 1995 Mar;168(1):47-61 [7883078.001]
  • [Cites] Invasion Metastasis. 1994-1995;14(1-6):38-49 [7657531.001]
  • [Cites] Mol Cell Biol. 1996 Sep;16(9):4842-51 [8756643.001]
  • [Cites] J Cell Biochem. 1998 Jun 15;69(4):377-91 [9620166.001]
  • [Cites] Oncogene. 1998 Jun 25;16(25):3285-9 [9681827.001]
  • [Cites] Exp Cell Res. 1999 Apr 10;248(1):1-9 [10094807.001]
  • [Cites] Oncogene. 1999 Mar 18;18(11):1993-2001 [10208421.001]
  • [Cites] Cancer Res. 2005 Feb 1;65(3):840-9 [15705882.001]
  • [Cites] Lancet. 2005 Feb 19-25;365(9460):671-9 [15721472.001]
  • [Cites] J Biol Chem. 2005 May 13;280(19):19373-80 [15757903.001]
  • [Cites] Nature. 2005 Aug 4;436(7051):636-7 [16079829.001]
  • [Cites] Nature. 2005 Aug 4;436(7051):660-5 [16079837.001]
  • [Cites] Cancer Res. 2006 Oct 1;66(19):9527-34 [17018609.001]
  • [Cites] Cancer Res. 2006 Nov 1;66(21):10391-8 [17079459.001]
  • [Cites] Lancet Oncol. 2007 Mar;8(3):203-11 [17329190.001]
  • [Cites] J Cell Biochem. 2000 May;78(2):210-21 [10842316.001]
  • (PMID = 18463397.001).
  • [ISSN] 1538-7445
  • [Journal-full-title] Cancer research
  • [ISO-abbreviation] Cancer Res.
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / P50 CA088843; United States / NCI NIH HHS / CA / P50 CA88843; United States / Intramural NIH HHS / / ; United States / NCI NIH HHS / CA / N01CO12400; United States / NCI NIH HHS / CO / N01-CO-12400
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, N.I.H., Intramural; Research Support, U.S. Gov't, Non-P.H.S.
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Homeodomain Proteins; 0 / Hoxb7 protein, mouse; EC 2.7.10.1 / Receptor, ErbB-2
  • [Other-IDs] NLM/ NIHMS485968; NLM/ PMC3715065
  •  go-up   go-down


57. Fukuoka H, Moriuchi M, Yano H, Nagayasu T, Moriuchi H: No association of mouse mammary tumor virus-related retrovirus with Japanese cases of breast cancer. J Med Virol; 2008 Aug;80(8):1447-51
MedlinePlus Health Information. consumer health - Breast Cancer.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] No association of mouse mammary tumor virus-related retrovirus with Japanese cases of breast cancer.
  • Mouse mammary tumor virus (MMTV) is the causative agent of breast tumors in mice.
  • However, the viral sequences have not been detected from any of breast cancer samples in several subsequent studies.
  • To demonstrate if MMTV-related retrovirus is involved in Japanese cases of breast cancer, breast tissue specimens from 46 breast cancer patients and 3 patients with benign mammary tumors were investigated.
  • Extensive analysis using PCR and Southern blot hybridization, however, could not detect the MMTV env gene-like sequence in any of the samples tested as well as in MCF7 cells that has previously been described as a positive control.
  • Thus, MMTV itself or MMTV-related retrovirus is not associated with breast carcinogenesis in Japanese women, and it is unclear whether this conclusion is merely a reflection of regional differences in its epidemics.
  • [MeSH-major] Breast Neoplasms. Gene Products, env / genetics. Genes, env. Mammary Tumor Virus, Mouse / isolation & purification
  • [MeSH-minor] Adenocarcinoma, Mucinous / epidemiology. Adenocarcinoma, Mucinous / genetics. Adenocarcinoma, Mucinous / virology. Adult. Aged. Aged, 80 and over. Animals. Blotting, Southern. Carcinoma, Ductal, Breast / epidemiology. Carcinoma, Ductal, Breast / genetics. Carcinoma, Ductal, Breast / virology. Carcinoma, Intraductal, Noninfiltrating / epidemiology. Carcinoma, Intraductal, Noninfiltrating / genetics. Carcinoma, Intraductal, Noninfiltrating / virology. Cell Line, Tumor. Female. Fibroadenoma / epidemiology. Fibroadenoma / genetics. Fibroadenoma / virology. Humans. Japan / epidemiology. Mice. Middle Aged. Nucleic Acid Hybridization. Phyllodes Tumor / epidemiology. Phyllodes Tumor / genetics. Phyllodes Tumor / virology. Polymerase Chain Reaction

  • Genetic Alliance. consumer health - Breast Cancer.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 18551605.001).
  • [ISSN] 1096-9071
  • [Journal-full-title] Journal of medical virology
  • [ISO-abbreviation] J. Med. Virol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Gene Products, env
  •  go-up   go-down


58. Courreges MC, Burzyn D, Nepomnaschy I, Piazzon I, Ross SR: Critical role of dendritic cells in mouse mammary tumor virus in vivo infection. J Virol; 2007 Apr;81(8):3769-77
COS Scholar Universe. author profiles.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Critical role of dendritic cells in mouse mammary tumor virus in vivo infection.
  • Mouse mammary tumor virus (MMTV) is a milk-transmitted betaretrovirus that causes mammary tumors in mice.
  • Although mammary epithelial cells are the ultimate targets of MMTV, the virus utilizes components of the host immune system to establish infection.

  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [Cites] J Exp Med. 1994 May 1;179(5):1457-66 [8163931.001]
  • [Cites] J Exp Med. 1994 Feb 1;179(2):439-46 [8294859.001]
  • [Cites] J Virol. 1994 Aug;68(8):5019-26 [8035502.001]
  • [Cites] J Exp Med. 1994 Nov 1;180(5):1829-40 [7525839.001]
  • [Cites] J Exp Med. 1994 Dec 1;180(6):2347-51 [7525852.001]
  • [Cites] Proc Natl Acad Sci U S A. 1995 May 23;92(11):4828-32 [7761408.001]
  • [Cites] J Virol. 1997 May;71(5):3895-903 [9094666.001]
  • [Cites] J Virol. 1997 Aug;71(8):6044-8 [9223496.001]
  • [Cites] J Virol. 1997 Oct;71(10):7289-94 [9311804.001]
  • [Cites] J Virol. 1997 Oct;71(10):7295-9 [9311805.001]
  • [Cites] Nature. 1998 Mar 19;392(6673):245-52 [9521319.001]
  • [Cites] J Virol. 1998 Apr;72(4):3066-71 [9525630.001]
  • [Cites] J Immunol. 1998 Aug 1;161(3):1083-6 [9686565.001]
  • [Cites] Eur J Immunol. 1998 Sep;28(9):2760-9 [9754563.001]
  • [Cites] Blood. 1998 Nov 15;92(10):3780-92 [9808572.001]
  • [Cites] J Immunol Methods. 1999 Feb 1;223(1):77-92 [10037236.001]
  • [Cites] J Immunol. 1999 Mar 1;162(5):2538-45 [10072493.001]
  • [Cites] J Virol. 1999 Oct;73(10):8403-10 [10482591.001]
  • [Cites] Int J Exp Pathol. 2005 Aug;86(4):187-204 [16045541.001]
  • [Cites] J Virol. 2006 Apr;80(7):3477-86 [16537615.001]
  • [Cites] Science. 1999 Dec 3;286(5446):1965-8 [10583962.001]
  • [Cites] Annu Rev Immunol. 2000;18:767-811 [10837075.001]
  • [Cites] Microbes Infect. 2000 Aug;2(10):1215-23 [11008111.001]
  • [Cites] Blood. 2002 Feb 15;99(4):1282-8 [11830477.001]
  • [Cites] Proc Natl Acad Sci U S A. 2002 Feb 19;99(4):2281-6 [11854525.001]
  • [Cites] J Immunol. 2002 Apr 1;168(7):3470-6 [11907107.001]
  • [Cites] Eur J Immunol. 2002 Apr;32(4):945-56 [11920560.001]
  • [Cites] Curr Opin Immunol. 2002 Jun;14(3):380-3 [11973138.001]
  • [Cites] Immunity. 2002 Aug;17(2):211-20 [12196292.001]
  • [Cites] Proc Natl Acad Sci U S A. 2002 Sep 17;99(19):12386-90 [12218182.001]
  • [Cites] Nat Immunol. 2003 Jun;4(6):573-8 [12730691.001]
  • [Cites] Curr Top Microbiol Immunol. 2003;276:1-30 [12797441.001]
  • [Cites] Nat Rev Immunol. 2003 Sep;3(9):697-709 [12949494.001]
  • [Cites] J Virol. 2003 Oct;77(19):10468-78 [12970432.001]
  • [Cites] Trends Microbiol. 2004 Jul;12(7):337-45 [15223061.001]
  • [Cites] Mol Immunol. 2005 Feb;42(2):229-37 [15488610.001]
  • [Cites] J Immunol. 1981 Mar;126(3):1075-9 [6970212.001]
  • [Cites] Proc Natl Acad Sci U S A. 1988 Dec;85(24):9655-9 [2849114.001]
  • [Cites] Arch Virol. 1989;107(3-4):191-205 [2554853.001]
  • [Cites] J Exp Med. 1993 May 1;177(5):1359-66 [8386743.001]
  • [Cites] Cell Microbiol. 2006 Apr;8(4):558-64 [16548882.001]
  • [Cites] J Virol. 2004 Jan;78(2):576-84 [14694089.001]
  • [Cites] Eur J Immunol. 1994 Jul;24(7):1612-9 [7913038.001]
  • (PMID = 17267484.001).
  • [ISSN] 0022-538X
  • [Journal-full-title] Journal of virology
  • [ISO-abbreviation] J. Virol.
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / R01 CA045954; United States / FIC NIH HHS / TW / R03TW01103; United States / NCI NIH HHS / CA / R01CA45954; United States / NIAID NIH HHS / AI / R21AI059625; United States / NIAID NIH HHS / AI / R21 AI059625; United States / FIC NIH HHS / TW / R03 TW001103
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Macrophage Inflammatory Proteins
  • [Other-IDs] NLM/ PMC1866091
  •  go-up   go-down


59. Cadieux C, Kedinger V, Yao L, Vadnais C, Drossos M, Paquet M, Nepveu A: Mouse mammary tumor virus p75 and p110 CUX1 transgenic mice develop mammary tumors of various histologic types. Cancer Res; 2009 Sep 15;69(18):7188-97
NCI CPTC Antibody Characterization Program. NCI CPTC Antibody Characterization Program .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Mouse mammary tumor virus p75 and p110 CUX1 transgenic mice develop mammary tumors of various histologic types.
  • The p75 and p110 isoforms of the CUX1 homeodomain protein are overexpressed in breast tumors and cancer cell lines.
  • To assess and compare the ability of these short CUX1 isoforms in driving mammary tumor development, we used site-specific transgenesis into the Hprt locus to generate transgenic mice expressing p75 or p110 CUX1 under the control of the mouse mammary tumor virus-long terminal repeat.
  • We report that mammary tumors developed after a long latency period, and although various histopathologies were observed, the proportion of adenosquamous carcinomas was significantly higher in p75 CUX1 than in p110 CUX1 transgenic mice.
  • Comparisons between tumors and adjacent normal mammary glands revealed that transgenes were overexpressed in most but not all tumors, yet in all cases tested, CUX1 DNA binding was increased, suggesting that both higher expression and changes in post-translational modifications can contribute to stimulate transgene activity.
  • Interestingly, higher expression of erbB2 mRNA was seen in most tumors, not only solid carcinomas but also adenosquamous carcinomas, whereas higher expression of various Wnt genes and activation of the beta-catenin pathway was observed primarily in adenosquamous carcinomas.
  • [MeSH-major] Homeodomain Proteins / genetics. Mammary Neoplasms, Experimental / genetics. Nuclear Proteins / genetics. Repressor Proteins / genetics
  • [MeSH-minor] Animals. Carcinoma, Adenosquamous / genetics. Carcinoma, Adenosquamous / metabolism. Carcinoma, Adenosquamous / pathology. Caseins / biosynthesis. Caseins / genetics. Female. Humans. Lung Neoplasms / genetics. Lung Neoplasms / secondary. Mammary Tumor Virus, Mouse / genetics. Mice. Mice, Transgenic. Protein Isoforms. RNA, Messenger / biosynthesis. RNA, Messenger / genetics. Receptor, ErbB-2 / biosynthesis. Receptor, ErbB-2 / genetics. Receptor, ErbB-2 / metabolism. Transgenes. Wnt Proteins / metabolism

  • KOMP Repository. gene/protein/disease-specific - KOMP Repository (subscription/membership/fee required).
  • Mouse Genome Informatics (MGI). Mouse Genome Informatics (MGI) .
  • NCI CPTAC Assay Portal. NCI CPTAC Assay Portal .
  • NCI CPTAC Assay Portal. NCI CPTAC Assay Portal .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 19738070.001).
  • [ISSN] 1538-7445
  • [Journal-full-title] Cancer research
  • [ISO-abbreviation] Cancer Res.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / CUX1 protein, human; 0 / Caseins; 0 / Homeodomain Proteins; 0 / Nuclear Proteins; 0 / Protein Isoforms; 0 / RNA, Messenger; 0 / Repressor Proteins; 0 / Wnt Proteins; EC 2.7.10.1 / Receptor, ErbB-2
  •  go-up   go-down


