[X] Close
You are about to erase all the values you have customized, search history, page format, etc.
Click here to RESET all values       Click here to GO BACK without resetting any value
Items 1 to 24 of about 24
1. Padar S, van Breemen C, Thomas DW, Uchizono JA, Livesey JC, Rahimian R: Differential regulation of calcium homeostasis in adenocarcinoma cell line A549 and its Taxol-resistant subclone. Br J Pharmacol; 2004 May;142(2):305-16
PDF icon [Fulltext service] Download fulltext PDF of this article and others, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Differential regulation of calcium homeostasis in adenocarcinoma cell line A549 and its Taxol-resistant subclone.
  • Drug resistance is a fundamental problem in cancer chemotherapy.
  • We investigated the regulatory role of [Ca2+](i) in Taxol resistance in the non-small-cell lung cancer cell line A549 and its chemoresistant subclone A549-T24.
  • Measurement of cytosolic calcium ([Ca2+](c)) in single cells and cell populations revealed similar levels of basal calcium in the two cell lines.
  • However, a reduced response to thapsigargin (a sarcoplasmic/endoplasmic reticulum Ca2+-ATPase (SERCA) inhibitor) in A549-T24 cells compared to the parent cell line suggested a lower ER Ca2+ content in these cells. mRNA expression of SERCA2b and SERCA3, major Ca2+ pumps involved in ER Ca2+ homeostasis, did not significantly differ between the two cell lines, as revealed by RT-PCR.
  • An altered calcium influx pathway in the Taxol-resistant cell line was observed.
  • Modulation of the ER calcium pools using CMC (4-chloro-m-cresol) and ATP revealed lower ryanodine receptor (RyR) and IP(3) receptor (IP(3)R)-sensitive Ca2+ stores in the chemoresistant cell line.
  • Western blot and RT-PCR studies suggested that A549-T24 cells expressed higher levels of the antiapoptotic protein Bcl-2 and the calcium-binding protein sorcin, respectively, in comparison to the parent cell line.
  • Both of these proteins have been previously implicated in chemoresistance, in part, due to their ability to modulate[Ca2+](i).

