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1. Andrade FH, Figueiroa FC, Bersano PR, Bissacot DZ, Rocha NS: Malignant mammary tumor in female dogs: environmental contaminants. Diagn Pathol; 2010;5:45
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  • [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

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  • (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
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2. 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
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  • [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.

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  • [Copyright] Copyright © 2010 AACR.
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  • (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
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3. 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
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  • [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


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4. 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
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  • [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

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  • (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
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5. 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
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  • [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.

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  • (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
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6. 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
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  • [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.

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  • [Copyright] ©2010 AACR.
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  • (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
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7. 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
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  • [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

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  • (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
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8. 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".

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  • [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
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9. 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.

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  • (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
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10. 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

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  • (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
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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.

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  • (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
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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.

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  • (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
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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.

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  • (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
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14. Cardiff RD, Kenney N: Mouse mammary tumor biology: a short history. Adv Cancer Res; 2007;98:53-116
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  • [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

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  • (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
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15. 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
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  • [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.

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  • (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
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16. 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
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  • [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

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  • (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
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17. 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
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  • [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.

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  • (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
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18. 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
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  • [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

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  • (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
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19. 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
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  • [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

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  • (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
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20. 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
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  • [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.

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  • (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
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21. 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
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  • [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

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  • (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
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22. 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
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  • [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

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  • (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
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23. Wali VB, Bachawal SV, Sylvester PW: Endoplasmic reticulum stress mediates gamma-tocotrienol-induced apoptosis in mammary tumor cells. Apoptosis; 2009 Nov;14(11):1366-77
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  • [Title] Endoplasmic reticulum stress mediates gamma-tocotrienol-induced apoptosis in mammary tumor cells.
  • However, previous studies have clearly demonstrated that gamma-tocotrienol-induced apoptosis in neoplastic mouse +SA mammary epithelial cells is not mediated through mitochondrial stress or death receptor apoptotic signaling.
  • Therefore, studies were conducted to determine the role of endoplasmic reticulum (ER) stress in mediating gamma-tocotrienol-induced apoptosis in +SA mammary tumor cells.
  • Intracellular levels of 3-hydroxy-3-methylglutaryl-coenzyme A (HMGCoA) reductase, an ER-transmembrane enzyme catalyzing the synthesis of mevalonate, decreased following gamma-tocotrienol treatment, but combined treatment with mevalonate did not reverse gamma-tocotrienol-induced apoptosis, suggesting that a decrease in HMGCoA reductase activity is not required for gamma-tocotrienol induced apoptosis.
  • These results demonstrate that ER stress apoptotic signaling is associated with gamma-tocotrienol-induced apoptosis in +SA mammary tumor cells.
  • [MeSH-major] Apoptosis / drug effects. Chromans / pharmacology. Endoplasmic Reticulum / pathology. Mammary Neoplasms, Animal / pathology. Vitamin E / analogs & derivatives
  • [MeSH-minor] Animals. Caspase 12 / metabolism. Cell Cycle Proteins / metabolism. Cell Line, Tumor. Cell Survival / drug effects. Dose-Response Relationship, Drug. Hydroxymethylglutaryl CoA Reductases / metabolism. Mice. Poly(ADP-ribose) Polymerases / metabolism. Signal Transduction / drug effects. Transcription Factor CHOP / metabolism

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  • (PMID = 19771520.001).
  • [ISSN] 1573-675X
  • [Journal-full-title] Apoptosis : an international journal on programmed cell death
  • [ISO-abbreviation] Apoptosis
  • [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 / Casp12 protein, mouse; 0 / Cell Cycle Proteins; 0 / Chromans; 0 / Ddit3 protein, mouse; 0 / TRB3 protein, mouse; 1406-18-4 / Vitamin E; 147336-12-7 / Transcription Factor CHOP; 4382-43-8 / plastochromanol 8; EC 1.1.1.- / Hydroxymethylglutaryl CoA Reductases; EC 2.4.2.30 / Poly(ADP-ribose) Polymerases; EC 3.4.22.- / Caspase 12
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24. 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
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  • [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.

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  • (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
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25. Lim HA, Kim JH, Kim JH, Sung MK, Kim MK, Park JH, Kim JS: Genistein induces glucose-regulated protein 78 in mammary tumor cells. J Med Food; 2006;9(1):28-32
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  • [Title] Genistein induces glucose-regulated protein 78 in mammary tumor cells.
  • Preliminary studies have shown that genistein modulates the expression of some heat shock proteins in mammary tumor cells.
  • However, induction of GRP78 by genistein appears not to be directly associated with inhibition of glucose uptake.
  • [MeSH-major] Breast Neoplasms / metabolism. Genistein / pharmacology. Heat-Shock Proteins / biosynthesis. Molecular Chaperones / biosynthesis
  • [MeSH-minor] Cell Line, Tumor. Dose-Response Relationship, Drug. Glucose / metabolism. Humans. Kinetics. Receptors, Estrogen / analysis

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  • (PMID = 16579725.001).
  • [ISSN] 1096-620X
  • [Journal-full-title] Journal of medicinal food
  • [ISO-abbreviation] J Med Food
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Heat-Shock Proteins; 0 / Molecular Chaperones; 0 / Receptors, Estrogen; 0 / molecular chaperone GRP78; DH2M523P0H / Genistein; IY9XDZ35W2 / Glucose
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26. 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
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  • [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

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  • (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
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27. Sotgia F, Casimiro MC, Bonuccelli G, Liu M, Whitaker-Menezes D, Er O, Daumer KM, Mercier I, Witkiewicz AK, Minetti C, Capozza F, Gormley M, Quong AA, Rui H, Frank PG, Milliman JN, Knudsen ES, Zhou J, Wang C, Pestell RG, Lisanti MP: Loss of caveolin-3 induces a lactogenic microenvironment that is protective against mammary tumor formation. Am J Pathol; 2009 Feb;174(2):613-29
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  • [Title] Loss of caveolin-3 induces a lactogenic microenvironment that is protective against mammary tumor formation.
  • Here, we show that functional loss of a single gene is sufficient to confer constitutive milk protein production and protection against mammary tumor formation.
  • We demonstrate that Cav-3 is also expressed in myoepithelial cells within the mammary gland.
  • To determine whether genetic ablation of Cav-3 expression affects adult mammary gland development, we studied the phenotype(s) of Cav-3(-/-)-null mice.
  • Interestingly, Cav-3(-/-) virgin mammary glands developed lobulo-alveolar hyperplasia, akin to the changes normally observed during pregnancy and lactation.
  • Genome-wide expression profiling revealed up-regulation of gene transcripts associated with pregnancy/lactation, mammary stem cells, and human breast cancers, consistent with a constitutive lactogenic phenotype.
  • Finally, using orthotopic tumor cell implantation, we demonstrated that virgin Cav-3(-/-) mice were dramatically protected against mammary tumor formation.
  • Thus, Cav-3(-/-) mice are a novel preclinical model to study the protective effects of a lactogenic microenvironment on mammary tumor onset and progression.