60. Fernandez-Twinn DS, Ekizoglou S, Martin-Gronert MS, Tarry-Adkins J, Wayman AP, Warner MJ, Luan JA, Gusterson BA, Ozanne SE: Poor early growth and excessive adult calorie intake independently and additively affect mitogenic signaling and increase mammary tumor susceptibility. Carcinogenesis; 2010 Oct;31(10):1873-81
NCI CPTC Antibody Characterization Program. NCI CPTC Antibody Characterization Program .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Poor early growth and excessive adult calorie intake independently and additively affect mitogenic signaling and increase mammary tumor susceptibility.
  • We previously showed that offspring of rat dams receiving a protein-restricted (low protein) diet throughout pregnancy and lactation develop mammary tumors more quickly.
  • Rapid post-weaning mammary growth and mammary tissue overexpression of insulin receptor, insulin-like growth factor-1 receptor (IGF-1R), estrogen receptor isoform alpha and v-erb-b2 erythroblastic leukemia viral oncogene homolog 2 (ERBB2), correlated with this risk.
  • We provide evidence for transcriptional upregulation of IGF-1R by Sp1 in LP mammary tissue (P < 0.01).
  • Feeding a highly palatable diet (HPD) to increase calorie intake from puberty, additively and independently increased early mammary tumor risk, which correlated with increased serum insulin and triglyceride concentrations (P < 0.05).
  • We conclude that poor early growth and excessive calorie intake exert independent and additive effects on mitogenic growth factor signaling to influence mammary tumor susceptibility.
  • [MeSH-major] Energy Intake. Growth Disorders / complications. Mammary Neoplasms, Animal / etiology. Signal Transduction
  • [MeSH-minor] Animals. Body Weight. Disease Susceptibility. Extracellular Signal-Regulated MAP Kinases / metabolism. Female. Gene Expression Profiling. Mammary Glands, Animal / chemistry. Mammary Glands, Animal / metabolism. Rats. Rats, Wistar. Receptor, ErbB-2 / genetics. Receptor, ErbB-2 / physiology. Receptor, IGF Type 1 / analysis. Receptor, IGF Type 1 / genetics. Sp1 Transcription Factor / analysis. Sp1 Transcription Factor / genetics


61. Pedersen K, Angelini PD, Laos S, Bach-Faig A, Cunningham MP, Ferrer-Ramón C, Luque-García A, García-Castillo J, Parra-Palau JL, Scaltriti M, Ramón y Cajal S, Baselga J, Arribas J: A naturally occurring HER2 carboxy-terminal fragment promotes mammary tumor growth and metastasis. Mol Cell Biol; 2009 Jun;29(12):3319-31
The Lens. Cited by Patents in .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] A naturally occurring HER2 carboxy-terminal fragment promotes mammary tumor growth and metastasis.
  • It is thought that transgenic mice overexpressing HER2 in the mammary glands develop tumors only after acquisition of activating mutations in the transgene.
  • In contrast, we show that expression of 611-CTF led to development of aggressive and invasive mammary tumors without the need for mutations.
  • These results demonstrate that 611-CTF is a potent oncogene capable of promoting mammary tumor progression and metastasis.
  • [MeSH-major] Breast Neoplasms / etiology. Peptide Fragments / physiology. Receptor, ErbB-2 / physiology
  • [MeSH-minor] Adenocarcinoma / etiology. Adenocarcinoma / genetics. Adenocarcinoma / pathology. Amino Acid Sequence. Animals. Cell Line, Tumor. Female. Gene Expression Regulation, Neoplastic. Humans. Male. Mammary Neoplasms, Experimental / etiology. Mammary Neoplasms, Experimental / genetics. Mammary Neoplasms, Experimental / pathology. Mice. Mice, Transgenic. Models, Biological. Molecular Sequence Data. Peptide Chain Initiation, Translational. Prognosis. Signal Transduction. Transfection


62. Shin SR, Sánchez-Velar N, Sherr DH, Sonenshein GE: 7,12-dimethylbenz(a)anthracene treatment of a c-rel mouse mammary tumor cell line induces epithelial to mesenchymal transition via activation of nuclear factor-kappaB. Cancer Res; 2006 Mar 1;66(5):2570-5
The Lens. Cited by Patents in .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] 7,12-dimethylbenz(a)anthracene treatment of a c-rel mouse mammary tumor cell line induces epithelial to mesenchymal transition via activation of nuclear factor-kappaB.
  • The aberrant expression of the nuclear factor-kappaB (NF-kappaB) c-Rel subunit that occurs in many human breast cancers can play a causal role in tumorigenesis as judged by findings with a mouse mammary tumor virus (MMTV)-c-rel transgenic mouse model, in which 31.6% of mice developed one or more mammary tumors after a long latency.
  • Interestingly, none of the cell lines established from the mammary tumors grew in soft agar.
  • To begin to test the hypothesis that a prototypic carcinogen insult can promote a more invasive, mesenchymal phenotype, a cell line established from a MMTV-c-rel mammary tumor rel-3983 was treated in culture with the polycyclic aromatic hydrocarbon 7,12-dimethylbenz(a)anthracene (DMBA; rel-3983D cells) or DMSO vehicle (rel-3983V cells).
  • Thus, DMBA treatment of c-Rel-transformed mammary tumor cells in culture is shown here for the first time to result in EMT via activation of NF-kappaB.
  • [MeSH-major] 9,10-Dimethyl-1,2-benzanthracene / pharmacology. Carcinoma, Adenosquamous / pathology. Cell Transformation, Neoplastic / chemically induced. Genes, rel. Mammary Neoplasms, Experimental / pathology. NF-kappa B / metabolism
  • [MeSH-minor] Animals. Cadherins / biosynthesis. Cell Adhesion / drug effects. Cell Growth Processes / drug effects. Cell Line, Tumor. Epithelial Cells / drug effects. Epithelial Cells / metabolism. Epithelial Cells / pathology. I-kappa B Proteins / biosynthesis. I-kappa B Proteins / genetics. Mesoderm / drug effects. Mesoderm / metabolism. Mesoderm / pathology. Mice. Mice, Transgenic. Proto-Oncogene Proteins c-rel / biosynthesis. Proto-Oncogene Proteins c-rel / genetics

  • Hazardous Substances Data Bank. 7,12-DIMETHYLBENZ(A)ANTHRACENE .
  • NCI CPTC Antibody Characterization Program. NCI CPTC Antibody Characterization Program .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 16510574.001).
  • [ISSN] 0008-5472
  • [Journal-full-title] Cancer research
  • [ISO-abbreviation] Cancer Res.
  • [Language] eng
  • [Grant] United States / NIEHS NIH HHS / ES / P01 ES11624
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Cadherins; 0 / I-kappa B Proteins; 0 / NF-kappa B; 0 / Proto-Oncogene Proteins c-rel; 139874-52-5 / NF-kappaB inhibitor alpha; 57-97-6 / 9,10-Dimethyl-1,2-benzanthracene
  •  go-up   go-down


63. Zhao Y, Li J, Wang J, Xing Y, Geng M: Role of cell surface oligosaccharides of mouse mammary tumor cell lines in cancer metastasis. Indian J Biochem Biophys; 2007 Jun;44(3):145-51

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Role of cell surface oligosaccharides of mouse mammary tumor cell lines in cancer metastasis.
  • In tumor cells, alterations in cellular glycosylation may play a key role in their metastatic behaviour.
  • In the present study, we have assessed the relationship between cell surface oligosaccharides and the metastasis ability of mouse mammary tumor cell lines 67NR and 4TO7.
  • The cell lines used in study have different metastasis abilities in vivo - the 67NR form primary tumors, but no tumor cells are detectable in any distant tissues, while cells of the 4TO7 line are able to spread to lung.
  • The study suggests that the sialic acids are not crucial for the cell migration and invasion in the 4TO7 cells.
  • [MeSH-major] Cell Membrane / metabolism. Mammary Neoplasms, Animal / metabolism. Mammary Neoplasms, Animal / pathology. Oligosaccharides / chemistry. Oligosaccharides / physiology
  • [MeSH-minor] Animals. Cell Adhesion. Cell Line, Tumor. Cell Movement. Cells. Glycosylation. Lectins / chemistry. Mice. Neoplasm Invasiveness. Neoplasm Metastasis. Polysaccharides / chemistry. Sialic Acids / chemistry

  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 17650582.001).
  • [ISSN] 0301-1208
  • [Journal-full-title] Indian journal of biochemistry & biophysics
  • [ISO-abbreviation] Indian J. Biochem. Biophys.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] India
  • [Chemical-registry-number] 0 / Lectins; 0 / Oligosaccharides; 0 / Polysaccharides; 0 / Sialic Acids
  •  go-up   go-down


64. Meng X, Shoemaker SF, McGee SO, Ip MM: t10,c12-Conjugated linoleic acid stimulates mammary tumor progression in Her2/ErbB2 mice through activation of both proliferative and survival pathways. Carcinogenesis; 2008 May;29(5):1013-21
NCI CPTC Antibody Characterization Program. NCI CPTC Antibody Characterization Program .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] t10,c12-Conjugated linoleic acid stimulates mammary tumor progression in Her2/ErbB2 mice through activation of both proliferative and survival pathways.
  • The t10,c12 isomer of conjugated linoleic acid (CLA) inhibits rat mammary carcinogenesis, metastasis from a transplantable mouse mammary tumor and angiogenesis; however, it stimulates mammary tumorigenesis in transgenic mice overexpressing ErbB2 in the mammary epithelium (ErbB2 transgenic mice).
  • In the current study, we report that a 4-week supplementation of the diet with 0.5% trans-10, cis-12 conjugated linoleic acid (t10,c12-CLA) stimulated the growth of established ErbB2-overexpressing mammary tumors by 30% and increased the number of new tumors from 11% to 82%.
  • Additionally, when t10,c12-CLA supplementation of ErbB2 transgenic mice was initiated at 21 weeks of age, a time just prior to tumor appearance, overall survival was decreased from 46.4 weeks in the control to 39.0 weeks in the CLA group, and survival after detection of a palpable tumor from 7.5 to 4.6 weeks.
  • Short-term supplementation from 10 to 14 weeks or 21 to 25 weeks of age temporarily accelerated tumor development, but over the long term, there was no significant effect on mammary tumorigenesis.
  • Long term as well as a short 4-week supplementation increased mammary epithelial hyperplasia and lobular development, and altered the mammary stroma; this was reversible in mice returned to the control diet. t10,c12-CLA altered proliferation and apoptosis of the mammary epithelium, although this differed depending on the length of administration and/or the age of the mice.
  • The increased tumor development with t10,c12-CLA was associated with increased phosphorylation of the IGF-I/insulin receptor, as well as increased signaling through the mitogen-activated protein kinase kinase (MEK)/extracellular signal-regulated kinase and phosphatidylinositol 3-kinase/Akt pathways; however, neither phospho-ErbB2 nor ErbB2 was altered.

  • COS Scholar Universe. author profiles.
  • KOMP Repository. gene/protein/disease-specific - KOMP Repository (subscription/membership/fee required).
  • Mouse Genome Informatics (MGI). Mouse Genome Informatics (MGI) .
  • NCI CPTAC Assay Portal. NCI CPTAC Assay Portal .
  • NCI CPTC Antibody Characterization Program. NCI CPTC Antibody Characterization Program .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [Cites] J Nutr. 1999 Dec;129(12):2135-42 [10573540.001]
  • [Cites] Breast Cancer Res Treat. 2008 Jan;107(2):181-94 [17611793.001]
  • [Cites] EMBO J. 2000 Jul 3;19(13):3159-67 [10880430.001]
  • [Cites] Cancer Epidemiol Biomarkers Prev. 2000 Jul;9(7):689-96 [10919739.001]
  • [Cites] Nat Rev Mol Cell Biol. 2001 Feb;2(2):127-37 [11252954.001]
  • [Cites] Nature. 2001 May 17;411(6835):355-65 [11357143.001]
  • [Cites] Breast Cancer Res. 2001;3(6):385-9 [11737890.001]
  • [Cites] J Steroid Biochem Mol Biol. 2002 Feb;80(2):239-56 [11897507.001]
  • [Cites] FASEB J. 2002 Sep;16(11):1447-9 [12205043.001]
  • [Cites] J Lipid Res. 2002 Sep;43(9):1400-9 [12235171.001]
  • [Cites] Nutr Cancer. 2002;43(1):52-8 [12467135.001]
  • [Cites] Cancer Lett. 2003 Feb 10;190(1):13-9 [12536072.001]
  • [Cites] Am J Physiol Gastrointest Liver Physiol. 2003 Jun;284(6):G996-1005 [12571082.001]
  • [Cites] J Nutr. 2003 Aug;133(8):2675-81 [12888657.001]
  • [Cites] Oncologist. 2003;8(4):307-25 [12897328.001]
  • [Cites] J Mammary Gland Biol Neoplasia. 2003 Jan;8(1):103-18 [14587866.001]
  • [Cites] Cancer Lett. 2003 Dec 8;202(1):81-7 [14643029.001]
  • [Cites] Br J Nutr. 2003 Nov;90(5):877-85 [14667181.001]
  • [Cites] J Nutr. 2004 Mar;134(3):674-80 [14988466.001]
  • [Cites] J Biol Chem. 2004 Jun 18;279(25):26735-47 [15067015.001]
  • [Cites] Science. 1987 Jan 9;235(4785):177-82 [3798106.001]
  • [Cites] Science. 1989 May 12;244(4905):707-12 [2470152.001]
  • [Cites] Oncogene. 1994 Aug;9(8):2109-23 [7913542.001]
  • [Cites] Cancer Res. 1997 Nov 15;57(22):5067-72 [9371504.001]
  • [Cites] Nat Rev Cancer. 2005 May;5(5):341-54 [15864276.001]
  • [Cites] Growth Factors. 2006 Mar;24(1):21-44 [16393692.001]
  • [Cites] J Mammary Gland Biol Neoplasia. 2006 Jan;11(1):27-39 [16947084.001]
  • [Cites] Oncogene. 2007 Feb 26;26(9):1338-45 [17322919.001]
  • [Cites] Biochem Biophys Res Commun. 2007 May 18;356(4):1044-9 [17400188.001]
  • [Cites] Oncogene. 2007 May 14;26(22):3227-39 [17496918.001]
  • [Cites] Carcinogenesis. 2007 Jun;28(6):1269-76 [17259656.001]
  • [Cites] Reproduction. 2007 Jul;134(1):41-9 [17641087.001]
  • [Cites] Oncogene. 2007 Oct 4;26(45):6469-87 [17471238.001]
  • [Cites] Cancer Lett. 2000 Mar 13;150(1):93-100 [10755392.001]
  • (PMID = 18339686.001).
  • [ISSN] 1460-2180
  • [Journal-full-title] Carcinogenesis
  • [ISO-abbreviation] Carcinogenesis
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / R01 CA061763-14; United States / NCI NIH HHS / CA / CA16056; United States / NCI NIH HHS / CA / CA61763
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Linoleic Acids, Conjugated; 0 / trans-10,cis-12-conjugated linoleic acid
  • [Other-IDs] NLM/ NIHMS145335; NLM/ PMC2777529
  •  go-up   go-down