  • COS Scholar Universe. author profiles.
  • Hazardous Substances Data Bank. TAXOL .
  • Hazardous Substances Data Bank. CALCIUM, ELEMENTAL .
  • NCI CPTAC Assay Portal. NCI CPTAC Assay Portal .
  • The Lens. Cited by Patents in .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [Cites] EMBO J. 2001 Jun 1;20(11):2690-701 [11387204.001]
  • [Cites] Trends Pharmacol Sci. 1998 Apr;19(4):131-5 [9612087.001]
  • [Cites] FASEB J. 2001 Aug;15(10):1727-38 [11481220.001]
  • [Cites] J Cell Sci. 2001 Jun;114(Pt 12):2223-9 [11493662.001]
  • [Cites] Mol Cell Biochem. 2001 Sep;225(1-):7-20 [11716366.001]
  • [Cites] Cell Calcium. 2001 Nov;30(5):343-50 [11733941.001]
  • [Cites] J Biol Chem. 2001 Dec 14;276(50):47266-76 [11579094.001]
  • [Cites] J Biol Chem. 2001 Dec 14;276(50):47608-14 [11606580.001]
  • [Cites] J Biol Chem. 2002 Feb 22;277(8):6504-10 [11724773.001]
  • [Cites] Chem Rec. 2001;1(3):195-211 [11895119.001]
  • [Cites] Biochem Pharmacol. 2002 Mar 15;63(6):1149-58 [11931848.001]
  • [Cites] Breast Cancer Res Treat. 2002 Feb;71(3):237-47 [12002342.001]
  • [Cites] Biochimie. 2002 Feb-Mar;84(2-3):195-201 [12022950.001]
  • [Cites] J Biol Chem. 2002 Aug 30;277(35):31381-9 [12077131.001]
  • [Cites] Cell Calcium. 2002 Oct;32(4):165-74 [12379176.001]
  • [Cites] Zhonghua Zhong Liu Za Zhi. 2002 Jul;24(4):370-4 [12408767.001]
  • [Cites] Nat Cell Biol. 2002 Nov;4(11):E263-72 [12415286.001]
  • [Cites] Biochim Biophys Acta. 2002 Nov 4;1600(1-2):51-60 [12445459.001]
  • [Cites] Exp Eye Res. 2002 Nov;75(5):583-90 [12457870.001]
  • [Cites] Leuk Res. 2003 Feb;27(2):125-31 [12526918.001]
  • [Cites] Brain Res Mol Brain Res. 2002 Dec 30;109(1-2):95-104 [12531519.001]
  • [Cites] Cell Calcium. 2002 Nov-Dec;32(5-6):413-20 [12543100.001]
  • [Cites] J Biol Chem. 2003 Mar 14;278(11):9100-6 [12509415.001]
  • [Cites] Biochem J. 2003 Nov 1;375(Pt 3):697-704 [12908873.001]
  • [Cites] Biochemistry. 1982 Aug 31;21(18):4511-6 [6215062.001]
  • [Cites] Cancer Res. 1984 Nov;44(11):5095-9 [6593116.001]
  • [Cites] J Biol Chem. 1985 Mar 25;260(6):3440-50 [3838314.001]
  • [Cites] Cell Calcium. 1986 Feb;7(1):1-12 [2420465.001]
  • [Cites] Arch Biochem Biophys. 1989 Feb 15;269(1):365-70 [2537063.001]
  • [Cites] Annu Rev Physiol. 1989;51:315-29 [2653185.001]
  • [Cites] Proc Natl Acad Sci U S A. 1990 Apr;87(7):2466-70 [2138778.001]
  • [Cites] Br J Cancer. 1991 Dec;64(6):1011-8 [1684906.001]
  • [Cites] Proc Natl Acad Sci U S A. 1994 Aug 2;91(16):7812-6 [7914372.001]
  • [Cites] Biochem Pharmacol. 1994 Aug 17;48(4):709-16 [8080443.001]
  • [Cites] Life Sci. 1994;55(16):313-9 [7934633.001]
  • [Cites] FASEB J. 1995 Feb;9(2):219-28 [7781924.001]
  • [Cites] Brain Res. 1995 Aug 14;689(1):141-6 [8528698.001]
  • [Cites] Cancer Res. 1998 Aug 15;58(16):3620-6 [9721870.001]
  • [Cites] Scanning Microsc. 1996;10(3):777-93; discussion 793-4 [9813639.001]
  • [Cites] Trends Pharmacol Sci. 1998 Dec;19(12):479-82 [9871407.001]
  • [Cites] Mech Ageing Dev. 1999 Mar 1;107(2):165-80 [10220045.001]
  • [Cites] J Exp Med. 1999 Jul 19;190(2):253-65 [10432288.001]
  • [Cites] Int J Cancer. 1999 Oct 8;83(2):151-6 [10471519.001]
  • [Cites] J Biol Chem. 2000 Feb 4;275(5):3403-11 [10652333.001]
  • [Cites] Cell Calcium. 1999 Jul-Aug;26(1-2):25-36 [10892568.001]
  • [Cites] J Biochem. 2000 Aug;128(2):329-36 [10920270.001]
  • [Cites] Mol Cell. 2000 Aug;6(2):421-31 [10983988.001]
  • [Cites] Endocrinology. 2000 Nov;141(11):4209-17 [11089555.001]
  • [Cites] Biosci Rep. 2000 Jun;20(3):129-38 [11095113.001]
  • [Cites] Am J Physiol Cell Physiol. 2001 Apr;280(4):C843-51 [11245601.001]
  • [Cites] Oncogene. 1996 Jun 6;12(11):2259-66 [8649765.001]
  • [Cites] Eur J Cancer. 1996 Jun;32A(6):1070-81 [8763349.001]
  • [Cites] J Clin Invest. 1997 Sep 1;100(5):1282-93 [9276747.001]
  • [Cites] J Biol Chem. 1997 Oct 3;272(40):25333-8 [9312152.001]
  • [Cites] Biochem J. 1998 Jan 15;329 ( Pt 2):349-57 [9425119.001]
  • [Cites] Am J Physiol. 1998 Jan;274(1 Pt 2):H123-31 [9458860.001]
  • [Cites] Nat Rev Mol Cell Biol. 2000 Oct;1(1):11-21 [11413485.001]
  • (PMID = 15066902.001).
  • [ISSN] 0007-1188
  • [Journal-full-title] British journal of pharmacology
  • [ISO-abbreviation] Br. J. Pharmacol.
  • [Language] ENG
  • [Grant] United States / NHLBI NIH HHS / HL / R15 HL071520; United States / NHLBI NIH HHS / HL / R15 HL 071520
  • [Publication-type] Journal Article; Research Support, U.S. Gov't, P.H.S.
  • [Publication-country] England
  • [Chemical-registry-number] P88XT4IS4D / Paclitaxel; SY7Q814VUP / Calcium
  • [Other-IDs] NLM/ PMC1574945
  •  go-up   go-down