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  • (PMID = 19164602.001).
  • [ISSN] 1525-2191
  • [Journal-full-title] The American journal of pathology
  • [ISO-abbreviation] Am. J. Pathol.
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / R01 CA075503; United States / NCI NIH HHS / CA / R01 CA098779; United States / NCI NIH HHS / CA / R01-CA-120876; United States / NCI NIH HHS / CA / R01 CA120876; United States / NCI NIH HHS / CA / R01-CA-70896; United States / NCI NIH HHS / CA / R01-CA-098779; United States / NCI NIH HHS / CA / R01-CA-86072; United States / NCI NIH HHS / CA / R01-CA-80250; United States / NCI NIH HHS / CA / P30-CA-56036; United States / NCI NIH HHS / CA / R01-CA-107382; United States / NCI NIH HHS / CA / R01 CA070896; United States / NCI NIH HHS / CA / R01-CA-75503; United States / NCI NIH HHS / CA / R01 CA080250; United States / NCI NIH HHS / CA / R01 CA086072; United States / NCI NIH HHS / CA / R01 CA107382; United States / NCI NIH HHS / CA / P30 CA056036
  • [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 / Caveolin 3
  • [Other-IDs] NLM/ PMC2630569
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28. 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
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  • [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.

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  • (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
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29. Tsuchiya F, Kano R, Sano J, Oguma K, Hasegawa A: Apoptosis of canine mammary tumor cells induced by small interfering RNA (siRNA) against Bcl-xL gene. J Vet Med Sci; 2006 Nov;68(11):1199-201
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  • [Title] Apoptosis of canine mammary tumor cells induced by small interfering RNA (siRNA) against Bcl-xL gene.
  • The inhibition of Bcl-xL mRNA expression and the acceleration of apoptotic cell rates in canine mammary tumor cell line (CF33) by the small interfering RNA (siRNA) were analyzed.
  • From these results, it was suggested that canine Bcl-xL might be an anticancer target of canine tumors.

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  • (PMID = 17146179.001).
  • [ISSN] 0916-7250
  • [Journal-full-title] The Journal of veterinary medical science
  • [ISO-abbreviation] J. Vet. Med. Sci.
  • [Language] ENG
  • [Publication-type] Comparative Study; Journal Article
  • [Publication-country] Japan
  • [Chemical-registry-number] 0 / DNA Primers; 0 / DNA, Complementary; 0 / Lipids; 0 / RNA, Small Interfering; 0 / bcl-X Protein; 0 / oligofectamine
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30. 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

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  • (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
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31. 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
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  • [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

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  • (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
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32. Quan X, Laes JF, Stieber D, Rivière M, Russo J, Wedekind D, Coppieters W, Farnir F, Georges M, Szpirer J, Szpirer C: Genetic identification of distinct loci controlling mammary tumor multiplicity, latency, and aggressiveness in the rat. Mamm Genome; 2006 Apr;17(4):310-21
SciCrunch. RGD: Data: Animal Model .

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  • [Title] Genetic identification of distinct loci controlling mammary tumor multiplicity, latency, and aggressiveness in the rat.
  • Therefore, understanding the genetic basis of susceptibility to mammary cancer in this species is of great interest.
  • Previous studies based on crosses involving the susceptible strain WF (crossed with the resistant strains COP or WKY) and focusing on tumor multiplicity as the susceptibility phenotype led to the identification of several loci that control chemically induced mammary cancer.
  • The present study was aimed to determine whether other loci can be identified by analyzing crosses derived from another susceptible strain on the one hand, and by including phenotypes other than tumor multiplicity on the other hand.
  • Female progeny were genotyped with microsatellite markers covering all rat autosomes, treated with a single dose of DMBA, and phenotyped with respect to tumor latency, tumor multiplicity, and tumor aggressiveness.
  • Seven loci controlling mammary tumor development were detected.
  • Different loci control tumor multiplicity, latency, and aggressiveness.
  • While some of these loci colocalize with loci identified in crosses involving the susceptible strain WF, new loci have been uncovered, indicating that the use of distinct susceptible and resistant strain pairs will help in establishing a comprehensive inventory of mammary cancer susceptibility loci.
  • [MeSH-major] Mammary Neoplasms, Animal / genetics. Mammary Neoplasms, Animal / pathology. Quantitative Trait Loci / genetics. Quantitative Trait, Heritable

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  • (PMID = 16596452.001).
  • [ISSN] 0938-8990
  • [Journal-full-title] Mammalian genome : official journal of the International Mammalian Genome Society
  • [ISO-abbreviation] Mamm. Genome
  • [Language] eng
  • [Publication-type] Comparative Study; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Carcinogens; 57-97-6 / 9,10-Dimethyl-1,2-benzanthracene
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33. Zábranský A, Hadravová R, Stokrová J, Sakalian M, Pichová I: Premature processing of mouse mammary tumor virus Gag polyprotein impairs intracellular capsid assembly. Virology; 2009 Feb 5;384(1):33-7
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Premature processing of mouse mammary tumor virus Gag polyprotein impairs intracellular capsid assembly.
  • Mouse mammary tumor virus (MMTV) is the prototypical member of the Betaretrovirus genus, but the processes of its morphogenesis are poorly characterized.
  • [MeSH-major] Gene Products, gag / genetics. Mammary Neoplasms, Animal / virology. Mammary Neoplasms, Experimental / virology. Mammary Tumor Virus, Mouse / genetics
  • [MeSH-minor] Amino Acid Substitution. Animals. Dexamethasone / pharmacology. Female. Humans. Kinetics. Mammary Glands, Animal / virology. Mice. Peptide Hydrolases / genetics. Peptide Hydrolases / metabolism. Promoter Regions, Genetic. Proviruses / genetics. Restriction Mapping. T-Lymphocytes / drug effects. T-Lymphocytes / virology. Transfection

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  • (PMID = 19046754.001).
  • [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 / Gene Products, gag; 7S5I7G3JQL / Dexamethasone; EC 3.4.- / Peptide Hydrolases
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34. Pawlowski KM, Krol M, Majewska A, Badowska-Kozakiewicz A, Mol JA, Malicka E, Motyl T: Comparison of cellular and tissue transcriptional profiles in canine mammary tumor. J Physiol Pharmacol; 2009 May;60 Suppl 1:85-94