65. Hakkak R, Holley AW, Macleod SL, Simpson PM, Fuchs GJ, Jo CH, Kieber-Emmons T, Korourian S: Obesity promotes 7,12-dimethylbenz(a)anthracene-induced mammary tumor development in female zucker rats. Breast Cancer Res; 2005;7(5):R627-33
Hazardous Substances Data Bank. 7,12-DIMETHYLBENZ(A)ANTHRACENE .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Obesity promotes 7,12-dimethylbenz(a)anthracene-induced mammary tumor development in female zucker rats.
  • Here we describe studies using 7,12-dimethylbenz(a)anthracene (DMBA) to investigate the role of obesity in DMBA-induced mammary tumor susceptibility in the female Zucker rat (fa/fa), which is the most widely used rat model of genetic obesity.
  • Rats were weighed and palpated twice weekly for detection of mammary tumors.
  • RESULTS: The first mammary tumor was detected in the obese group at 49 days after DMBA treatment, as compared with 86 days in the lean group (P < 0.001).
  • The median tumor-free time was significantly lower in the obese group (P < 0.001).
  • Using the days after DMBA treatment at which 25% of the rats had developed mammary tumors as the marker of tumor latency, the obese group had a significantly shorter latency period (66 days) than did the lean group (118 days).
  • At the end of the study, obese rats had developed a significantly (P < 0.001) greater mammary tumor incidence (68% versus 32%) compared with the lean group.
  • The tumor histology of the mammary tumors revealed that obesity was associated with a significant (P < 0.05) increase in the number of rats with at least one invasive ductal and lobular carcinoma compared with lean rats.
  • CONCLUSION: Our results indicate that obesity increases the susceptibility of female Zucker rats to DMBA-induced mammary tumors, further supporting the hypothesis that obesity and some of its mediators play a significant role in carcinogenesis.
  • [MeSH-major] 9,10-Dimethyl-1,2-benzanthracene / toxicity. Mammary Neoplasms, Experimental / epidemiology. Obesity / complications

  • MedlinePlus Health Information. consumer health - Obesity.
  • COS Scholar Universe. author profiles.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [Cites] Cancer Lett. 2001 Jan 26;162(2):155-60 [11146220.001]
  • [Cites] Breast Cancer Res Treat. 2004 Aug;86(3):191-6 [15567935.001]
  • [Cites] Cancer Causes Control. 2002 Oct;13(8):741-51 [12420953.001]
  • [Cites] Cancer Epidemiol Biomarkers Prev. 2000 Jan;9(1):113-7 [10667471.001]
  • [Cites] Dig Dis Sci. 2000 May;45(5):890-5 [10795750.001]
  • [Cites] Carcinogenesis. 2000 Jul;21(7):1281-9 [10874004.001]
  • [Cites] Am J Epidemiol. 2000 Sep 15;152(6):514-27 [10997541.001]
  • [Cites] J Natl Cancer Inst. 2002 Nov 20;94(22):1704-11 [12441326.001]
  • [Cites] JAMA. 2003 Jan 1;289(1):76-9 [12503980.001]
  • [Cites] N Engl J Med. 2003 Apr 24;348(17):1625-38 [12711737.001]
  • [Cites] Int J Cancer. 2004 Sep 20;111(5):762-71 [15252848.001]
  • [Cites] Arch Surg. 2004 Sep;139(9):954-58; discussion 958-60 [15381612.001]
  • [Cites] Br J Nutr. 2004 Sep;92(3):347-55 [15469638.001]
  • [Cites] J Lipid Res. 1972 Mar;13(2):234-43 [5016304.001]
  • [Cites] Fed Proc. 1977 Feb;36(2):148-53 [320051.001]
  • [Cites] J Toxicol Environ Health. 1982 Jul;10(1):131-42 [6290678.001]
  • [Cites] Int J Cancer. 1989 May 15;43(5):922-5 [2497075.001]
  • [Cites] Cancer Res. 1989 Aug 1;49(15):4130-4 [2501021.001]
  • [Cites] Vitam Horm. 1989;45:1-125 [2688303.001]
  • [Cites] Proc Soc Exp Biol Med. 1991 Apr;196(4):381-4 [1901169.001]
  • [Cites] Fundam Appl Toxicol. 1994 Jul;23(1):44-52 [7958562.001]
  • [Cites] Cell. 1995 Dec 29;83(7):1263-71 [8548812.001]
  • [Cites] Cancer Res. 1996 Jan 15;56(2):287-93 [8542582.001]
  • [Cites] Science. 1996 Feb 16;271(5251):994-6 [8584938.001]
  • [Cites] Am J Clin Nutr. 1996 Mar;63(3 Suppl):437S-41S [8615337.001]
  • [Cites] Breast Cancer Res Treat. 1996;39(1):7-20 [8738602.001]
  • [Cites] Environ Health Perspect. 1996 Sep;104(9):938-67 [8899375.001]
  • [Cites] Proc Soc Exp Biol Med. 1997 Mar;214(3):222-32 [9083255.001]
  • [Cites] J Nutr. 1997 May;127(5 Suppl):921S-923S [9164264.001]
  • [Cites] Proc Soc Exp Biol Med. 1997 Oct;216(1):28-43 [9316608.001]
  • [Cites] Cancer Causes Control. 1998 Mar;9(2):217-24 [9578299.001]
  • [Cites] J Nutr. 1963 May;80:6-19 [14004033.001]
  • [Cites] J Nutr. 2001 Dec;131(12):3281-7 [11739881.001]
  • (PMID = 16168107.001).
  • [ISSN] 1465-542X
  • [Journal-full-title] Breast cancer research : BCR
  • [ISO-abbreviation] Breast Cancer Res.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 57-97-6 / 9,10-Dimethyl-1,2-benzanthracene
  • [Other-IDs] NLM/ PMC1242129
  •  go-up   go-down


66. Davie SA, Maglione JE, Manner CK, Young D, Cardiff RD, MacLeod CL, Ellies LG: Effects of FVB/NJ and C57Bl/6J strain backgrounds on mammary tumor phenotype in inducible nitric oxide synthase deficient mice. Transgenic Res; 2007 Apr;16(2):193-201
Mouse Genome Informatics (MGI). Mouse Genome Informatics (MGI) .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Effects of FVB/NJ and C57Bl/6J strain backgrounds on mammary tumor phenotype in inducible nitric oxide synthase deficient mice.
  • The ability to genetically manipulate mice has led to rapid progress in our understanding of the roles of different gene products in human disease.
  • Genetic modifiers have been shown to modulate mammary tumor latency in mouse models of breast cancer and it is commonly known that the FVB strain is susceptible to mammary tumors while the B6 strain is more resistant.
  • Our results reveal that the large difference in mean tumor latencies in the two backgrounds of 53 and 92 days respectively affect the ability to discern smaller differences in latency due to the Nos2 genetic mutation.
  • Furthermore, the longer latency in the B6 strain enables a more detailed analysis of tumor formation indicating that individual tumor development is not stoichastic, but is initiated in the #1 glands and proceeds in early and late phases.
  • NO production affects tumors that develop early suggesting an association of iNOS-induced NO with a more aggressive tumor phenotype, consistent with human clinical data positively correlating iNOS expression with breast cancer progression.

  • COS Scholar Universe. author profiles.
  • Jackson Laboratory JAX®Mice Database. culture/stock collections - B6.FVB-Tg(MMTV-PyVT)634Mul/LellJ (subscription/membership/fee required).
  • KOMP Repository. gene/protein/disease-specific - KOMP Repository (subscription/membership/fee required).
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [Cites] J Biol Chem. 2004 Dec 3;279(49):51630-46 [15355971.001]
  • [Cites] Dev Biol. 2006 Jul 1;295(1):219-31 [16678815.001]
  • [Cites] Development. 2006 Jun;133(12):2325-35 [16720875.001]
  • [Cites] Cancer Cell. 2005 Jun;7(6):575-89 [15950906.001]
  • [Cites] Oncol Rep. 2005 Apr;13(4):559-83 [15756426.001]
  • [Cites] Eur J Cancer. 2005 Jan;41(2):265-71 [15661552.001]
  • [Cites] J Natl Cancer Inst. 1965 Apr;34:521-7 [14317645.001]
  • [Cites] Development. 2002 Jan;129(1):53-60 [11782400.001]
  • [Cites] J Mammary Gland Biol Neoplasia. 1999 Jan;4(1):105-22 [10219910.001]
  • [Cites] Int J Cancer. 1998 Aug 12;77(4):640-4 [9679770.001]
  • [Cites] Cancer Lett. 1998 Apr 10;126(1):49-57 [9563648.001]
  • [Cites] Mol Cell Biol. 1998 Apr;18(4):2344-59 [9528804.001]
  • [Cites] Proc Natl Acad Sci U S A. 1995 Nov 7;92(23):10688-92 [7479866.001]
  • [Cites] Genes Dev. 1994 Jan;8(1):23-32 [7507074.001]
  • [Cites] Virology. 1992 Dec;191(2):724-31 [1333121.001]
  • [Cites] Mol Cell Biol. 1992 Mar;12(3):954-61 [1312220.001]
  • [Cites] Hepatology. 1991 Jan;13(1):15-20 [1988335.001]
  • [Cites] Proc Natl Acad Sci U S A. 1985 Sep;82(17):5940-3 [3875855.001]
  • [Cites] Proc Natl Acad Sci U S A. 1967 Apr;57(4):1068-75 [4291920.001]
  • [Cites] Cancer Res. 2004 Sep 1;64(17):5973-81 [15342376.001]
  • [Cites] J Anat. 2004 Jul;205(1):1-13 [15255957.001]
  • [Cites] J Mammary Gland Biol Neoplasia. 2003 Jul;8(3):321-34 [14973376.001]
  • [Cites] Dev Dyn. 2004 Feb;229(2):349-56 [14745960.001]
  • [Cites] Comp Med. 2003 Jun;53(3):250-3 [12868567.001]
  • [Cites] Int J Cancer. 2003 Aug 10;106(1):1-7 [12794750.001]
  • [Cites] Am J Pathol. 2002 Sep;161(3):1087-97 [12213737.001]
  • [Cites] Nat Genet. 2003 Jan;33(1):49-54 [12469122.001]
  • [Cites] Proc Natl Acad Sci U S A. 2003 May 13;100(10):5974-9 [12714683.001]
  • [Cites] Nat Rev Mol Cell Biol. 2002 Sep;3(9):697-702 [12209129.001]
  • [Cites] Mamm Genome. 2000 Oct;11(10):883-9 [11003704.001]
  • [Cites] J Exp Med. 2001 Mar 19;193(6):727-40 [11257139.001]
  • [Cites] Br J Cancer. 2001 May 4;84(9):1188-92 [11336469.001]
  • [Cites] J Mammary Gland Biol Neoplasia. 2001 Jan;6(1):1-5 [11467445.001]
  • (PMID = 17206489.001).
  • [ISSN] 0962-8819
  • [Journal-full-title] Transgenic research
  • [ISO-abbreviation] Transgenic Res.
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / K08 CA088035; United States / NCI NIH HHS / CA / K08-CA88035; United States / NCI NIH HHS / CA / R01-CA81376
  • [Publication-type] Comparative Study; Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
  • [Publication-country] Netherlands
  • [Chemical-registry-number] EC 1.14.13.39 / Nitric Oxide Synthase Type II
  • [Other-IDs] NLM/ PMC1829418
  •  go-up   go-down