2. Singh B, Cook KR, Vincent L, Hall CS, Berry JA, Multani AS, Lucci A: Cyclooxygenase-2 induces genomic instability, BCL2 expression, doxorubicin resistance, and altered cancer-initiating cell phenotype in MCF7 breast cancer cells. J Surg Res; 2008 Jun 15;147(2):240-6
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Cyclooxygenase-2 induces genomic instability, BCL2 expression, doxorubicin resistance, and altered cancer-initiating cell phenotype in MCF7 breast cancer cells.
  • INTRODUCTION: Cyclooxygenase (COX2) expression in primary breast cancer correlates with a worse prognosis.
  • We reported previously that COX2 expression in MCF10A breast epithelial cells of basal subtype induces genomic instability.
  • To understand the role of COX2 in estrogen receptor-positive (non-basal) breast cancer, we transfected the MCF7 cell line with COX2 and analyzed its chromosomal profile, BCL2 protein expression, and resistance to doxorubicin.
  • We also analyzed cell cultures grown as mammospheres to determine whether COX2 expression affects the cancer-initiating ("stem") cell phenotype in MCF7 cells.
  • Sensitivity of cells to drug treatment was analyzed by MTT assay.
  • CONCLUSIONS: We found that COX2 expression in MCF7 breast cancer cells induced genomic instability, BCL2 expression, and doxorubicin resistance, thus making them significantly more tumorigenic.
  • This data suggests that COX-2 may be an important target for breast cancer treatment.
  • [MeSH-major] Adenocarcinoma / enzymology. Breast Neoplasms / enzymology. Cell Transformation, Neoplastic. Cyclooxygenase 2 / metabolism. Genomic Instability / physiology
  • [MeSH-minor] Antibiotics, Antineoplastic / administration & dosage. Cell Culture Techniques. Cell Line, Tumor. Colony-Forming Units Assay. Cytogenetic Analysis. DNA, Complementary. Doxorubicin / administration & dosage. Drug Resistance, Neoplasm / physiology. Female. Humans. Phenotype. Proto-Oncogene Proteins c-bcl-2 / metabolism. Transfection

  • Genetic Alliance. consumer health - Breast Cancer.
  • MedlinePlus Health Information. consumer health - Breast Cancer.
  • Hazardous Substances Data Bank. DOXORUBICIN .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 18498876.001).
  • [ISSN] 0022-4804
  • [Journal-full-title] The Journal of surgical research
  • [ISO-abbreviation] J. Surg. Res.
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / CA16672; United States / NIDDK NIH HHS / DK / R21 DK067682
  • [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] 0 / Antibiotics, Antineoplastic; 0 / DNA, Complementary; 0 / Proto-Oncogene Proteins c-bcl-2; 80168379AG / Doxorubicin; EC 1.14.99.1 / Cyclooxygenase 2; EC 1.14.99.1 / PTGS2 protein, human
  •  go-up   go-down


3. Immonen E, Serpi R, Vähäkangas K, Myllynen P: Responses of PhIP (2-amino-1-methyl-6-phenylimidazo[4,5-b]pyridine) in MCF-7 cells are culture condition dependent. Chem Biol Interact; 2009 Nov 10;182(1):73-83
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • Effects of PhIP and estradiol on cell viability and proliferation were determined by ATP analysis and Ki-67 immunocytochemistry.
  • Expression of estrogen receptor alpha, cell stress markers (p53 and ERK) and estrogen responsive proteins (c-myc and ERK) were immunoblotted.
  • All concentrations of estradiol induced cell proliferation, viability and changes in protein expression, typical for estrogenic responses.
  • No changes in protein expressions by PhIP were noted, not even when switching cells from steroid-containing to -deprived medium which down-regulated the expression of proteins at basal level.
  • [MeSH-major] Carcinogens / pharmacology. Cell Culture Techniques / methods. Estrogen Receptor alpha / metabolism. Imidazoles / pharmacology
  • [MeSH-minor] Adenocarcinoma / metabolism. Adenocarcinoma / pathology. Adenosine Triphosphate / metabolism. Breast Neoplasms / metabolism. Breast Neoplasms / pathology. Cell Line, Tumor. Cell Survival / drug effects. Cell Survival / physiology. Dose-Response Relationship, Drug. Estradiol / pharmacology. Extracellular Signal-Regulated MAP Kinases / metabolism. Humans. Immunoblotting. Immunohistochemistry. Ki-67 Antigen / metabolism. Proto-Oncogene Proteins c-myc / metabolism. Tumor Suppressor Protein p53 / metabolism