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Comparison of cellular and tissue transcriptional profiles in canine mammary tumor.
  • Tumor-derived cell lines are widely used as in vitro cancer models.
  • Cell lines historically served as the primary experimental model systems for exploration of tumor cell biology and pharmacology.
  • This complication has led to difficulties in the extrapolation of biology observed in cell lines to tumor biology in vivo.
  • The aim of our study was to compare gene expression profiles in canine mammary tumor tissue and cell cultures derived from those tumors using cDNA microarrays.
  • Tumors of two different origins were used; chondrosarcoma and adenocarcinoma and their primary cell cultures.
  • It has been found that cell culture gene expression profiles closely resembled those of their corresponding in vivo tumor.
  • These experiments revealed that transcriptome of our primary cell culture corresponds to transcriptome of its parental tumor tissue and for this reason cell culture represents the reliable in vitro model for oncogenomic and pharmacogenomic studies.
  • [MeSH-major] Adenocarcinoma / metabolism. Cell Line, Tumor / metabolism. Chondrosarcoma, Mesenchymal / metabolism. Gene Expression Profiling. Mammary Neoplasms, Animal / metabolism

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  • (PMID = 19609017.001).
  • [ISSN] 1899-1505
  • [Journal-full-title] Journal of physiology and pharmacology : an official journal of the Polish Physiological Society
  • [ISO-abbreviation] J. Physiol. Pharmacol.
  • [Language] eng
  • [Publication-type] Comparative Study; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Poland
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35. Bhadra S, Lozano MM, Dudley JP: Conversion of mouse mammary tumor virus to a lymphomagenic virus. J Virol; 2005 Oct;79(19):12592-6
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  • [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.

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  • (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
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36. Bhadra S, Lozano MM, Dudley JP: BALB/Mtv-null mice responding to strong mouse mammary tumor virus superantigens restrict mammary tumorigenesis. J Virol; 2009 Jan;83(1):484-8
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  • [Title] BALB/Mtv-null mice responding to strong mouse mammary tumor virus superantigens restrict mammary tumorigenesis.
  • The absence of endogenous mouse mammary tumor viruses (MMTVs) in the congenic mouse strain, BALB/Mtv-null, restricts the early steps of exogenous C3H MMTV infection, preventing the superantigen (Sag) response and mammary tumorigenesis.
  • Here we demonstrate that BALB/Mtv-null mice also resist tumor induction by FM MMTV, which encodes a stronger Sag compared to C3H MMTV.
  • Neither virus shows significant replication in the spleen or mammary gland.
  • Thus, Mtv-null mice restrict MMTV replication and mammary tumorigenesis even after a robust Sag response.
  • [MeSH-major] Mammary Neoplasms, Experimental / immunology. Mammary Tumor Virus, Mouse / immunology. Retroviridae Infections / immunology. Superantigens / immunology. Tumor Virus Infections / immunology
  • [MeSH-minor] Animals. Female. Incidence. Mammary Glands, Animal / virology. Mice. Mice, Inbred BALB C. Mice, Knockout. Spleen / virology

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  • [Cites] Microbes Infect. 2000 Aug;2(10):1215-23 [11008111.001]
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  • (PMID = 18922863.001).
  • [ISSN] 1098-5514
  • [Journal-full-title] Journal of virology
  • [ISO-abbreviation] J. Virol.
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / R01 CA116813
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Superantigens
  • [Other-IDs] NLM/ PMC2612332
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37. 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
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  • [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.

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  • (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
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38. 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
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  • [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

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  • (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
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39. 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
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  • [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

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  • (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
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40. 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
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  • [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.

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  • (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
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41. Gattelli A, Zimberlin MN, Meiss RP, Castilla LH, Kordon EC: Selection of early-occurring mutations dictates hormone-independent progression in mouse mammary tumor lines. J Virol; 2006 Nov;80(22):11409-15
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  • [Title] Selection of early-occurring mutations dictates hormone-independent progression in mouse mammary tumor lines.
  • Mice harboring three mouse mammary tumor virus (MMTV) variants develop pregnancy-dependent (PD) tumors that progress to pregnancy-independent (PI) behavior through successive passages.
  • Herein, we identified 10 predominant insertions in PI transplants from 8 independent tumor lines.
  • In addition, we identified a new viral insertion upstream of the gene Rspo3, which is overexpressed in three of the eight independent tumor lines and codes for a protein very similar to the recently described protein encoded by Int7.

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  • (PMID = 16971449.001).
  • [ISSN] 0022-538X
  • [Journal-full-title] Journal of virology
  • [ISO-abbreviation] J. Virol.
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / R01 CA096983; United States / FIC NIH HHS / TW / R01 TW006212; United States / FIC NIH HHS / TW / R01TW006212
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Other-IDs] NLM/ PMC1642155
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42. 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

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  • (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
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43. Fierz Y, Novosyadlyy R, Vijayakumar A, Yakar S, LeRoith D: Insulin-sensitizing therapy attenuates type 2 diabetes-mediated mammary tumor progression. Diabetes; 2010 Mar;59(3):686-93
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  • [Title] Insulin-sensitizing therapy attenuates type 2 diabetes-mediated mammary tumor progression.
  • Thus, we hypothesized that pharmacological reduction of elevated insulin levels would attenuate type 2 diabetes-mediated mammary tumor progression.
  • RESEARCH DESIGN AND METHODS: We studied mammary tumor development in MKR(+/+) mice, a nonobese, hyperinsulinemic mouse model of type 2 diabetes.
  • MKR(+/+) mice were either crossed with mice expressing the polyoma virus middle T oncogene specifically in the mammary gland or inoculated orthotopically with the mouse mammary tumor cell lines Met-1 and MCNeuA.
  • MKR(+/+) or control mice harboring tumors were treated with CL-316243, a specific beta3-adrenergic receptor agonist, which sensitizes insulin action but has no direct effect on the mouse mammary epithelium or Met-1 and MCNeuA cells.
  • RESULTS: CL-316243 treatment significantly reduced the elevated insulin levels in MKR(+/+) mice and, as a consequence, attenuated mammary tumor progression in the three tumor models tested.
  • This effect was accompanied by reductions in phosphorylation of insulin and IGF-I receptors in transformed mammary tissue.
  • CONCLUSIONS: Insulin-sensitizing treatment is sufficient to abrogate type 2 diabetes-mediated mammary tumor progression.
  • [MeSH-major] Diabetes Mellitus, Type 2 / drug therapy. Dioxoles / pharmacology. Hyperinsulinism / drug therapy. Hypoglycemic Agents / pharmacology. Mammary Neoplasms, Animal / drug therapy
  • [MeSH-minor] Animals. Body Composition / drug effects. Cell Line, Tumor. Comorbidity. Disease Models, Animal. Disease Progression. Eating / drug effects. Epithelial Cells / cytology. Epithelial Cells / drug effects. Female. Insulin / blood. Lipids / blood. Male. Mammary Glands, Animal / drug effects. Mammary Glands, Animal / pathology. Mice. Mice, Inbred Strains. Mice, Transgenic. Polyomavirus / genetics. Risk Factors