67. Lowther W, Wiley K, Smith GH, Callahan R: A new common integration site, Int7, for the mouse mammary tumor virus in mouse mammary tumors identifies a gene whose product has furin-like and thrombospondin-like sequences. J Virol; 2005 Aug;79(15):10093-6
The Lens. Cited by Patents in .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] A new common integration site, Int7, for the mouse mammary tumor virus in mouse mammary tumors identifies a gene whose product has furin-like and thrombospondin-like sequences.
  • A novel common integration site for the mouse mammary tumor virus (MMTV) was identified (designated Int7) in five independently arising mouse mammary tumors.
  • Expression of Int7 is normally very low or silent during various stages of mammary gland development, but MMTV integration at this site results in the activation of high steady-state levels of expression of the gene.
  • These five tumors were also found to have two or three additional viral insertions, which in each case occurred flanking a member of either the Wnt and/or FGF gene family.
  • [MeSH-major] Chromosomes / genetics. Mammary Neoplasms, Experimental / genetics. Mammary Tumor Virus, Mouse / physiology. Mice / genetics. Retroviridae Infections / genetics. Tumor Virus Infections / genetics. Virus Integration

  • COS Scholar Universe. author profiles.
  • KOMP Repository. gene/protein/disease-specific - KOMP Repository (subscription/membership/fee required).
  • Mouse Genome Informatics (MGI). Mouse Genome Informatics (MGI) .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [Cites] Oncogene. 2000 Feb 21;19(8):992-1001 [10713682.001]
  • [Cites] Oncogene. 2002 Oct 17;21(47):7247-55 [12370816.001]
  • [Cites] Nature. 2002 Dec 5;420(6915):563-73 [12466851.001]
  • [Cites] Nucleic Acids Res. 2004 Jan 1;32(Database issue):D523-7 [14681473.001]
  • [Cites] J Virol. 2004 Feb;78(4):1971-80 [14747562.001]
  • [Cites] J Virol. 1987 Jan;61(1):218-20 [3023699.001]
  • [Cites] Cancer Res. 2004 Jul 1;64(13):4419-27 [15231650.001]
  • [Cites] J Virol. 1989 May;63(5):1924-8 [2704070.001]
  • [Cites] Mol Cell Biol. 1992 Jan;12(1):147-54 [1530875.001]
  • [Cites] Proc Natl Acad Sci U S A. 1993 Jan 15;90(2):740-4 [8380647.001]
  • [Cites] J Virol. 1995 Mar;69(3):1932-8 [7853537.001]
  • [Cites] J Virol. 1995 Apr;69(4):2501-7 [7884899.001]
  • [Cites] Proc Natl Acad Sci U S A. 1995 Mar 14;92(6):2268-72 [7892260.001]
  • [Cites] EMBO J. 1988 Jul;7(7):2089-95 [3416834.001]
  • (PMID = 16014973.001).
  • [ISSN] 0022-538X
  • [Journal-full-title] Journal of virology
  • [ISO-abbreviation] J. Virol.
  • [Language] eng
  • [Publication-type] Comparative Study; Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Thrombospondin 1; EC 3.4.21.75 / Furin
  • [Other-IDs] NLM/ PMC1181551
  •  go-up   go-down


68. Hakkak R, Shaaf S, Jo CH, MacLeod S, Korourian S: Dehydroepiandrosterone intake protects against 7,12-dimethylbenz(a)anthracene-induced mammary tumor development in the obese Zucker rat model. Oncol Rep; 2010 Aug;24(2):357-62
COS Scholar Universe. author profiles.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Dehydroepiandrosterone intake protects against 7,12-dimethylbenz(a)anthracene-induced mammary tumor development in the obese Zucker rat model.
  • Dehydroepiandrosterone (DHEA) is an over-the-counter dietary supplement used as an immunomodulating, anti-depressant, anti-aging, anti-cardiovascular disease, and anti-cancer agent and anti-obesity supplement.
  • The objectives of this study were to investigate the long-term effects of obesity and DHEA treatment on body weight gain and on 7,12-dimethylbenz(a)anthracene (DMBA)-induced mammary tumor development.
  • Rats were weighed and palpated twice weekly for detection of mammary tumors and sacrificed 155 days post-DMBA treatment.
  • At the end of the experiment, 55% of the control diet group developed mammary tumors, while no tumors were detected in the DHEA diet group (P<0.001).
  • Our results suggest that DHEA treatment can reduce body weight gain and protects against DMBA-induced mammary tumor development in the obese Zucker rat model.
  • [MeSH-major] Benz(a)Anthracenes. Carcinoma, Ductal, Breast / chemically induced. Carcinoma, Ductal, Breast / prevention & control. Dehydroepiandrosterone / pharmacology. Mammary Neoplasms, Experimental / chemically induced. Mammary Neoplasms, Experimental / prevention & control. Obesity / complications

  • MedlinePlus Health Information. consumer health - Breast Cancer.
  • MedlinePlus Health Information. consumer health - Obesity.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 20596621.001).
  • [ISSN] 1791-2431
  • [Journal-full-title] Oncology reports
  • [ISO-abbreviation] Oncol. Rep.
  • [Language] eng
  • [Publication-type] Comparative Study; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Greece
  • [Chemical-registry-number] 0 / Benz(a)Anthracenes; 0 / Carcinogens; 2564-65-0 / 7,12-dihydroxymethylbenz(a)anthracene; 459AG36T1B / Dehydroepiandrosterone
  •  go-up   go-down


69. Simian M, Manzur T, Rodriguez V, de Kier Joffé EB, Klein S: A spontaneous estrogen dependent, tamoxifen sensitive mouse mammary tumor: a new model system to study hormone-responsiveness in immune competent mice. Breast Cancer Res Treat; 2009 Jan;113(1):1-8
Hazardous Substances Data Bank. TAMOXIFEN .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] A spontaneous estrogen dependent, tamoxifen sensitive mouse mammary tumor: a new model system to study hormone-responsiveness in immune competent mice.
  • Currently, an in vivo spontaneous model of estrogen dependent, tamoxifen sensitive breast cancer does not exist.
  • We show here the characterization of the M05 mammary tumor that appeared spontaneously in a 1-year-old virgin female BALB/c mouse in our animal facility.
  • The M05 tumor is a semi-differentiated adenocarcinoma that expresses estrogen and progesterone receptors.
  • When it was transplanted to either male or ovariectomized female mice it did not grow.
  • Moreover, ovariectomy or treatment with tamoxifen of tumor bearing mice led to a halt in tumor growth.
  • Treatment of ovariectomized mice that had been inoculated with the M05 tumor showed that only estradiol, but not progesterone, promoted the re-growth of the tumor.
  • Finally, after passage nine, tumor growth was achieved in male and ovariectomized female mice suggesting that the tumor had progressed to hormone independence.
  • [MeSH-major] Mammary Neoplasms, Experimental / drug therapy. Tamoxifen / therapeutic use
  • [MeSH-minor] Adenocarcinoma / drug therapy. Adenocarcinoma / immunology. Adenocarcinoma / pathology. Animals. Cell Division. Female. Immunocompetence. Male. Mice. Mice, Inbred BALB C. Neoplasm Transplantation / methods. Neoplasm Transplantation / pathology. Ovariectomy. Receptors, Estrogen / metabolism. Receptors, Progesterone / metabolism

  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 18183485.001).
  • [ISSN] 1573-7217
  • [Journal-full-title] Breast cancer research and treatment
  • [ISO-abbreviation] Breast Cancer Res. Treat.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Netherlands
  • [Chemical-registry-number] 0 / Receptors, Estrogen; 0 / Receptors, Progesterone; 094ZI81Y45 / Tamoxifen
  •  go-up   go-down


70. Ross SR, Schmidt JW, Katz E, Cappelli L, Hultine S, Gimotty P, Monroe JG: An immunoreceptor tyrosine activation motif in the mouse mammary tumor virus envelope protein plays a role in virus-induced mammary tumors. J Virol; 2006 Sep;80(18):9000-8
eagle-i research resources. PMID 16940512 (University of Pennsylvania) .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] An immunoreceptor tyrosine activation motif in the mouse mammary tumor virus envelope protein plays a role in virus-induced mammary tumors.
  • Mouse mammary tumor virus (MMTV) induces breast cancer with almost 100% efficiency in susceptible strains through insertional activation of protooncogenes, such as members of the wnt and fibroblast growth factor (fgf) families.
  • We previously showed that expression of the MMTV envelope protein (Env) in normal immortalized mammary epithelial cells grown in three-dimensional cultures caused their morphological transformation, and that this phenotype depended on an immunoreceptor tyrosine-based activation motif (ITAM) present in Env and signaling through the Syk tyrosine kinase (E.
  • Here, we examined the role of the Env protein in virus-induced mammary tumorigenesis in vivo.
  • Similar to the effect seen in vitro, Env expression in the mammary glands of transgenic mice bearing either full-length wild-type provirus or only Env transgenes showed increased lobuloalveolar budding.
  • Moreover, replication-competent MMTV bearing the ITAM mutation in Env infected lymphoid and mammary tissue at the same level as wild-type MMTV and was transmitted through milk.
  • However, mammary tumor induction was greatly attenuated, and the pattern of oncogene activation was altered.
  • Taken together, these studies indicate that the MMTV Env protein participates in mammary epithelial cell transformation in vivo and that this requires a functional ITAM in the envelope protein.

  • COS Scholar Universe. author profiles.
  • Hazardous Substances Data Bank. L-TYROSINE .
  • NCI CPTAC Assay Portal. NCI CPTAC Assay Portal .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [Cites] Virology. 1999 Oct 25;263(2):418-26 [10544114.001]
  • [Cites] J Biol Chem. 1991 Oct 15;266(29):19384-95 [1655786.001]
  • [Cites] J Virol. 1999 Dec;73(12):9810-5 [10559292.001]
  • [Cites] Oncogene. 2000 Feb 21;19(8):992-1001 [10713682.001]
  • [Cites] Nature. 2000 Aug 17;406(6797):742-7 [10963601.001]
  • [Cites] J Virol. 1993 Dec;67(12):7690-4 [8230492.001]
  • [Cites] EMBO J. 1993 Dec 15;12(13):5105-12 [8262054.001]
  • [Cites] J Exp Med. 1994 Feb 1;179(2):439-46 [8294859.001]
  • [Cites] J Virol. 1994 Aug;68(8):5019-26 [8035502.001]
  • [Cites] EMBO J. 1995 Jan 16;14(2):247-56 [7835336.001]
  • [Cites] Nucleic Acids Res. 1995 Feb 25;23(4):628-33 [7899083.001]
  • [Cites] J Virol. 1995 Jul;69(7):4137-41 [7769672.001]
  • [Cites] J Virol. 1996 Feb;70(2):1246-9 [8551589.001]
  • [Cites] Virology. 1996 Jun 15;220(2):265-6 [8661376.001]
  • [Cites] J Exp Med. 2005 Feb 7;201(3):431-9 [15684322.001]
  • [Cites] Nature. 2005 Apr 14;434(7035):904-7 [15829964.001]
  • [Cites] Blood. 2005 May 15;105(10):3987-94 [15665117.001]
  • [Cites] Immunol Lett. 2006 Apr 15;104(1-2):29-37 [16332394.001]
  • [Cites] Nat Rev Immunol. 2006 Apr;6(4):283-94 [16557260.001]
  • [Cites] Oncogene. 2006 May 4;25(19):2748-57 [16369490.001]
  • [Cites] Immunol Lett. 1996 Dec;54(2-3):163-9 [9052872.001]
  • [Cites] Virology. 1997 Sep 1;235(2):241-51 [9281504.001]
  • [Cites] J Virol. 1998 Apr;72(4):3066-71 [9525630.001]
  • [Cites] Receptors Channels. 1998;5(5):243-53 [9666518.001]
  • [Cites] Mol Cell Biol. 1998 Aug;18(8):4872-82 [9671496.001]
  • [Cites] Mol Cell Biol. 1998 Sep;18(9):5219-28 [9710606.001]
  • [Cites] J Immunol. 1998 Sep 1;161(5):2375-82 [9725233.001]
  • [Cites] Proc Natl Acad Sci U S A. 1999 May 11;96(10):5704-9 [10318948.001]
  • [Cites] Immunol Lett. 1999 May 3;68(1):3-15 [10397150.001]
  • [Cites] J Virol. 2000 Oct;74(19):8876-83 [10982330.001]
  • [Cites] J Virol. 2000 Oct;74(19):9115-24 [10982358.001]
  • [Cites] Dev Biol. 2001 Apr 1;232(1):219-32 [11254359.001]
  • [Cites] Proc Natl Acad Sci U S A. 2001 Apr 10;98(8):4443-8 [11296287.001]
  • [Cites] Proc Natl Acad Sci U S A. 2001 Apr 10;98(8):4449-54 [11296288.001]
  • [Cites] J Virol. 2001 Jul;75(13):5891-8 [11390590.001]
  • [Cites] Eur J Immunol. 2001 Sep;31(9):2603-11 [11536158.001]
  • [Cites] J Exp Med. 2001 Dec 3;194(11):1583-96 [11733573.001]
  • [Cites] J Virol. 2002 Mar;76(5):2363-74 [11836414.001]
  • [Cites] Nat Genet. 2002 Sep;32(1):153-9 [12185366.001]
  • [Cites] Proc Natl Acad Sci U S A. 2002 Sep 17;99(19):12386-90 [12218182.001]
  • [Cites] Immunity. 2002 Oct;17(4):401-12 [12387735.001]
  • [Cites] J Virol. 2003 Feb;77(3):1951-63 [12525629.001]
  • [Cites] Proc Natl Acad Sci U S A. 2003 Jul 8;100(14):8454-9 [12832623.001]
  • [Cites] J Virol. 2003 Oct;77(19):10468-78 [12970432.001]
  • [Cites] Curr Opin Cell Biol. 2003 Oct;15(5):515-24 [14519385.001]
  • [Cites] J Virol. 2004 Jan;78(1):454-63 [14671125.001]
  • [Cites] Proc Natl Acad Sci U S A. 2003 Dec 23;100(26):15853-8 [14668450.001]
  • [Cites] Proc Natl Acad Sci U S A. 2004 Apr 13;101(15):5598-603 [15034168.001]
  • [Cites] J Biol Chem. 2004 Jul 30;279(31):32308-15 [15173175.001]
  • [Cites] J Virol. 2004 Aug;78(16):8506-12 [15280459.001]
  • [Cites] Adv Cancer Res. 1979;29:347-418 [89801.001]
  • [Cites] J Mol Appl Genet. 1982;1(4):327-41 [6286831.001]
  • [Cites] Cell. 1982 Nov;31(1):99-109 [6297757.001]
  • [Cites] Cancer Res. 1983 Dec;43(12 Pt 1):5879-82 [6315219.001]
  • [Cites] Cell. 1984 Jun;37(2):529-36 [6327073.001]
  • [Cites] EMBO J. 1986 May;5(5):919-24 [3013624.001]
  • [Cites] J Virol. 1987 Oct;61(10):3013-9 [3041021.001]
  • [Cites] Cell. 1988 Nov 18;55(4):619-25 [3180222.001]
  • [Cites] Proc Natl Acad Sci U S A. 1988 Dec;85(24):9655-9 [2849114.001]
  • [Cites] EMBO J. 1990 Mar;9(3):907-13 [1690126.001]
  • [ErratumIn] J Virol. 2007 Nov;81(22):12718
  • (PMID = 16940512.001).
  • [ISSN] 0022-538X
  • [Journal-full-title] Journal of virology
  • [ISO-abbreviation] J. Virol.
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / R01 CA073746; United States / NCI NIH HHS / CA / R01 CA 73746
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Viral Envelope Proteins; 42HK56048U / Tyrosine
  • [Other-IDs] NLM/ PMC1563925
  •  go-up   go-down