  • Hazardous Substances Data Bank. 2-Amino-1-methyl-6-phenylimidazo[4,5-b]pyridine .
  • Hazardous Substances Data Bank. ESTRADIOL .
  • NCI CPTAC Assay Portal. NCI CPTAC Assay Portal .
  • NCI CPTAC Assay Portal. NCI CPTAC Assay Portal .
  • NCI CPTAC Assay Portal. NCI CPTAC Assay Portal .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 19647730.001).
  • [ISSN] 1872-7786
  • [Journal-full-title] Chemico-biological interactions
  • [ISO-abbreviation] Chem. Biol. Interact.
  • [Language] eng
  • [Publication-type] Comparative Study; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Ireland
  • [Chemical-registry-number] 0 / Carcinogens; 0 / Estrogen Receptor alpha; 0 / Imidazoles; 0 / Ki-67 Antigen; 0 / MYC protein, human; 0 / Proto-Oncogene Proteins c-myc; 0 / Tumor Suppressor Protein p53; 4TI98Z838E / Estradiol; 8L70Q75FXE / Adenosine Triphosphate; 909C6UN66T / 2-amino-1-methyl-6-phenylimidazo(4,5-b)pyridine; EC 2.7.11.24 / Extracellular Signal-Regulated MAP Kinases
  •  go-up   go-down


Advertisement
4. Landesman-Bollag E, Song DH, Romieu-Mourez R, Sussman DJ, Cardiff RD, Sonenshein GE, Seldin DC: Protein kinase CK2: signaling and tumorigenesis in the mammary gland. Mol Cell Biochem; 2001 Nov;227(1-2):153-65
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • Breast cancer is a major cause of cancer death in women, and the genetic abnormalities leading to the common sporadic forms of the disease are still under active investigation.
  • CK2 has been reported to be upregulated in human breast cancer, which these studies confirm; CK2 is also upregulated in rat carcinogen-induced breast tumors.
  • CK2 is known to phosphorylate IkappaB and thereby regulate basal NFkappaB levels; in the mammary cell lines and tumors, CK2 activity correlates with NFkappaB levels and inhibition of CK2 downregulates NFkappaB.
  • Thus, CK2 may promote breast cancer through dysregulation of key pathways of transcriptional control in the mammary epithelium, and inhibition of CK2 has a potential role in the treatment of breast and other cancers.
  • [MeSH-major] Breast Neoplasms / metabolism. Mammary Neoplasms, Animal / metabolism. Protein-Serine-Threonine Kinases / metabolism. Protein-Serine-Threonine Kinases / physiology. Zebrafish Proteins
  • [MeSH-minor] Adenocarcinoma / genetics. Adenocarcinoma / metabolism. Animals. Apigenin. Blotting, Western. Casein Kinase II. DNA, Complementary / metabolism. Dose-Response Relationship, Drug. Down-Regulation. Flavonoids / pharmacology. Gene Expression Regulation, Enzymologic. Gene Expression Regulation, Neoplastic. Genes, Reporter. Humans. Immunohistochemistry. Mice. Mice, Transgenic. NF-kappa B / genetics. NF-kappa B / metabolism. Neoplasms, Experimental. Phosphorylation. Precipitin Tests. Proto-Oncogene Proteins / metabolism. Proto-Oncogene Proteins c-myc / metabolism. Rats. Signal Transduction. Time Factors. Transcription, Genetic. Up-Regulation. Wnt Proteins