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  • (PMID = 19959755.001).
  • [ISSN] 1939-327X
  • [Journal-full-title] Diabetes
  • [ISO-abbreviation] Diabetes
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / R01 CA128799; United States / NCI NIH HHS / CA / 1R01CA128799-01A1
  • [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 / Dioxoles; 0 / Hypoglycemic Agents; 0 / Insulin; 0 / Lipids; 138908-40-4 / disodium (R,R)-5-(2-((2-(3-chlorophenyl)-2-hydroxyethyl)-amino)propyl)-1,3-benzodioxole-2,3-dicarboxylate
  • [Other-IDs] NLM/ PMC2828655
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44. 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
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  • [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.

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  • (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
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45. Sfacteria A, Mazzullo G, Bertani C, Calabrò P, De Vico G, Macrì B: Erythropoietin receptor expression in canine mammary tumor: an immunohistochemical study. Vet Pathol; 2005 Nov;42(6):837-40

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Erythropoietin receptor expression in canine mammary tumor: an immunohistochemical study.
  • Recently, it has been demonstrated that EPO and its receptor (EPOR) are expressed in several neoplastic cell lines and solid tumors.
  • Furthermore, in vitro and in vivo studies have shown that EPO could promote human breast carcinoma growth by means of the binding with its receptor, although a clear function for EPO in this setting has not been yet established.
  • The aim of the present study was to investigate the immunohistochemical expression of EPOR in canine mammary gland dysplastic and neoplastic lesions.
  • On the basis of these findings, this study describes, for the first time, the evidence for EPOR expression in canine mammary gland tumor and suggests a feasible EPO's role for canine mammary tumor progression.
  • [MeSH-major] Dog Diseases / metabolism. Gene Expression Regulation, Neoplastic. Mammary Neoplasms, Animal / metabolism. Receptors, Erythropoietin / metabolism

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  • (PMID = 16301583.001).
  • [ISSN] 0300-9858
  • [Journal-full-title] Veterinary pathology
  • [ISO-abbreviation] Vet. Pathol.
  • [Language] eng
  • [Publication-type] Comparative Study; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Receptors, Erythropoietin
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46. Bangari DS, Stevenson GW: Carcinoma in a mixed mammary tumor in a llama (Lama glama). J Vet Diagn Invest; 2007 Jul;19(4):450-3

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  • [Title] Carcinoma in a mixed mammary tumor in a llama (Lama glama).
  • A 13-year-old female llama was presented to the referring veterinarian for swelling and firmness of the right rear mammary gland, for a duration of 2 months, which had been unresponsive to antibiotics.
  • A formalin-fixed wedge biopsy specimen from the affected quarter was submitted to Purdue University Animal Disease Diagnostic Laboratory for histopathology.
  • The presence of osseous metaplasia in the proliferative mesenchymal component justified classification as a mixed tumor.
  • The llama was in good health after about 1 year of initial presentation, and metastasis to regional lymph nodes was not reported.
  • Mammary neoplasia is rare in camelids.
  • To the authors' knowledge, this is the first report of a carcinoma in a mixed mammary tumor in a llama.
  • [MeSH-major] Camelids, New World. Carcinoma / veterinary. Mammary Neoplasms, Animal / diagnosis
  • [MeSH-minor] Animals. Female. Mammary Glands, Animal / pathology

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  • (PMID = 17609363.001).
  • [ISSN] 1040-6387
  • [Journal-full-title] Journal of veterinary diagnostic investigation : official publication of the American Association of Veterinary Laboratory Diagnosticians, Inc
  • [ISO-abbreviation] J. Vet. Diagn. Invest.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
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47. 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
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  • [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


48. 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
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  • [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

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  • (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
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49. 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
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  • [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

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  • (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
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50. Lam JB, Chow KH, Xu A, Lam KS, Liu J, Wong NS, Moon RT, Shepherd PR, Cooper GJ, Wang Y: Adiponectin haploinsufficiency promotes mammary tumor development in MMTV-PyVT mice by modulation of phosphatase and tensin homolog activities. PLoS One; 2009;4(3):e4968
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  • [Title] Adiponectin haploinsufficiency promotes mammary tumor development in MMTV-PyVT mice by modulation of phosphatase and tensin homolog activities.
  • However, the precise role of adiponectin deficiency in mammary carcinogenesis remains elusive.
  • METHODOLOGY/PRINCIPAL FINDINGS: In the present study, MMTV-polyomavirus middle T antigen (MMTV-PyVT) transgenic mice with reduced adiponectin expressions were established and the stromal effects of adiponectin haploinsufficiency on mammary tumor development evaluated.
  • In mice from both FVB/N and C57BL/6J backgrounds, insufficient adiponectin production promoted mammary tumor onset and development.
  • A distinctive basal-like subtype of tumors, with a more aggressive phenotype, was derived from adiponectin haplodeficient MMTV-PyVT mice.
  • Comparing with those from control MMTV-PyVT mice, the isolated mammary tumor cells showed enhanced tumor progression in re-implanted nude mice, accelerated proliferation in primary cultures, and hyperactivated phosphatidylinositol-3-kinase (PI3K)/Akt/beta-catenin signaling, which at least partly attributed to the decreased phosphatase and tensin homolog (PTEN) activities.
  • Increased association of PTEN-thioredoxin complexes was detected in tumors derived from mice with reduced adiponectin levels.
  • The activities of thioredoxin (Trx1) and thioredoxin reductase (TrxR1) were significantly elevated, whereas treatment with either curcumin, an irreversible inhibitor of TrxR1, or adiponectin largely attenuated their activities and resulted in the re-activation of PTEN in these tumor cells.
  • CONCLUSION: Adiponectin haploinsufficiency facilitated mammary tumorigenesis by down-regulation of PTEN activity and activation of PI3K/Akt signalling pathway through a mechanism involving Trx1/TrxR1 redox regulations.