71. Hembruff SL, Jokar I, Yang L, Cheng N: Loss of transforming growth factor-beta signaling in mammary fibroblasts enhances CCL2 secretion to promote mammary tumor progression through macrophage-dependent and -independent mechanisms. Neoplasia; 2010 May;12(5):425-33

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Loss of transforming growth factor-beta signaling in mammary fibroblasts enhances CCL2 secretion to promote mammary tumor progression through macrophage-dependent and -independent mechanisms.
  • Whereas the accumulation of fibroblasts and macrophages in breast cancer is a well-documented phenomenon and correlates with metastatic disease, the functional contributions of these stromal cells on breast cancer progression still remain largely unclear.
  • Previous studies have uncovered a potentially important role for CCL2 inflammatory chemokine signaling in regulating metastatic disease through a macrophage-dependent mechanism.
  • In these studies, we demonstrate a significant regulatory mechanism for CCL2 expression in fibroblasts in mediating mammary tumor progression and characterize multiple functions for CCL2 in regulating stromal-epithelial interactions.
  • Targeted ablation of the transforming growth factor-beta (TGF-beta) type 2 receptor in fibroblasts (Tgfbr2(FspKO)) results in a high level of secretion of CCL2, and cografts of Tgfbr2(FspKO) fibroblasts with 4T1 mammary carcinoma cells enhanced tumor progression associated with recruitment of tumor-associated macrophages (TAMs).
  • Antibody neutralization of CCL2 in tumor-bearing mice inhibits primary tumor growth and liver metastases as evidenced by reduced cell proliferation, survival, and TAM recruitment.
  • Both high and low stable expressions of small interfering RNA to CCL2 in Tgfbr2(FspKO) fibroblasts significantly reduce liver metastases without significantly affecting primary tumor growth, cell proliferation, or TAM recruitment.
  • High but not low knockdown of CCL2 enhances tumor cell apoptosis.
  • These data indicate that CCL2 enhances primary tumor growth, survival, and metastases in a dose-dependent manner, through TAM-dependent and -independent mechanisms, with important implications on the potential effects of targeting CCL2 chemokine signaling in the metastatic disease.

  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [Cites] J Biol Chem. 2009 Oct 16;284(42):29087-96 [19720836.001]
  • [Cites] Int J Cancer. 2009 Sep 15;125(6):1276-84 [19479998.001]
  • [Cites] Neoplasia. 2009 Dec;11(12):1309-17 [20019839.001]
  • [Cites] Blood. 2000 Jul 1;96(1):34-40 [10891427.001]
  • [Cites] Clin Cancer Res. 2000 Aug;6(8):3282-9 [10955814.001]
  • [Cites] Cell Immunol. 2001 Feb 1;207(2):81-8 [11243697.001]
  • [Cites] Trends Cell Biol. 2001 Nov;11(11):S44-51 [11684442.001]
  • [Cites] Science. 2002 Apr 19;296(5567):550-3 [11910072.001]
  • [Cites] Virology. 2003 May 10;309(2):196-202 [12758167.001]
  • [Cites] J Gen Virol. 2003 Sep;84(Pt 9):2389-400 [12917460.001]
  • [Cites] J Med Genet. 2004 May;41(5):e59 [15121787.001]
  • [Cites] Cancer Cell. 2004 Oct;6(4):409-21 [15488763.001]
  • [Cites] Clin Cancer Res. 2004 Oct 15;10(20):6789-95 [15501955.001]
  • [Cites] Cytokine. 1993 May;5(3):264-75 [8218939.001]
  • [Cites] J Exp Med. 1997 Nov 17;186(10):1757-62 [9362535.001]
  • [Cites] J Clin Invest. 1997 Nov 15;100(10):2552-61 [9366570.001]
  • [Cites] J Exp Med. 1998 Feb 16;187(4):601-8 [9463410.001]
  • [Cites] Pathol Res Pract. 1998;194(5):335-40 [9651946.001]
  • [Cites] Differentiation. 1998 Jul;63(3):131-40 [9697307.001]
  • [Cites] Trends Pharmacol Sci. 1999 Apr;20(4):151-6 [10322500.001]
  • [Cites] Oncogene. 2005 Jul 28;24(32):5053-68 [15856015.001]
  • [Cites] Cell. 2005 Dec 16;123(6):985-7 [16360028.001]
  • [Cites] Cancer Res. 2006 Jan 15;66(2):605-12 [16423985.001]
  • [Cites] Cell. 2006 Jan 27;124(2):263-6 [16439202.001]
  • [Cites] Biochem Biophys Res Commun. 2006 Sep 22;348(2):406-12 [16884687.001]
  • [Cites] Cancer Res. 2007 May 15;67(10):4869-77 [17495323.001]
  • [Cites] Adv Exp Med Biol. 2007;604:67-86 [17695721.001]
  • [Cites] Front Biosci. 2008;13:2548-77 [17981734.001]
  • [Cites] J Neurooncol. 2008 Jan;86(2):153-63 [17703277.001]
  • [Cites] Crit Rev Oncol Hematol. 2008 Apr;66(1):1-9 [17913510.001]
  • [Cites] Sci Signal. 2008;1(10):pe13 [18334714.001]
  • [Cites] Nat Med. 2008 May;14(5):518-27 [18438415.001]
  • [Cites] Cytokine. 2008 Oct;44(1):191-200 [18790652.001]
  • [Cites] J Virol. 2009 Jan;83(2):522-39 [18987138.001]
  • [Cites] Neoplasia. 2009 Nov;11(11):1235-42 [19881959.001]
  • (PMID = 20454514.001).
  • [ISSN] 1476-5586
  • [Journal-full-title] Neoplasia (New York, N.Y.)
  • [ISO-abbreviation] Neoplasia
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / K99 CA127357; United States / NCI NIH HHS / CA / 1K99CA127357-01A2
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Chemokine CCL2; 0 / RNA, Small Interfering; 0 / Transforming Growth Factor beta
  • [Other-IDs] NLM/ PMC2864480
  •  go-up   go-down


72. Lamb CA, Fabris V, Gorostiaga MA, Helguero LA, Efeyan A, Bottino MC, Simian M, Soldati R, Sanjuan N, Molinolo A, Lanari C: Isolation of a stromal cell line from an early passage of a mouse mammary tumor line: a model for stromal parenchymal interactions. J Cell Physiol; 2005 Mar;202(3):672-82
NCI CPTAC Assay Portal. NCI CPTAC Assay Portal .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Isolation of a stromal cell line from an early passage of a mouse mammary tumor line: a model for stromal parenchymal interactions.
  • We have developed a murine mammary tumor cell line, MC4-L4, and after 15 passages, a spindle-shaped population became evident.
  • The cuboidal cells, MC4-L4E, cloned by limit dilution, proved to be epithelial tumor cells.
  • These tumors regressed after anti-progestin treatment and stopped growing after 17-beta-estradiol administration.
  • Cells were polyploid and shared the same four common marker chromosomes present in the parental tumor in addition to an exclusive marker.
  • They were cytokeratin negative, showed mesenchymal features by electron microscopy, differentiated to adipocytes when treated with an adipogenic cocktail, were stimulated by TGFbeta1 and EGF, showed a wild-type p53, and did not exhibit the marker chromosomes of the parental tumor.
  • Their unique characteristics make them an excellent model to be used in studies of epithelial-stromal interactions in the context of hormone responsiveness in hormone related tumors.
  • [MeSH-major] Breast Neoplasms. Cell Line, Tumor. Mammary Glands, Animal / cytology. Stromal Cells
  • [MeSH-minor] Animals. Antineoplastic Agents, Hormonal / metabolism. Cell Culture Techniques / methods. Cell Differentiation. Cell Shape. Coculture Techniques. Epidermal Growth Factor / metabolism. Estradiol / metabolism. Female. Fibroblasts / cytology. Fibroblasts / metabolism. Genetic Markers. Hormone Antagonists / metabolism. Humans. Keratins / metabolism. Medroxyprogesterone Acetate / metabolism. Mice. Mice, Inbred BALB C. Mifepristone / metabolism. Mutation. Neoplasm Transplantation. Receptors, Estrogen / metabolism. Receptors, Progesterone / metabolism. Transforming Growth Factor beta / metabolism. Transforming Growth Factor beta1. Tumor Suppressor Protein p53 / genetics. Tumor Suppressor Protein p53 / metabolism

  • MedlinePlus Health Information. consumer health - Breast Cancer.
  • Hazardous Substances Data Bank. ESTRADIOL .
  • Hazardous Substances Data Bank. MIFEPRISTONE .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [Copyright] 2004 Wiley-Liss, Inc.
  • (PMID = 15389583.001).
  • [ISSN] 0021-9541
  • [Journal-full-title] Journal of cellular physiology
  • [ISO-abbreviation] J. Cell. Physiol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antineoplastic Agents, Hormonal; 0 / Genetic Markers; 0 / Hormone Antagonists; 0 / Receptors, Estrogen; 0 / Receptors, Progesterone; 0 / TGFB1 protein, human; 0 / Tgfb1 protein, mouse; 0 / Transforming Growth Factor beta; 0 / Transforming Growth Factor beta1; 0 / Tumor Suppressor Protein p53; 320T6RNW1F / Mifepristone; 4TI98Z838E / Estradiol; 62229-50-9 / Epidermal Growth Factor; 68238-35-7 / Keratins; C2QI4IOI2G / Medroxyprogesterone Acetate
  •  go-up   go-down


73. Koyama H, Hibi T, Isogai Z, Yoneda M, Fujimori M, Amano J, Kawakubo M, Kannagi R, Kimata K, Taniguchi S, Itano N: Hyperproduction of hyaluronan in neu-induced mammary tumor accelerates angiogenesis through stromal cell recruitment: possible involvement of versican/PG-M. Am J Pathol; 2007 Mar;170(3):1086-99
SciCrunch. Marmoset Gene list: Data: Gene Annotation .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Hyperproduction of hyaluronan in neu-induced mammary tumor accelerates angiogenesis through stromal cell recruitment: possible involvement of versican/PG-M.
  • Here, we investigated the roles of hyaluronan in carcinogenesis and cancer progression using the mouse mammary tumor virus (MMTV)-Neu transgenic model of spontaneous breast cancer.
  • In expressing Cre recombinase under the control of the MMTV promoter, the bigenic mice bearing Has2 and neu transgenes exhibited a deposition of hyaluronan matrix and aggressive growth of Neu-initiated mammary tumors.
  • Notably, forced expression of Has2 impaired intercellular adhesion machinery and elicited cell survival signals in tumor cells.
  • Concurrent with these alterations of tumor cells, intratumoral stroma and microvessels were markedly induced.
  • Administration of hyaluronan-versican aggregates, but not native hyaluronan alone, promoted stromal cell recruitment concurrently with the infiltration of endothelial cells.
  • Taken together, these results suggest that hyaluronan overproduction accelerates tumor angiogenesis through stromal reaction, notably in the presence of versican.
  • [MeSH-major] Hyaluronic Acid / biosynthesis. Mammary Neoplasms, Experimental / metabolism. Neovascularization, Pathologic / metabolism. Stromal Cells / metabolism. Versicans / metabolism