  • MedlinePlus Health Information. consumer health - Breast Cancer.
  • Gene Ontology. gene/protein/disease-specific - Gene Ontology annotations from this paper .
  • Hazardous Substances Data Bank. APIGENIN .
  • The Lens. Cited by Patents in .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [Cites] Mol Cell Biol. 1996 Mar;16(3):899-906 [8622692.001]
  • [Cites] J Biol Chem. 1997 Dec 19;272(51):32606-12 [9405476.001]
  • [Cites] Oncogene. 1997 Mar 13;14(10):1249-53 [9121776.001]
  • [Cites] Cell Growth Differ. 1997 Oct;8(10):1049-59 [9342183.001]
  • [Cites] Science. 1995 Feb 10;267(5199):894-7 [7846532.001]
  • [Cites] Cancer Res. 1994 May 15;54(10):2615-21 [8168088.001]
  • [Cites] Science. 1998 Sep 4;281(5382):1509-12 [9727977.001]
  • [Cites] Nat Genet. 1999 Sep;23(1):118-21 [10471512.001]
  • [Cites] EMBO J. 1996 Oct 1;15(19):5160-6 [8895560.001]
  • [Cites] Biochem Pharmacol. 1997 Jun 1;53(11):1649-57 [9264317.001]
  • [Cites] J Biol Chem. 1996 Jun 7;271(23 ):13868-74 [8662925.001]
  • [Cites] Cancer Res. 2001 May 1;61(9):3810-8 [11325857.001]
  • [Cites] Trends Genet. 1999 Jun;15(6):229-35 [10354583.001]
  • [Cites] FASEB J. 1995 Mar;9(5):313-23 [7896000.001]
  • [Cites] Cancer Res. 1996 Oct 1;56(19):4320-3 [8813115.001]
  • [Cites] J Exp Med. 1992 Sep 1;176(3):787-92 [1512542.001]
  • [Cites] Virchows Arch B Cell Pathol Incl Mol Pathol. 1992;62(6):365-70 [1360723.001]
  • [Cites] Proc Natl Acad Sci U S A. 1990 Jun;87(12):4727-31 [2191300.001]
  • [Cites] Carcinogenesis. 2000 May;21(5):871-9 [10783306.001]
  • [Cites] J Mammary Gland Biol Neoplasia. 1999 Jan;4(1):105-22 [10219910.001]
  • [Cites] Trends Cell Biol. 2000 Apr;10 (4):129-33 [10740266.001]
  • [Cites] Mol Cell Biol. 1997 Sep;17 (9):5386-99 [9271416.001]
  • [Cites] Toxicol Pathol. 1996 Nov-Dec;24(6):710-6 [8994298.001]
  • [Cites] Nature. 1961 Jan 21;189:204-7 [13716610.001]
  • [Cites] Mol Cell Biol. 1997 Jul;17(7):3629-39 [9199297.001]
  • [Cites] Mol Cell Biol. 1996 Apr;16(4):1401-9 [8657113.001]
  • [Cites] In Vitro. 1983 Jan;19(1):58-66 [6295922.001]
  • [Cites] Mol Cell Biol. 1996 Jul;16(7):3554-9 [8668171.001]
  • [Cites] Cell. 1988 Nov 18;55(4):619-25 [3180222.001]
  • [Cites] EMBO J. 1997 Jun 2;16(11):3089-96 [9214626.001]
  • [Cites] Oncogene. 1998 Jun 11;16(23):2965-74 [9662328.001]
  • [Cites] J Clin Invest. 1997 Dec 15;100(12):2952-60 [9399940.001]
  • [Cites] Exp Cell Res. 1997 Feb 25;231(1):163-72 [9056423.001]
  • [Cites] Prog Cell Cycle Res. 1997;3:77-97 [9552408.001]
  • [Cites] Am J Pathol. 1999 Jan;154(1):29-35 [9916915.001]
  • [Cites] J Mammary Gland Biol Neoplasia. 1996 Jan;1(1):61-73 [10887481.001]
  • [Cites] J Biol Chem. 1987 Jul 5;262(19):9136-40 [3474230.001]
  • [Cites] Eur J Biochem. 1990 Apr 30;189(2):251-7 [2159876.001]
  • [Cites] Cell. 1984 Oct;38(3):627-37 [6488314.001]
  • [Cites] Cell. 1987 May 22;49(4):465-75 [3032456.001]
  • [Cites] Eur J Biochem. 1999 Jan;259(1-2):253-61 [9914500.001]
  • [Cites] J Mol Biol. 2000 Apr 14;297(5):1245-58 [10764587.001]
  • [Cites] J Biol Chem. 2000 Jul 14;275(28):21278-86 [10801847.001]
  • (PMID = 11827167.001).
  • [ISSN] 0300-8177
  • [Journal-full-title] Molecular and cellular biochemistry
  • [ISO-abbreviation] Mol. Cell. Biochem.
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / R01 CA 82742; United States / NCI NIH HHS / CA / R01 CA63929
  • [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] Netherlands
  • [Chemical-registry-number] 0 / DNA, Complementary; 0 / Flavonoids; 0 / NF-kappa B; 0 / Proto-Oncogene Proteins; 0 / Proto-Oncogene Proteins c-myc; 0 / Wnt Proteins; 0 / Zebrafish Proteins; 7V515PI7F6 / Apigenin; EC 2.7.11.1 / Casein Kinase II; EC 2.7.11.1 / Protein-Serine-Threonine Kinases
  •  go-up   go-down