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  • [ErratumIn] PLoS One. 2009;4(4). doi: 10.1371/annotation/14cb7d7e-a921-4ae6-a405-99c60656579f
  • (PMID = 19319191.001).
  • [ISSN] 1932-6203
  • [Journal-full-title] PloS one
  • [ISO-abbreviation] PLoS ONE
  • [Language] ENG
  • [Grant] United States / NHLBI NIH HHS / HL / R01 HL051586
  • [Publication-type] Journal Article; 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 / Txn1 protein, mouse; 52500-60-4 / Thioredoxins; EC 1.8.1.9 / Thioredoxin Reductase 1; EC 1.8.1.9 / Txnrd1 protein, mouse; EC 2.7.1.- / Phosphatidylinositol 3-Kinases; EC 2.7.11.1 / Proto-Oncogene Proteins c-akt; EC 3.1.3.48 / Pten protein, mouse; EC 3.1.3.67 / PTEN Phosphohydrolase
  • [Other-IDs] NLM/ PMC2656613
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51. Lee JJ, Chen PB, Yang SH, Cheng CH, Chueh LL, Pang VF, Hsiao M, Lin CT: Effect of the VP3 gene of chicken anemia virus on canine mammary tumor cells. Am J Vet Res; 2007 Apr;68(4):411-22
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  • [Title] Effect of the VP3 gene of chicken anemia virus on canine mammary tumor cells.
  • OBJECTIVE: To investigate the antitumor effect of the chicken anemia virus (CAV) VP3 gene in canine mammary tumor (CMT) cells.
  • SAMPLE POPULATIONS: Established primary canine cell lines that originated from epithelial cells of resected CMTs and nonneoplastic mammary gland epithelial (MGE) cells.
  • Among the fusion protein-expressing CMT cells, most underwent characteristic changes of apoptosis, whereas apoptosis was not detected in fusion protein-expressing, nonneoplastic MGE cells.
  • Induction of apoptosis by VP3 gene overexpression in CMT cells was associated with the caspase-9-, but not the caspase-8-, mediated apoptosis pathway.
  • CONCLUSIONS AND CLINICAL RELEVANCE: These data indicate that the VP3 gene of the CAV induces apoptosis in malignant CMT cells, but not in nonneoplastic canine MGE cells.
  • On the basis of such tumor cell-specific killing, the VP3 gene may be a promising agent for the treatment of malignant mammary gland tumors in dogs.
  • [MeSH-major] Apoptosis / drug effects. Capsid Proteins / therapeutic use. Chicken anemia virus / genetics. Dog Diseases / therapy. Gene Expression Regulation, Neoplastic / drug effects. Genetic Therapy / methods. Mammary Neoplasms, Animal / therapy
  • [MeSH-minor] Animals. Blotting, Western / veterinary. Cell Line, Tumor. Dogs. Genetic Vectors. In Situ Nick-End Labeling / veterinary. Lentivirus. Microscopy, Fluorescence / veterinary

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  • (PMID = 17397298.001).
  • [ISSN] 0002-9645
  • [Journal-full-title] American journal of veterinary research
  • [ISO-abbreviation] Am. J. Vet. Res.
  • [Language] eng
  • [Publication-type] Comparative Study; Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Capsid Proteins; 0 / VP3 protein, Chicken anemia virus
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52. Wang H, Teske D, Tess A, Kohlhepp R, Choi Y, Kendziorski C, Moser AR: Identification of novel modifier loci of Apc Min affecting mammary tumor development. Cancer Res; 2007 Dec 1;67(23):11226-33
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  • [Title] Identification of novel modifier loci of Apc Min affecting mammary tumor development.
  • Genetic background affects the susceptibility to mammary tumor development in Apc(Min/+) mice.
  • Here we report the identification of four novel modifier loci that influence different aspects of mammary tumor development in Apc(Min/+) mice.
  • Analysis of tumor development in a backcross of (FVBB6 Apc(Min/+)) x B6 Apc(Min/+) mice has identified a modifier on chromosome 9 that significantly affects tumor multiplicity, and a modifier on chromosome 4 that significantly affects tumor latency and affects tumor number with suggestive significance.
  • A modifier on chromosome 18 specifically affects tumor latency but not tumor number.
  • Kaplan-Meier analysis suggests there is at least an additive interaction affecting tumor latency between the loci on chromosomes 4 and 18.
  • We also identified a modifier locus on chromosome 6 that interacts with the loci on chromosome 4 and chromosome 9 to affect tumor number.
  • These results suggest that multiple genetic loci control different aspects of mammary tumor development.
  • None of these modifiers is associated with intestinal tumor susceptibility, which indicates that these modifiers act on tumor development in a tissue-specific manner.
  • [MeSH-major] Genes, APC. Mammary Glands, Animal / pathology. Mammary Neoplasms, Experimental / epidemiology. Mammary Neoplasms, Experimental / genetics
  • [MeSH-minor] Alkylating Agents / toxicity. Alleles. Animals. Chromosome Mapping. Crosses, Genetic. Effect Modifier, Epidemiologic. Ethylnitrosourea / toxicity. Female. Genetic Predisposition to Disease. Hyperplasia / genetics. Intestinal Neoplasms / genetics. Male. Mice. Mice, Inbred C57BL

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  • (PMID = 18056448.001).
  • [ISSN] 1538-7445
  • [Journal-full-title] Cancer research
  • [ISO-abbreviation] Cancer Res.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, U.S. Gov't, Non-P.H.S.
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Alkylating Agents; P8M1T4190R / Ethylnitrosourea
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53. 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
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  • [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

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  • (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
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54. Kim JH, Hubbard NE, Ziboh V, Erickson KL: Conjugated linoleic acid reduction of murine mammary tumor cell growth through 5-hydroxyeicosatetraenoic acid. Biochim Biophys Acta; 2005 Feb 21;1687(1-3):103-9
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Conjugated linoleic acid reduction of murine mammary tumor cell growth through 5-hydroxyeicosatetraenoic acid.
  • However, the mechanism of its action has not been clarified.
  • The goal of this study was to determine whether CLA altered mouse mammary tumor cell growth and whether specific metabolites of the lipoxygenase pathway were involved in CLA action.
  • Both t10, c12-CLA and a lipoxygenase inhibitor, but not c9, t11-CLA or linoleic acid (LA), reduced mouse mammary tumor cell viability and growth by inducing apoptosis and reducing cell proliferation. t10, c12-CLA reduced the production of the 5-lipoxygenase metabolite, 5-hydroxyeicosatetraenoic acid (5-HETE).
  • That effect was not seen with c9, t11-CLA or LA.
  • Adding 5-HETE back to tumor cells reduced the t10, c12-CLA effect on both apoptosis and cell proliferation.
  • These data suggest that t10, c12-CLA reduction of tumor cell growth may involve the suppression of the 5-lipoxygenase metabolite, 5-HETE, with subsequent effects on apoptosis and cell proliferation.
  • [MeSH-major] Cell Proliferation / drug effects. Chemotactic Factors / metabolism. Hydroxyeicosatetraenoic Acids / metabolism. Linoleic Acids, Conjugated / pharmacology. Mammary Neoplasms, Animal / metabolism
  • [MeSH-minor] Animals. Apoptosis / drug effects. Cell Line, Tumor. Cell Survival / drug effects. Dose-Response Relationship, Drug. Female. Humans. Mice