  • Hazardous Substances Data Bank. HYALURONIC ACID .
  • KOMP Repository. gene/protein/disease-specific - KOMP Repository (subscription/membership/fee required).
  • Mouse Genome Informatics (MGI). Mouse Genome Informatics (MGI) .
  • NCI CPTAC Assay Portal. NCI CPTAC Assay Portal .
  • NCI CPTC Antibody Characterization Program. NCI CPTC Antibody Characterization Program .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [Cites] Nat Rev Cancer. 2006 May;6(5):392-401 [16572188.001]
  • [Cites] Acta Biochim Pol. 2000;47(4):1081-91 [11996098.001]
  • [Cites] Am J Pathol. 2006 Jul;169(1):325-36 [16816384.001]
  • [Cites] J Biol Chem. 2006 Sep 8;281(36):26512-9 [16809345.001]
  • [Cites] Am J Pathol. 2000 Feb;156(2):529-36 [10666382.001]
  • [Cites] J Clin Invest. 2000 Aug;106(3):349-60 [10930438.001]
  • [Cites] Mol Biol Cell. 2001 Jun;12(6):1859-68 [11408591.001]
  • [Cites] Neurosurgery. 2002 Jun;50(6):1311-8 [12015850.001]
  • [Cites] Curr Opin Cell Biol. 2002 Oct;14(5):617-23 [12231358.001]
  • [Cites] J Biol Chem. 2002 Oct 11;277(41):38013-20 [12145277.001]
  • [Cites] J Biol Chem. 2002 Dec 6;277(49):47626-35 [12221092.001]
  • [Cites] Am J Pathol. 2003 Feb;162(2):391-402 [12547698.001]
  • [Cites] Int J Cancer. 2003 Nov 10;107(3):359-64 [14506734.001]
  • [Cites] J Biol Chem. 2003 Nov 14;278(46):45801-10 [12954618.001]
  • [Cites] J Biol Chem. 2004 Apr 30;279(18):18679-87 [14724275.001]
  • [Cites] Nat Rev Cancer. 2004 Jul;4(7):528-39 [15229478.001]
  • [Cites] EMBO J. 2004 Jul 21;23(14):2800-10 [15229650.001]
  • [Cites] Cell. 2004 Aug 6;118(3):277-9 [15294153.001]
  • [Cites] Int J Dev Biol. 2004;48(5-6):509-17 [15349825.001]
  • [Cites] Science. 1985 Jun 14;228(4705):1324-6 [2408340.001]
  • [Cites] J Biol Chem. 1986 Oct 15;261(29):13517-25 [3759975.001]
  • [Cites] FASEB J. 1992 Apr;6(7):2397-404 [1563592.001]
  • [Cites] J Cell Sci. 1994 Sep;107 ( Pt 9):2581-90 [7531202.001]
  • [Cites] Int J Cancer. 1996 May 29;66(5):664-8 [8647630.001]
  • [Cites] Cancer Res. 1996 Sep 1;56(17):3902-8 [8752156.001]
  • [Cites] Gene. 1996 Nov 28;181(1-2):207-12 [8973332.001]
  • [Cites] Histochem J. 1997 Jan;29(1):21-30 [9088942.001]
  • [Cites] Int J Cancer. 1997 Apr 10;71(2):251-6 [9139851.001]
  • [Cites] Biochem Biophys Res Commun. 1997 Aug 18;237(2):318-24 [9268708.001]
  • [Cites] Cancer Res. 1999 Mar 1;59(5):1141-5 [10070975.001]
  • [Cites] Arterioscler Thromb Vasc Biol. 1999 Apr;19(4):1004-13 [10195929.001]
  • [Cites] Cancer Res. 1999 May 15;59(10):2499-504 [10344764.001]
  • [Cites] J Biol Chem. 1999 Aug 27;274(35):25085-92 [10455188.001]
  • [Cites] Nat Rev Cancer. 2004 Nov;4(11):839-49 [15516957.001]
  • [Cites] Breast Cancer Res. 2004;6(2):93-101 [14979914.001]
  • [Cites] Semin Cancer Biol. 2005 Apr;15(2):132-7 [15652458.001]
  • [Cites] Mol Biol Cell. 2005 Mar;16(3):1330-40 [15635104.001]
  • [Cites] Cell. 2005 May 6;121(3):335-48 [15882617.001]
  • [Cites] J Biol Chem. 2005 Jun 24;280(25):24195-204 [15843382.001]
  • [Cites] Tumour Biol. 2005 Jul-Aug;26(4):173-85 [16006771.001]
  • [Cites] J Biol Chem. 2005 Sep 9;280(36):31890-7 [16014622.001]
  • [Cites] Curr Opin Cell Biol. 2005 Oct;17(5):548-58 [16098727.001]
  • [Cites] Cancer Res. 2001 Jul 1;61(13):5207-14 [11431361.001]
  • [Cites] Br J Cancer. 2001 Aug 17;85(4):600-7 [11506502.001]
  • [Cites] J Biol Chem. 2001 Sep 28;276(39):36770-8 [11448954.001]
  • [Cites] Dis Markers. 2001;17(3):153-7 [11790880.001]
  • [Cites] J Biol Chem. 2002 Feb 15;277(7):4589-92 [11717317.001]
  • [Cites] J Biol Chem. 2002 Mar 22;277(12):10050-7 [11790779.001]
  • [Cites] Proc Natl Acad Sci U S A. 2002 Mar 19;99(6):3609-14 [11891291.001]
  • [Cites] Stem Cells. 2006 Apr;24(4):928-35 [16306150.001]
  • (PMID = 17322391.001).
  • [ISSN] 0002-9440
  • [Journal-full-title] The American journal of pathology
  • [ISO-abbreviation] Am. J. Pathol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 126968-45-4 / Versicans; 9004-61-9 / Hyaluronic Acid; EC 2.4.1.- / Has2 protein, mouse; EC 2.4.1.17 / Glucuronosyltransferase; EC 2.7.10.1 / Receptor, ErbB-2
  • [Other-IDs] NLM/ PMC1864876
  •  go-up   go-down


74. Luijten M, Verhoef A, Dormans JA, Beems RB, Cremers HW, Nagelkerke NJ, Adlercreutz H, Peñalvo JL, Piersma AH: Modulation of mammary tumor development in Tg.NK (MMTV/c-neu) mice by dietary fatty acids and life stage-specific exposure to phytoestrogens. Reprod Toxicol; 2007 Apr-May;23(3):407-13
NCI CPTC Antibody Characterization Program. NCI CPTC Antibody Characterization Program .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Modulation of mammary tumor development in Tg.NK (MMTV/c-neu) mice by dietary fatty acids and life stage-specific exposure to phytoestrogens.
  • We investigated spontaneous mammary tumor development in female heterozygous MMTV/c-neu (Tg.NK) mice upon isoflavone exposure on background diets rich in either n-6 or n-3 polyunsaturated fatty acids (PUFAs).
  • Mice fed diets high in n-3 PUFAs developed mammary tumors 15 weeks later than mice fed n-6 PUFA diets.
  • In the latter mice, isoflavone exposure from weaning onwards resulted in a significant decrease in tumor incidence and a delay in tumor onset.
  • Therefore, the effects of phytoestrogen exposure on tumor formation appear to depend on the composition of the background diet and on the timing of exposure within the life cycle.
  • [MeSH-major] Dietary Fats / toxicity. Isoflavones / pharmacology. Mammary Neoplasms, Animal / prevention & control. Phytoestrogens / pharmacology
  • [MeSH-minor] Animals. Body Weight / drug effects. Fatty Acids, Omega-3 / administration & dosage. Fatty Acids, Omega-3 / toxicity. Fatty Acids, Omega-6 / administration & dosage. Fatty Acids, Omega-6 / toxicity. Female. Humans. Male. Mammary Glands, Animal / drug effects. Mammary Glands, Animal / metabolism. Mammary Glands, Animal / pathology. Mice. Mice, Transgenic. Postpartum Period. Pregnancy. Receptor, ErbB-2 / genetics. Time Factors. Weaning

  • MedlinePlus Health Information. consumer health - Dietary Fats.
  • KOMP Repository. gene/protein/disease-specific - KOMP Repository (subscription/membership/fee required).
  • Mouse Genome Informatics (MGI). Mouse Genome Informatics (MGI) .
  • NCI CPTAC Assay Portal. NCI CPTAC Assay Portal .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 17229545.001).
  • [ISSN] 0890-6238
  • [Journal-full-title] Reproductive toxicology (Elmsford, N.Y.)
  • [ISO-abbreviation] Reprod. Toxicol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Dietary Fats; 0 / Fatty Acids, Omega-3; 0 / Fatty Acids, Omega-6; 0 / Isoflavones; 0 / Phytoestrogens; EC 2.7.10.1 / Receptor, ErbB-2
  •  go-up   go-down


75. Jabrane-Ferrat N, Campbell MJ, Esserman LJ, Peterlin BM: Challenge with mammary tumor cells expressing MHC class II and CD80 prevents the development of spontaneously arising tumors in MMTV-neu transgenic mice. Cancer Gene Ther; 2006 Nov;13(11):1002-10
NCI CPTC Antibody Characterization Program. NCI CPTC Antibody Characterization Program .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Challenge with mammary tumor cells expressing MHC class II and CD80 prevents the development of spontaneously arising tumors in MMTV-neu transgenic mice.
  • Indeed, transgenic MMTV-neu mice expressing this oncogene from the mammary tumor virus long terminal repeat develop spontaneous mammary tumors and die within 1 year of life.
  • We have expressed the class II transactivator (CIITA) and/or the costimulatory molecule CD80 (B7.1) in a mammary carcinoma cell line (MCNeuA) derived from these mice.
  • When injected into MMTV-neu mice, tumor cells expressing CD80 or CD80 and CIITA, were rejected completely.
  • In addition, following the rejection of dual expressing cells, 75% of the mice were protected against the development of subsequent spontaneous tumors.
  • Cells expressing only CD80 or CIITA were not as effective as antitumor vaccines in preventing the development of spontaneous tumors.
  • [MeSH-major] Antigens, CD80 / genetics. Genes, MHC Class II / genetics. Mammary Neoplasms, Animal / immunology. Mammary Tumor Virus, Mouse / genetics. Receptor, ErbB-2 / genetics
  • [MeSH-minor] Animals. Blotting, Western. Cell Line. Cell Line, Tumor. Female. Flow Cytometry. Humans. Immunohistochemistry. Immunoprecipitation. Lymphocytes / immunology. Mice. Mice, Transgenic. Nuclear Proteins / genetics. Nuclear Proteins / immunology. Nuclear Proteins / metabolism. Rats. Trans-Activators / genetics. Trans-Activators / immunology. Trans-Activators / metabolism

  • COS Scholar Universe. author profiles.
  • NCI CPTAC Assay Portal. NCI CPTAC Assay Portal .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 16841083.001).
  • [ISSN] 0929-1903
  • [Journal-full-title] Cancer gene therapy
  • [ISO-abbreviation] Cancer Gene Ther.
  • [Language] eng
  • [Grant] United States / NIAID NIH HHS / AI / AI050770
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Antigens, CD80; 0 / MHC class II transactivator protein; 0 / Nuclear Proteins; 0 / Trans-Activators; EC 2.7.10.1 / Receptor, ErbB-2
  •  go-up   go-down


76. Nkhata KJ, Ray A, Dogan S, Grande JP, Cleary MP: Mammary tumor development from T47-D human breast cancer cells in obese ovariectomized mice with and without estradiol supplements. Breast Cancer Res Treat; 2009 Mar;114(1):71-83
NCI CPTAC Assay Portal. NCI CPTAC Assay Portal .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Mammary tumor development from T47-D human breast cancer cells in obese ovariectomized mice with and without estradiol supplements.
  • Obesity is a risk factor for postmenopausal breast cancer, particularly for development of estrogen-receptor (ER)-positive tumors.
  • Our goal was to address how obesity and/or elevated serum leptin affects tumor formation from ER-positive T47-D cells.
  • In Study 1 no mice developed tumors.
  • In Study 2 mice with placebo pellets developed more tumors than mice with estrogen pellets, 50% vs. 13%.
  • GTG-obese mice with placebo pellets had a 100% tumor incidence compared to 50% and 20% for GTG-lean and controls without estrogen.
  • Serum leptin was higher in obese compared to lean mice and adiponectin was not affected by body weight.
  • Leptin, leptin receptor and signaling protein expression were determined in mammary and tumor tissue.
  • Leptin and STAT3 were most abundant in tumors.
  • These findings suggest that in vivo estrogen suppressed proliferation of T47-D cells but without supplemental estrogen obesity enhanced tumor development.
  • The exact reason for this is not presently clear.
  • [MeSH-major] Breast Neoplasms / physiopathology
  • [MeSH-minor] Animals. Disease Models, Animal. Estradiol / administration & dosage. Estrogens / administration & dosage. Female. Leptin / blood. Mice. Mice, Nude. Mice, Obese. Neoplasm Transplantation. Ovariectomy. Receptors, Estrogen

  • MedlinePlus Health Information. consumer health - Breast Cancer.
  • COS Scholar Universe. author profiles.
  • Hazardous Substances Data Bank. ESTRADIOL .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 18392696.001).
  • [ISSN] 1573-7217
  • [Journal-full-title] Breast cancer research and treatment
  • [ISO-abbreviation] Breast Cancer Res. Treat.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Netherlands
  • [Chemical-registry-number] 0 / Estrogens; 0 / Leptin; 0 / Receptors, Estrogen; 4TI98Z838E / Estradiol
  •  go-up   go-down


77. Wendt MK, Smith JA, Schiemann WP: p130Cas is required for mammary tumor growth and transforming growth factor-beta-mediated metastasis through regulation of Smad2/3 activity. J Biol Chem; 2009 Dec 4;284(49):34145-56
antibodies-online. View related products from antibodies-online.com (subscription/membership/fee required).