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  • (PMID = 15708358.001).
  • [ISSN] 0006-3002
  • [Journal-full-title] Biochimica et biophysica acta
  • [ISO-abbreviation] Biochim. Biophys. Acta
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Netherlands
  • [Chemical-registry-number] 0 / Chemotactic Factors; 0 / Hydroxyeicosatetraenoic Acids; 0 / Linoleic Acids, Conjugated; 467RNW8T91 / 5-hydroxy-6,8,11,14-eicosatetraenoic acid
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55. Fernandez-Twinn DS, Ekizoglou S, Gusterson BA, Luan J, Ozanne SE: Compensatory mammary growth following protein restriction during pregnancy and lactation increases early-onset mammary tumor incidence in rats. Carcinogenesis; 2007 Mar;28(3):545-52
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Compensatory mammary growth following protein restriction during pregnancy and lactation increases early-onset mammary tumor incidence in rats.
  • Offspring postnatal mammary gland development was assessed by morphometry.
  • To identify potential growth mechanisms, we measured protein expression of receptors involved in insulin and hormone signaling, both in cleared mammary gland lysates and isolated epithelial cells.
  • Mammary tumor incidence and latency (n=96) was monitored after three weekly intraperitoneal nitrosomethylurea injections (50 mg/kg body wt).
  • LP offspring displayed reduced postnatal ductal branching and epithelial invasion at 3 weeks, followed by compensatory mammary growth 1 week later coinciding with increased protein expression of receptors to insulin, IGF-1 and estrogen.
  • Significantly, early-mammary tumor incidence (0-16 weeks post-treatment) was doubled in LP offspring [RR, 2.13 (1.02, 4.45); P=0.046].
  • The data suggest that poor early nutrition has an important influence on the mammary primordium, and increases future susceptibility to breast cancer.
  • Up-regulated growth factor and hormone signaling during compensatory mammary growth may mediate this increased susceptibility and present potential targets for intervention.
  • [MeSH-major] Lactation / physiology. Mammary Neoplasms, Animal / pathology
  • [MeSH-minor] Animals. Animals, Suckling. Body Weight. Breast Neoplasms / epidemiology. Disease Susceptibility. Estradiol / blood. Female. Humans. Male. Nutritional Status. Pregnancy. Rats. Rats, Wistar

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  • (PMID = 16952910.001).
  • [ISSN] 0143-3334
  • [Journal-full-title] Carcinogenesis
  • [ISO-abbreviation] Carcinogenesis
  • [Language] eng
  • [Grant] United States / NIA NIH HHS / AG / AG-20608-02
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 4TI98Z838E / Estradiol
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56. 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
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  • [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

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  • [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
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57. Bar-Sinai A, Bassa N, Fischette M, Gottesman MM, Love DC, Hanover JA, Hochman J: Mouse mammary tumor virus Env-derived peptide associates with nucleolar targets in lymphoma, mammary carcinoma, and human breast cancer. Cancer Res; 2005 Aug 15;65(16):7223-30
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  • [Title] Mouse mammary tumor virus Env-derived peptide associates with nucleolar targets in lymphoma, mammary carcinoma, and human breast cancer.
  • We have previously shown that the leader peptide (p14) of the Env-precursor of mouse mammary tumor virus is translocated into the nucleoli of murine T cell lymphomas that harbor this virus.
  • Using a polyclonal antibody against recombinant p14, we show here that p14 is also localized to the nucleoli of murine mammary carcinomas and some human breast cancer samples.
  • Taken together, these findings point towards a more general involvement of p14 in lymphomagenesis and mammary carcinogenesis.
  • [MeSH-major] Breast Neoplasms / virology. Cell Nucleolus / virology. Lymphoma, T-Cell / virology. Mammary Neoplasms, Experimental / metabolism. Mammary Tumor Virus, Mouse / metabolism. Viral Envelope Proteins / metabolism

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  • (PMID = 16103073.001).
  • [ISSN] 0008-5472
  • [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 / Antibodies, Viral; 0 / Viral Envelope Proteins
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58. 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
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  • [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

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  • (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
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59. Bachawal SV, Wali VB, Sylvester PW: Combined gamma-tocotrienol and erlotinib/gefitinib treatment suppresses Stat and Akt signaling in murine mammary tumor cells. Anticancer Res; 2010 Feb;30(2):429-37
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 gamma-tocotrienol and erlotinib/gefitinib treatment suppresses Stat and Akt signaling in murine mammary tumor cells.
  • However, combination treatment of TKIs with gamma-tocotrienol targets multiple ErbB receptors and significantly inhibit +SA murine mammary tumor cell growth.
  • CONCLUSION: Combined treatment of gamma-tocotrienol with erlotinib or gefitinib prevents ErbB receptor heterodimer cooperation and inhibits EGF-dependent mitogenic signaling in +SA murine mammary tumor cells.
  • [MeSH-major] Antineoplastic Combined Chemotherapy Protocols / pharmacology. Chromans / pharmacology. Mammary Neoplasms, Animal / drug therapy. Proto-Oncogene Proteins c-akt / metabolism. STAT Transcription Factors / metabolism. Signal Transduction / drug effects. Vitamin E / analogs & derivatives


60. 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.

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  • (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
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61. 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


62. 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

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  • [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
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63. 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

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  • (PMID = 18032509.001).
  • [ISSN] 1098-5514
  • [Journal-full-title] Journal of virology
  • [ISO-abbreviation] J. Virol.
  • [Language] eng
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  • [Publication-type] Comparative Study; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Other-IDs] NLM/ PMC2224419
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64. Martin MD, Fingleton B, Lynch CC, Wells S, McIntyre JO, Piston DW, Matrisian LM: Establishment and quantitative imaging of a 3D lung organotypic model of mammary tumor outgrowth. Clin Exp Metastasis; 2008;25(8):877-85
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Establishment and quantitative imaging of a 3D lung organotypic model of mammary tumor outgrowth.
  • To better understand the interaction between tumor and host cells in this important secondary site, we have developed a 3D in vitro organotypic model of breast tumor metastatic growth in the lung.
  • In our model, cells isolated from mouse lungs are placed in a collagen sponge to serve as a scaffold and co-cultured with a green fluorescent protein-labeled polyoma virus middle T antigen (PyVT) mammary tumor cell line.
  • Our studies determined that host lung cells influence the ability of tumor cells to grow, as the presence of lung parenchyma positively affected the proliferation of the mammary tumor cells in culture.
  • In summary, we have developed a novel in vitro model of breast tumor cells in a common metastatic site that can be used to study tumor/host interactions in an important microenvironment.

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  • (PMID = 18787962.001).
  • [ISSN] 1573-7276
  • [Journal-full-title] Clinical & experimental metastasis
  • [ISO-abbreviation] Clin. Exp. Metastasis
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / CA084360-04; United States / NCI NIH HHS / CA / R01 CA084360; United States / NCI NIH HHS / CA / R01 CA084360-04; United States / NCI NIH HHS / CA / R01-CA84360
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural
  • [Publication-country] Netherlands
  • [Chemical-registry-number] 147336-22-9 / Green Fluorescent Proteins
  • [Other-IDs] NLM/ NIHMS66754; NLM/ PMC2588650
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65. Bachawal SV, Wali VB, Sylvester PW: Enhanced antiproliferative and apoptotic response to combined treatment of gamma-tocotrienol with erlotinib or gefitinib in mammary tumor cells. BMC Cancer; 2010 Mar 08;10:84
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  • [Title] Enhanced antiproliferative and apoptotic response to combined treatment of gamma-tocotrienol with erlotinib or gefitinib in mammary tumor cells.
  • METHODS: Highly malignant mouse +SA mammary epithelial cells were maintained in culture on serum-free defined media containing 10 ng/ml EGF as a mitogen.
  • RESULTS: Treatment with 3.5 microM gamma-tocotrienol, 0.5 microM erlotinib or 1.0 microM gefitinib alone, significantly inhibited +SA tumor cell growth.
  • CONCLUSION: Combination treatment of gamma-tocotrienol with specific ErbB receptor inhibitors is more effective in reducing mammary tumor cell growth and viability than high dose monotherapy, suggesting that targeting multiple ErbB receptors with combination therapy may significantly improve the therapeutic response in breast cancer patients.

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  • (PMID = 20211018.001).
  • [ISSN] 1471-2407
  • [Journal-full-title] BMC cancer
  • [ISO-abbreviation] BMC Cancer
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / CA 86833
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Antibodies, Monoclonal; 0 / Antibodies, Monoclonal, Humanized; 0 / Chromans; 0 / Culture Media, Serum-Free; 0 / Quinazolines; 1406-18-4 / Vitamin E; 4382-43-8 / plastochromanol 8; DA87705X9K / Erlotinib Hydrochloride; EC 2.7.10.1 / Receptor, Epidermal Growth Factor; P188ANX8CK / Trastuzumab; S65743JHBS / gefitinib
  • [Other-IDs] NLM/ PMC2841143
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66. El-Refaei MF, Sarkar NH: Snake venom inhibits the growth of mouse mammary tumor cells in vitro and in vivo. Toxicon; 2009 Jul;54(1):33-41

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Snake venom inhibits the growth of mouse mammary tumor cells in vitro and in vivo.
  • However, it is not known if Cerastes cerastes venom (CCV) obtained from the Egyptian desert possesses any anti-tumor activity.
  • In the present study we examined in vitro the effect of CCV on the growth rate and morphology of a mouse mammary tumor virus-induced mammary tumor cell line (RIII/Sa-MT).
  • CCV (1 microg/mouse), administered once per week directly into growing tumors for a period of 4 weeks, was found to reduce tumor load by 54%, and as a consequence the CCV-treated mice lived for more than 35 days longer than untreated mice.
  • Histological and ultrastructural examination of the cells and tumors, as well as nuclear staining of the cells and DNA fragmentation studies, led us to conclude that necrosis is most likely the underlying mechanism by which CCV inhibited the growth of mouse mammary tumor cells both in vitro and in vivo.
  • [MeSH-major] Mammary Neoplasms, Animal / drug therapy. Viper Venoms / therapeutic use. Viperidae / physiology
  • [MeSH-minor] Animals. Body Weight / drug effects. Cell Line, Tumor. Cell Survival / drug effects. DNA Fragmentation / drug effects. Dose-Response Relationship, Drug. Female. Immunohistochemistry. Mice. Microscopy, Electron. Necrosis / pathology

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  • [ErratumIn] Toxicon. 2011 Apr;57(5):826. El-Refael, Mohamed F [corrected to El-Refaei, Mohamed F]
  • (PMID = 19327376.001).
  • [ISSN] 1879-3150
  • [Journal-full-title] Toxicon : official journal of the International Society on Toxinology
  • [ISO-abbreviation] Toxicon
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Viper Venoms
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67. 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
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  • [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

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  • (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
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68. 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
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  • [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.

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  • (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
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69. Fierz Y, Novosyadlyy R, Vijayakumar A, Yakar S, LeRoith D: Mammalian target of rapamycin inhibition abrogates insulin-mediated mammary tumor progression in type 2 diabetes. Endocr Relat Cancer; 2010 Dec;17(4):941-51
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  • [Title] Mammalian target of rapamycin inhibition abrogates insulin-mediated mammary tumor progression in type 2 diabetes.
  • The mammalian target of rapamycin (mTOR) is activated by insulin and is a key regulator of mammary tumor progression.
  • Pharmacological mTOR inhibition suppresses tumor growth in numerous mammary tumor models in the non-diabetic setting.
  • However, the role of the mTOR pathway in type 2 diabetes-induced tumor growth remains elusive.
  • Herein, we investigated whether the mTOR pathway is implicated in insulin-induced mammary tumor progression in a transgenic mouse model of type 2 diabetes (MKR mice) and evaluated the impact of mTOR inhibition on the diabetic state.
  • Mammary tumor progression was studied in the double transgenic MMTV-Polyoma Virus middle T antigen (PyVmT)/MKR mice and by orthotopic inoculation of PyVmT- and Neu/ErbB2-driven mammary tumor cells (Met-1 and MCNeuA cells respectively).
  • mTOR inhibition by rapamycin markedly suppressed tumor growth in both wild-type and MKR mice.
  • In diabetic animals, however, the promoting action of insulin on tumor growth was completely blunted by rapamycin, despite a worsening of the carbohydrate and lipid metabolism.
  • Taken together, pharmacological mTOR blockade is sufficient to abrogate mammary tumor progression in the setting of hyperinsulinemia, and thus mTOR inhibitors may be an attractive therapeutic modality for breast cancer patients with type 2 diabetes.