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] p130Cas is required for mammary tumor growth and transforming growth factor-beta-mediated metastasis through regulation of Smad2/3 activity.
  • During breast cancer progression, transforming growth factor-beta (TGF-beta) switches from a tumor suppressor to a pro-metastatic molecule.
  • Indeed, elevating expression of either the full-length (FL) or just the carboxyl terminus (CT) of p130Cas in mammary epithelial cells (MECs) diminished the ability of TGF-beta1 to activate Smad2/3, but increased its coupling to p38 MAPK.
  • Furthermore, rendering metastatic MECs deficient in p130Cas enhanced TGF-beta-stimulated Smad2/3 activity, which restored TGF-beta-induced growth inhibition both in vitro and in mammary tumors produced in mice.
  • Importantly, depleting p130Cas expression in TbetaR-II-expressing metastatic MECs significantly increased their activation of Smad2/3, which (i) reestablished the physiologic balance between canonical and noncanonical TGF-beta signaling, and (ii) reversed cellular invasion and early mammary tumor cell dissemination stimulated by TGF-beta.
  • Collectively, our findings identify p130Cas as a molecular rheostat that regulates the delicate balance between canonical and noncanonical TGF-beta signaling, a balance that is critical to maintaining the tumor suppressor function of TGF-beta during breast cancer progression.

  • MedlinePlus Health Information. consumer health - Breast Cancer.
  • Faculty of 1000. commentaries/discussion - See the articles recommended by F1000Prime's Faculty of more than 8,000 leading experts in Biology and Medicine. (subscription/membership/fee required).
  • NCI CPTC Antibody Characterization Program. NCI CPTC Antibody Characterization Program .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [Cites] Cell. 2009 Apr 3;137(1):87-98 [19345189.001]
  • [Cites] Mol Cell. 2008 Sep 26;31(6):918-24 [18922473.001]
  • [Cites] Breast Cancer Res. 2009;11(5):R68 [19740433.001]
  • [Cites] N Engl J Med. 2000 May 4;342(18):1350-8 [10793168.001]
  • [Cites] Int J Cancer. 2000 Sep 20;89(5):465-8 [11008210.001]
  • [Cites] J Natl Cancer Inst. 2000 Nov 1;92(21):1717-30 [11058615.001]
  • [Cites] J Biol Chem. 2000 Nov 24;275(47):36818-22 [11016919.001]
  • [Cites] Breast Cancer Res Treat. 2001 Jan;65(2):101-10 [11261825.001]
  • [Cites] J Mammary Gland Biol Neoplasia. 2001 Jan;6(1):67-82 [11467453.001]
  • [Cites] J Clin Invest. 2002 Jun;109(12):1551-9 [12070302.001]
  • [Cites] J Clin Invest. 2003 Oct;112(7):1116-24 [14523048.001]
  • [Cites] Nat Rev Cancer. 2003 Nov;3(11):807-21 [14557817.001]
  • [Cites] Lancet Oncol. 2004 Apr;5(4):229-39 [15050954.001]
  • [Cites] Oncogene. 2004 Sep 23;23(44):7406-15 [15273716.001]
  • [Cites] Science. 1987 Jul 17;237(4812):291-3 [3474783.001]
  • [Cites] Cancer Res. 1992 Mar 15;52(6):1399-405 [1540948.001]
  • [Cites] Am J Pathol. 1996 Jan;148(1):313-9 [8546221.001]
  • [Cites] Biochem Cell Biol. 1996;74(6):833-51 [9164652.001]
  • [Cites] Cell Growth Differ. 1997 Jul;8(7):821-7 [9218876.001]
  • [Cites] Proc Natl Acad Sci U S A. 1997 Sep 30;94(20):10669-74 [9380693.001]
  • [Cites] Nat Genet. 1998 Aug;19(4):361-5 [9697697.001]
  • [Cites] Prog Biophys Mol Biol. 1999;71(3-4):435-78 [10354709.001]
  • [Cites] Cancer Res. 2006 May 1;66(9):4672-80 [16651418.001]
  • [Cites] Cancer Cell. 2006 Sep;10(3):203-14 [16959612.001]
  • [Cites] Science. 2006 Oct 13;314(5797):298-300 [17038622.001]
  • [Cites] Cell. 2006 Dec 1;127(5):879-81 [17129774.001]
  • [Cites] Future Oncol. 2006 Dec;2(6):743-63 [17155901.001]
  • [Cites] Breast Cancer Res. 2006;8(4):R42 [16859511.001]
  • [Cites] Ann N Y Acad Sci. 2006 Nov;1089:119-26 [17261761.001]
  • [Cites] J Cell Biochem. 2007 May 1;101(1):9-33 [17340614.001]
  • [Cites] Cancer Res. 2007 Apr 15;67(8):3752-8 [17440088.001]
  • [Cites] Expert Rev Anticancer Ther. 2007 May;7(5):609-11 [17492924.001]
  • [Cites] Oncogene. 2007 Dec 6;26(55):7684-91 [17546043.001]
  • [Cites] Oncogene. 2008 Feb 28;27(10):1461-71 [17724466.001]
  • [Cites] Cancer Res. 2008 Nov 1;68(21):8796-804 [18974122.001]
  • [Cites] Carcinogenesis. 2008 Nov;29(11):2227-35 [18725385.001]
  • [Cites] Future Oncol. 2009 Mar;5(2):259-71 [19284383.001]
  • [Cites] Carcinogenesis. 2008 Feb;29(2):244-51 [18174260.001]
  • [Cites] Mol Biol Cell. 2008 May;19(5):2135-46 [18321991.001]
  • [Cites] Cancer Res. 2008 May 15;68(10):3835-43 [18483268.001]
  • [Cites] Cell. 2008 May 16;133(4):704-15 [18485877.001]
  • [Cites] Biol Reprod. 2008 Oct;79(4):711-7 [18614704.001]
  • [Cites] Nat Cell Biol. 2008 Oct;10(10):1199-207 [18758450.001]
  • [Cites] Mol Oncol. 2007 Jun;1(1):84-96 [18516279.001]
  • (PMID = 19822523.001).
  • [ISSN] 1083-351X
  • [Journal-full-title] The Journal of biological chemistry
  • [ISO-abbreviation] J. Biol. Chem.
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / R01 CA129359; United States / NCI NIH HHS / CA / CA129359
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't; Research Support, U.S. Gov't, Non-P.H.S.
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / BCAR1 protein, human; 0 / Bcar1 protein, mouse; 0 / Crk-Associated Substrate Protein; 0 / Smad2 Protein; 0 / Smad3 Protein; 0 / Transforming Growth Factor beta
  • [Other-IDs] NLM/ PMC2797185
  •  go-up   go-down


78. WATANABE M, CHEN IY, ISHIKURA Y, NAKAGAWA T, MOCHIZUKI M, NISHIMURA R, SASAKI N, SUGANO S: Tumor cell growth inhibition and cell differentiation analysis in a canine mammary tumor cell line (MCM-B2) treated with four chemical reagents. J Vet Med Sci; 2009 Nov;71(11):1413-7
NCI CPTC Antibody Characterization Program. NCI CPTC Antibody Characterization Program .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Tumor cell growth inhibition and cell differentiation analysis in a canine mammary tumor cell line (MCM-B2) treated with four chemical reagents.
  • In this study, we examined the effects of four chemical reagents, 5 azacytidine (5azaC), all-trans-retinoic acid (ATRA), Phorbol 12-myristate 13-acetate (TPA) and trichostatin A (TSA), on an MCM-B2 canine mammary tumor cell line.
  • Both ATRA-treated and 5azaC-treated cells showed decreased expression of cell cycle related molecules and increased expressions of the mammary epithelial marker cytokeratin 18 and underwent morphological changes.
  • These results demonstrated the growth-inhibiting, differentiation-inducing and antitumor effects of each of these four chemicals on the unique phenotype of canine mammary tumors.

  • NCI CPTAC Assay Portal. NCI CPTAC Assay Portal .
  • NCI CPTAC Assay Portal. NCI CPTAC Assay Portal .
  • NCI CPTC Antibody Characterization Program. NCI CPTC Antibody Characterization Program .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 19959889.001).
  • [ISSN] 0916-7250
  • [Journal-full-title] The Journal of veterinary medical science
  • [ISO-abbreviation] J. Vet. Med. Sci.
  • [Language] ENG
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Japan
  • [Chemical-registry-number] 0 / Antineoplastic Agents
  •  go-up   go-down


79. Lee HJ, So JY, DeCastro A, Smolarek A, Paul S, Maehr H, Uskokovic M, Suh N: Gemini vitamin D analog suppresses ErbB2-positive mammary tumor growth via inhibition of ErbB2/AKT/ERK signaling. J Steroid Biochem Mol Biol; 2010 Jul;121(1-2):408-12
NCI CPTC Antibody Characterization Program. NCI CPTC Antibody Characterization Program .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Gemini vitamin D analog suppresses ErbB2-positive mammary tumor growth via inhibition of ErbB2/AKT/ERK signaling.
  • However, the inhibitory effects of naturally occurring 1alpha,25-dihydroxyvitamin D3 or its synthetic analogs on ErbB2 overexpressing mammary tumorigenesis have not been reported.
  • Gemini vitamin D analogs are novel synthetic vitamin D derivatives with a unique structure of two six-carbon chains at C-20.
  • We have previously shown that Gemini vitamin D analogs significantly inhibited carcinogen-induced estrogen receptor (ER)-positive mammary tumorigenesis and reduced ER-negative MCF10DCIS.com xenograft tumor growth without hypercalcemic toxicity.
  • In the present study, we have determined the inhibitory effect of a potent Gemini vitamin D analog BXL0124 (1alpha,25-dihydroxy-20R-21(3-hydroxy-3-deuteromethyl-4,4,4-trideuterobutyl)-23-yne-26,27-hexafluoro-cholecalciferol) on the ErbB2/Her-2/neu overexpressing mammary tumorigenesis.
  • The Gemini BXL0124 inhibits ErbB2-positive mammary tumor growth and down-regulates the phosphorylation of ErbB2, ERK and AKT in tumors of MMTV-ErbB2/neu transgenic mice.
  • These effects of Gemini BXL0124 in vivo were confirmed by using the ErbB2 overexpressing tumor cells derived from the mammary tumors of MMTV-ErbB2/neu mice.
  • In conclusion, the Gemini vitamin D analog BXL0124 inhibits the growth of ErbB2 overexpressing mammary tumors through regulating the ErbB2/AKT/ERK signaling pathways, suggesting that Gemini vitamin D analog may be considered for translational studies.

  • COS Scholar Universe. author profiles.
  • Hazardous Substances Data Bank. 1,25-DIHYDROXYCHOLECALCIFEROL .
  • Hazardous Substances Data Bank. CHOLECALCIFEROL .
  • Hazardous Substances Data Bank. CALCIUM, ELEMENTAL .
  • NCI CPTAC Assay Portal. NCI CPTAC Assay Portal .
  • NCI CPTAC Assay Portal. NCI CPTAC Assay Portal .
  • NCI CPTC Antibody Characterization Program. NCI CPTC Antibody Characterization Program .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [Copyright] Copyright (c) 2010 Elsevier Ltd. All rights reserved.
  • [Cites] J Steroid Biochem Mol Biol. 2003 Feb;84(2-3):199-209 [12711004.001]
  • [Cites] Nat Rev Cancer. 2009 Jul;9(7):463-75 [19536107.001]
  • [Cites] Proc Natl Acad Sci U S A. 1992 Nov 15;89(22):10578-82 [1359541.001]
  • [Cites] Nat Rev Cancer. 2005 May;5(5):341-54 [15864276.001]
  • [Cites] Am J Physiol Renal Physiol. 2005 Jul;289(1):F8-28 [15951480.001]
  • [Cites] J Steroid Biochem Mol Biol. 2005 Oct;97(1-2):111-20 [16154354.001]
  • [Cites] Carcinogenesis. 2006 Mar;27(3):551-9 [16195238.001]
  • [Cites] Biochem Pharmacol. 2006 Jul 28;72(3):332-43 [16737686.001]
  • [Cites] Cancer Res. 2006 Sep 1;66(17):8565-73 [16951169.001]
  • [Cites] Science. 2006 Oct 13;314(5797):268-74 [16959974.001]
  • [Cites] J Steroid Biochem Mol Biol. 2006 Dec;102(1-5):156-62 [17113979.001]
  • [Cites] Nature. 2007 Jan 25;445(7126):437-41 [17206155.001]
  • [Cites] J Steroid Biochem Mol Biol. 2007 Mar;103(3-5):277-81 [17254779.001]
  • [Cites] J Steroid Biochem Mol Biol. 2007 Mar;103(3-5):757-62 [17368190.001]
  • [Cites] Nat Rev Cancer. 2007 May;7(5):357-69 [17446857.001]
  • [Cites] Nat Rev Cancer. 2007 May;7(5):389-97 [17446858.001]
  • [Cites] Nat Rev Cancer. 2007 Sep;7(9):659-72 [17721431.001]
  • [Cites] Nat Rev Cancer. 2007 Sep;7(9):684-700 [17721433.001]
  • [Cites] Clin Cancer Res. 2007 Oct 15;13(20):6224-31 [17947490.001]
  • [Cites] Cancer Prev Res (Phila). 2008 Jun;1(1):45-55 [19138935.001]
  • [Cites] Cancer Prev Res (Phila). 2008 Nov;1(6):476-84 [19138995.001]
  • [Cites] Clin Cancer Res. 2009 Jun 15;15(12):4242-9 [19509159.001]
  • [Cites] Proc Natl Acad Sci U S A. 2003 Jul 22;100(15):8933-8 [12853564.001]
  • (PMID = 20304052.001).
  • [ISSN] 1879-1220
  • [Journal-full-title] The Journal of steroid biochemistry and molecular biology
  • [ISO-abbreviation] J. Steroid Biochem. Mol. Biol.
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / R03 CA112642; United States / NCI NIH HHS / CA / R01 CA127645-01A1; United States / NCI NIH HHS / CA / R01 CA127645-02; United States / NCI NIH HHS / CA / R01 CA127645-03; United States / NCI NIH HHS / CA / R01 CA127645-02S1; United States / NCI NIH HHS / CA / CA127645-02S1; United States / NCI NIH HHS / CA / R01 CA127645; United States / NCI NIH HHS / CA / CA127645-03; United States / NCI NIH HHS / CA / CA127645-02; United States / NCI NIH HHS / CA / CA112642-02; United States / NCI NIH HHS / CA / R03 CA112642-02
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / 1,25-dihydroxy-21-(3-hydroxy-3-methyl-4,4,4-tributyl)-23-yne-26,27-hexafluorocholecalciferol; 0 / 1,25-dihydroxy-21-(3-hydroxy-3-methylbutyl)vitamin D(3); 0 / Carcinogens; 1C6V77QF41 / Cholecalciferol; EC 2.7.10.1 / Erbb2 protein, mouse; EC 2.7.10.1 / Receptor, ErbB-2; EC 2.7.11.1 / Proto-Oncogene Proteins c-akt; EC 2.7.11.24 / Mitogen-Activated Protein Kinase 3; FXC9231JVH / Calcitriol; SY7Q814VUP / Calcium
  • [Other-IDs] NLM/ NIHMS195239; NLM/ PMC2906695
  •  go-up   go-down