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  • (PMID = 20801951.001).
  • [ISSN] 1479-6821
  • [Journal-full-title] Endocrine-related cancer
  • [ISO-abbreviation] Endocr. Relat. Cancer
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / R01 CA128799; United States / NCI NIH HHS / CA / 1R01CA128799
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Antibiotics, Antineoplastic; 0 / Blood Glucose; 0 / Insulin; 0 / Triglycerides; EC 2.7.1.1 / TOR Serine-Threonine Kinases; EC 2.7.1.1 / mTOR protein, mouse; W36ZG6FT64 / Sirolimus
  • [Other-IDs] NLM/ NIHMS598328; NLM/ PMC4082826
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70. 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 .

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  • [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.

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  • (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
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71. 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
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  • [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

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  • (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
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72. Wei N, Wang B, Zhang QY, Mi MT, Zhu JD, Yu XP, Yuan JL, Chen K, Wang J, Chang H: Effects of different dietary fatty acids on the fatty acid compositions and the expression of lipid metabolic-related genes in mammary tumor tissues of rats. Nutr Cancer; 2008;60(6):810-25
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  • [Title] Effects of different dietary fatty acids on the fatty acid compositions and the expression of lipid metabolic-related genes in mammary tumor tissues of rats.
  • In this study, the effects of dietary fatty acids on the fatty acid compositions and lipid metabolic-related genes expression in N-methyl-N-nitrosourea (MNU)-induced rat mammary carcinogenesis were evaluated.
  • There was no mammary tumor occurrence in the control and MNU-treated n-3 PUFA groups after 18 wk. n-3 PUFA diet retarded the weight growth of rats.
  • 1:1 n-6/n-3 diet significantly reduced the MNU-induced tumor incidence and tumor multiplicity compared with SFA, MUFA, n-6 PUFA, 5:1 n-6/n-3, 10:1 n-6/n-3 and 1:2:1 S/M/P diets (42.86% vs. 83.33%-92.31%, 0.79 vs. 2.62-2.85, P < 0.01).
  • Additionally, 1:1 n-6/n-3 diet substantially increased cis-5,8,11,14,17-eicosapentaenoic acid and cis-4,7,10,13,16,19-docosahexaenoic acid levels, whereas it decreased C20:4 level and the mRNA expressions of fatty acid synthase, Cyclooxygenase-2 (COX-2), and 5-lipoxygenase (5-LOX) in mammary tissues (P < 0.05).
  • These results suggest that 1:1 n-6/n-3 in the diet is effective in the prevention of mammary tumor development by increasing the n-3 PUFA content and reducing the expression of lipid metabolic-related genes.
  • [MeSH-major] Dietary Fats / administration & dosage. Fatty Acids / analysis. Mammary Neoplasms, Experimental / prevention & control
  • [MeSH-minor] Animals. Arachidonate 5-Lipoxygenase / genetics. Arachidonic Acid / metabolism. Cyclooxygenase 2 / genetics. Fatty Acid Synthases / genetics. Fatty Acids, Omega-3 / administration & dosage. Fatty Acids, Omega-6 / administration & dosage. Female. Mammary Glands, Animal / chemistry. Rats. Rats, Sprague-Dawley. Weight Gain

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  • (PMID = 19005981.001).
  • [ISSN] 1532-7914
  • [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 / Dietary Fats; 0 / Fatty Acids; 0 / Fatty Acids, Omega-3; 0 / Fatty Acids, Omega-6; 27YG812J1I / Arachidonic Acid; EC 1.13.11.34 / Arachidonate 5-Lipoxygenase; EC 1.14.99.1 / Cyclooxygenase 2; EC 2.3.1.85 / Fatty Acid Synthases
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73. 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 .

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  • [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

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  • (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
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74. 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
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  • [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

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  • (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
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75. 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
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  • [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.

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  • (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
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76. 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
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  • [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

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  • (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
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77. 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
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  • [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

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  • (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
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78. 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
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  • [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.

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  • (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
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79. 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.


80. 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

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  • (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
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81. 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
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  • [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.

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  • (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
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82. MacLean PS, Giles ED, Johnson GC, McDaniel SM, Fleming-Elder BK, Gilman KA, Andrianakos AG, Jackman MR, Shroyer KR, Schedin PJ: A surprising link between the energetics of ovariectomy-induced weight gain and mammary tumor progression in obese rats. Obesity (Silver Spring); 2010 Apr;18(4):696-703
Hazardous Substances Data Bank. N-NITROSO-N-METHYLUREA .

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  • [Title] A surprising link between the energetics of ovariectomy-induced weight gain and mammary tumor progression in obese rats.
  • The rats were ovariectomized (OVX) at approximately 24 weeks of age and the change in tumor multiplicity and burden, weight gain, energy intake, tumor estrogen receptor (ER) status, and humoral metabolite and cytokine profiles were examined.
  • The survival and growth of tumors increased in obese rats in response to OVX.
  • During this time, feed efficiency (mg gain/kcal intake) was lower in obese rats, and this reduced storage efficiency of ingested fuels predicted the OVX-induced changes in tumor multiplicity (r = -0.64, P < 0.001) and burden (r = -0.57, P < 0.001).
  • Tumors from obese rats contained more cells that expressed ERalpha, and post-OVX plasma from rats with the lowest feed efficiency had lower interleukin (IL)-2 and IL-4 levels.
  • Our observations suggest a novel link between obesity and mammary tumor promotion that involves impaired fuel metabolism during OVX-induced weight gain.

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  • (PMID = 19798068.001).
  • [ISSN] 1930-739X
  • [Journal-full-title] Obesity (Silver Spring, Md.)
  • [ISO-abbreviation] Obesity (Silver Spring)
  • [Language] ENG
  • [Grant] United States / NIDDK NIH HHS / DK / DK67403; United States / NIDDK NIH HHS / DK / P30 DK048520; United States / NIDDK NIH HHS / DK / R01 DK038088; United States / NIDDK NIH HHS / DK / DK38088; United States / NIDDK NIH HHS / DK / DK48520; United States / NIDDK NIH HHS / DK / K01 DK067403
  • [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 / Alkylating Agents; 0 / Dietary Fats; 0 / Estrogen Receptor alpha; 0 / Estrogens; 0 / Interleukin-2; 207137-56-2 / Interleukin-4; 684-93-5 / Methylnitrosourea
  • [Other-IDs] NLM/ NIHMS765005; NLM/ PMC4973619
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83. 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) .

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  • [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.

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  • (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
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84. 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
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  • [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