80. Grandi F, Colodel MM, Monteiro LN, Leão JR, Rocha NS: Extramedullary hematopoiesis in a case of benign mixed mammary tumor in a female dog: cytological and histopathological assessment. BMC Vet Res; 2010;6:45

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Extramedullary hematopoiesis in a case of benign mixed mammary tumor in a female dog: cytological and histopathological assessment.
  • Mammary EMH is a rare condition either in human and veterinary medicine and can be associated with benign mixed mammary tumors, similarly to that described in this case.
  • CASE PRESENTATION: Hematopoietic stem cells were found in a benign mixed mammary tumor of a 7-year-old female mongrel dog that presents a nodule in the left inguinal mammary gland.
  • The patient did not have any hematological abnormalities.
  • Histological examination confirmed the presence of an active hematopoietic bone marrow within the bone tissue of a benign mammary mixed tumor.
  • CONCLUSIONS: EMH is a rare condition described in veterinary medicine that can be associated with mammary mixed tumors.
  • It's detection can be associated with several neoplastic and non-neoplastic mammary lesions, i.e. osteosarcomas, mixed tumors and bone metaplasia.
  • [MeSH-major] Hematopoiesis, Extramedullary / immunology. Mammary Neoplasms, Animal / complications

  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [Cites] Ann Oncol. 2001 Feb;12(2):267-70 [11300336.001]
  • [Cites] Vet Clin Pathol. 2009 Dec;38(4):521-8 [19392751.001]
  • [Cites] Am J Surg Pathol. 1980 Jun;4(3):281-5 [7396068.001]
  • [Cites] Diagn Imaging. 1982;51(1):19-24 [7060437.001]
  • [Cites] Virchows Arch A Pathol Anat Histopathol. 1983;401(2):203-7 [6415904.001]
  • [Cites] Blood. 1985 Apr;65(4):803-9 [3978228.001]
  • [Cites] Vet Pathol. 1986 Nov;23(6):649-55 [3811129.001]
  • [Cites] J Comput Assist Tomogr. 1987 May-Jun;11(3):541-2 [3571606.001]
  • [Cites] J Comp Pathol. 1989 Nov;101(4):443-50 [2607016.001]
  • [Cites] J Clin Ultrasound. 1993 Nov-Dec;21(9):631-5 [8227393.001]
  • [Cites] Vet Pathol. 1995 Jul;32(4):437-40 [7483223.001]
  • [Cites] Pathol Res Pract. 1997;193(3):219-22; discussion 223-4 [9198107.001]
  • [Cites] Head Neck. 1998 May;20(3):204-7 [9570625.001]
  • [Cites] Vet J. 1999 Jul;158(1):39-47 [10409415.001]
  • [Cites] J Clin Pathol. 2005 Apr;58(4):448 [15790723.001]
  • [Cites] Ann Clin Lab Sci. 2006 Autumn;36(4):475-8 [17127738.001]
  • [Cites] Cytopathology. 2007 Jun;18(3):191-6 [17573766.001]
  • [Cites] BMC Cancer. 2007;7:218 [18045453.001]
  • [Cites] Prev Vet Med. 2001 Sep 20;51(1-2):125-36 [11530199.001]
  • (PMID = 20846427.001).
  • [ISSN] 1746-6148
  • [Journal-full-title] BMC veterinary research
  • [ISO-abbreviation] BMC Vet. Res.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Hemoglobins
  • [Other-IDs] NLM/ PMC2954924
  •  go-up   go-down


81. Puppe J, Drost R, Liu X, Joosse SA, Evers B, Cornelissen-Steijger P, Nederlof P, Yu Q, Jonkers J, van Lohuizen M, Pietersen AM: BRCA1-deficient mammary tumor cells are dependent on EZH2 expression and sensitive to Polycomb Repressive Complex 2-inhibitor 3-deazaneplanocin A. Breast Cancer Res; 2009;11(4):R63
The Lens. Cited by Patents in .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] BRCA1-deficient mammary tumor cells are dependent on EZH2 expression and sensitive to Polycomb Repressive Complex 2-inhibitor 3-deazaneplanocin A.
  • INTRODUCTION: Treatment of breast cancer is becoming more individualized with the recognition of tumor subgroups that respond differently to available therapies.
  • Breast cancer 1 gene (BRCA1)-deficient tumors are usually of the basal subtype and associated with poor survival rates, highlighting the need for more effective therapy.
  • METHODS: We investigated a mouse model that closely mimics breast cancer arising in BRCA1-mutation carriers to better understand the molecular mechanism of tumor progression and tested whether targeting of the Polycomb-group protein EZH2 would be a putative therapy for BRCA1-deficient tumors.
  • RESULTS: Gene expression analysis demonstrated that EZH2 is overexpressed in BRCA1-deficient mouse mammary tumors.
  • By immunohistochemistry we show that an increase in EZH2 protein levels is also evident in tumors from BRCA1-mutation carriers.
  • EZH2 is responsible for repression of genes driving differentiation and could thus be involved in the undifferentiated phenotype of these tumors.
  • In addition, a chemical inhibitor of EZH2, 3-deazaneplanocin A (DZNep), is about 20-fold more effective in killing BRCA1-deficient cells compared to BRCA1-proficient mammary tumor cells.
  • [MeSH-major] Adenosine / analogs & derivatives. BRCA1 Protein / deficiency. Breast Neoplasms / genetics. Genes, BRCA1. Histone-Lysine N-Methyltransferase / physiology
  • [MeSH-minor] Animals. Cell Line, Tumor / drug effects. Cell Line, Tumor / metabolism. DNA Repair / genetics. Drug Delivery Systems. Female. Gene Knockdown Techniques. Humans. Mice. Mutation. Polycomb Repressive Complex 2. RNA, Messenger / biosynthesis. RNA, Neoplasm / biosynthesis. RNA, Small Interfering / pharmacology. Recombinant Fusion Proteins / physiology

  • MedlinePlus Health Information. consumer health - Breast Cancer.
  • Hazardous Substances Data Bank. Adenosine .
  • NCI CPTAC Assay Portal. NCI CPTAC Assay Portal .
  • NCI CPTC Antibody Characterization Program. NCI CPTC Antibody Characterization Program .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [Cites] Mol Cell. 1999 Oct;4(4):511-8 [10549283.001]
  • [Cites] N Engl J Med. 2009 Jul 9;361(2):123-34 [19553641.001]
  • [Cites] Semin Surg Oncol. 2000 Jun;18(4):287-95 [10805950.001]
  • [Cites] Nature. 2000 Aug 17;406(6797):747-52 [10963602.001]
  • [Cites] Genesis. 2001 Feb;29(2):72-7 [11170347.001]
  • [Cites] Cancer Res. 2001 May 15;61(10):4092-7 [11358831.001]
  • [Cites] Mol Cell Biol. 2001 Jul;21(13):4330-6 [11390661.001]
  • [Cites] Nat Genet. 2001 Dec;29(4):418-25 [11694875.001]
  • [Cites] Nature. 2002 Jan 31;415(6871):530-6 [11823860.001]
  • [Cites] Science. 2002 Nov 1;298(5595):1039-43 [12351676.001]
  • [Cites] N Engl J Med. 2002 Dec 19;347(25):1999-2009 [12490681.001]
  • [Cites] Proc Natl Acad Sci U S A. 2003 Jul 8;100(14):8418-23 [12829800.001]
  • [Cites] Proc Natl Acad Sci U S A. 2003 Sep 30;100(20):11606-11 [14500907.001]
  • [Cites] EMBO J. 2003 Oct 15;22(20):5323-35 [14532106.001]
  • [Cites] Neoplasia. 2003 Nov-Dec;5(6):481-8 [14965441.001]
  • [Cites] Nat Rev Cancer. 2004 Oct;4(10):814-9 [15510162.001]
  • [Cites] Nucleic Acids Res. 2005;33(4):e36 [15731329.001]
  • [Cites] Neoplasia. 2005 Nov;7(11):1011-9 [16331887.001]
  • [Cites] J Clin Oncol. 2006 Jan 10;24(2):268-73 [16330673.001]
  • [Cites] Clin Cancer Res. 2006 Feb 15;12(4):1168-74 [16489070.001]
  • [Cites] Cell. 2006 Apr 21;125(2):301-13 [16630818.001]
  • [Cites] Genes Dev. 2006 May 1;20(9):1123-36 [16618801.001]
  • [Cites] BMC Genomics. 2006;7:96 [16643655.001]
  • [Cites] Oncogene. 2006 Sep 25;25(43):5846-53 [16998499.001]
  • [Cites] Nat Rev Cancer. 2006 Nov;6(11):846-56 [17060944.001]
  • [Cites] Nat Genet. 2007 Feb;39(2):237-42 [17211412.001]
  • [Cites] Genes Dev. 2007 Mar 1;21(5):525-30 [17344414.001]
  • [Cites] Cell. 2007 Mar 9;128(5):991-1002 [17350581.001]
  • [Cites] Genes Dev. 2007 May 1;21(9):1050-63 [17437993.001]
  • [Cites] Proc Natl Acad Sci U S A. 2007 Jun 19;104(25):10476-81 [17566110.001]
  • [Cites] Proc Natl Acad Sci U S A. 2007 Jul 17;104(29):12111-6 [17626182.001]
  • [Cites] Expert Rev Anticancer Ther. 2007 Aug;7(8):1065-7 [17725409.001]
  • [Cites] Cancer Res. 2007 Sep 15;67(18):8671-81 [17875707.001]
  • [Cites] Proc Natl Acad Sci U S A. 2008 Feb 5;105(5):1680-5 [18230721.001]
  • [Cites] Mol Cell Biol. 2008 Mar;28(5):1702-12 [18160714.001]
  • [Cites] Cancer Res. 2008 Feb 15;68(4):989-97 [18281472.001]
  • [Cites] Curr Opin Cell Biol. 2008 Apr;20(2):201-7 [18291635.001]
  • [Cites] Nat Genet. 2008 May;40(5):499-507 [18443585.001]
  • [Cites] Breast Cancer Res. 2008;10(3):R53 [18559090.001]
  • [Cites] Proc Natl Acad Sci U S A. 2008 Nov 4;105(44):17079-84 [18971340.001]
  • [Cites] Ann Surg Oncol. 2008 Dec;15(12):3614-5; author reply 3616 [18521683.001]
  • [Cites] Oncogene. 2009 Feb 12;28(6):843-53 [19079346.001]
  • [Cites] Breast Cancer Res. 2008;10(6):R109 [19099573.001]
  • [Cites] Cancer Res. 2009 Apr 15;69(8):3625-33 [19336573.001]
  • [CommentIn] Breast Cancer Res. 2009;11(5):108 [19804613.001]
  • (PMID = 19709408.001).
  • [ISSN] 1465-542X
  • [Journal-full-title] Breast cancer research : BCR
  • [ISO-abbreviation] Breast Cancer Res.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / BRCA1 Protein; 0 / BRCA1 protein, human; 0 / RNA, Messenger; 0 / RNA, Neoplasm; 0 / RNA, Small Interfering; 0 / Recombinant Fusion Proteins; 102052-95-9 / 3-deazaneplanocin; EC 2.1.1.43 / Ezh2 protein, mouse; EC 2.1.1.43 / Histone-Lysine N-Methyltransferase; EC 2.1.1.43 / Polycomb Repressive Complex 2; K72T3FS567 / Adenosine
  • [Other-IDs] NLM/ PMC2750125
  •  go-up   go-down


82. Xuan W, Li YJ, Liu G, Ben-David Y, Archer MC: Interleukin-24 induces expression of beta4 integrin but suppresses anchorage-independent growth of rat mammary tumor cells by a mechanism that is independent of beta4. Mol Cancer Res; 2009 Mar;7(3):433-42
NCI CPTAC Assay Portal. NCI CPTAC Assay Portal .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Interleukin-24 induces expression of beta4 integrin but suppresses anchorage-independent growth of rat mammary tumor cells by a mechanism that is