5. Darash-Yahana M, Pikarsky E, Abramovitch R, Zeira E, Pal B, Karplus R, Beider K, Avniel S, Kasem S, Galun E, Peled A: Role of high expression levels of CXCR4 in tumor growth, vascularization, and metastasis. FASEB J; 2004 Aug;18(11):1240-2
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • Positive staining for CXCL12, the ligand for CXCR4, was mainly present in the tumor-associated blood vessels and basal cell hyperplasia.
  • Similar effects of CXCR4 overexpression on tumor growth in vivo were also noted in two breast cancer lines, suggesting that the observed effect of CXCR4 is not unique to prostate tumor cells.
  • [MeSH-major] Adenocarcinoma / metabolism. Neoplasm Metastasis / genetics. Neoplasm Proteins / physiology. Neovascularization, Pathologic / genetics. Prostatic Neoplasms / metabolism. Receptors, CXCR4 / physiology
  • [MeSH-minor] Animals. Bone Marrow / pathology. Bone Neoplasms / secondary. Breast Neoplasms / pathology. Cell Adhesion / drug effects. Cell Line, Tumor / drug effects. Cell Line, Tumor / metabolism. Cell Line, Tumor / pathology. Cell Movement / drug effects. Chemokine CXCL12. Chemokines, CXC / analysis. Chemokines, CXC / pharmacology. Female. Humans. Hyperplasia. Lung Neoplasms / secondary. Lymphatic Metastasis. Magnetic Resonance Imaging. Male. Mice. Mice, Inbred NOD. Mice, SCID. Organ Specificity. Ovarian Neoplasms / pathology. Phenotype. Recombinant Fusion Proteins / physiology. Transplantation, Heterologous. Vascular Endothelial Growth Factor A / secretion

  • MedlinePlus Health Information. consumer health - Prostate Cancer.
  • The Lens. Cited by Patents in .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 15180966.001).
  • [ISSN] 1530-6860
  • [Journal-full-title] FASEB journal : official publication of the Federation of American Societies for Experimental Biology
  • [ISO-abbreviation] FASEB J.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / CXCL12 protein, human; 0 / Chemokine CXCL12; 0 / Chemokines, CXC; 0 / Cxcl12 protein, mouse; 0 / Neoplasm Proteins; 0 / Receptors, CXCR4; 0 / Recombinant Fusion Proteins; 0 / Vascular Endothelial Growth Factor A
  •  go-up   go-down


6. Newill H, Loske R, Wagner J, Johannes C, Lorenz RL, Lehmann L: Oxidation products of stigmasterol interfere with the action of the female sex hormone 17beta-estradiol in cultured human breast and endometrium cell lines. Mol Nutr Food Res; 2007 Jul;51(7):888-98
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Oxidation products of stigmasterol interfere with the action of the female sex hormone 17beta-estradiol in cultured human breast and endometrium cell lines.
  • Phytosterols are constituents of plant membranes and are thus contained in low concentrations in vegetable products as well as at high concentrations in functional food designed to reduce serum cholesterol levels.
  • Although oxyphytosterols have been detected in the serum of healthy human subjects, little is known of their biological activity.
  • Therefore, the estrogenic and antiestrogenic activities of a mixture of six oxidation products of stigmasterol (oxy-StOL) were determined at the following endpoints: (i) the affinity to isolated human estrogen receptors (ER), (ii) the basal and 17beta-estradiol (E2)-induced expression of the alkaline phosphatase (AlP) in human endometrial adenocarcinoma (Ishikawa) cells, and (iii) the basal and E2-induced proliferation of human breast adenocarcinoma (MCF-7) cells.
  • [MeSH-minor] Alkaline Phosphatase / genetics. Breast Neoplasms. Cell Division / drug effects. Cell Line, Tumor. Endometrial Neoplasms. Estrogen Receptor alpha / metabolism. Estrogen Receptor beta / metabolism. Female. Gene Expression / drug effects. Humans. Oxidation-Reduction. RNA, Messenger / analysis. Recombinant Proteins / metabolism

  • Hazardous Substances Data Bank. ESTRADIOL .
  • Hazardous Substances Data Bank. STIGMASTEROL .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 17579897.001).
  • [ISSN] 1613-4125
  • [Journal-full-title] Molecular nutrition & food research
  • [ISO-abbreviation] Mol Nutr Food Res
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Germany
  • [Chemical-registry-number] 0 / Estrogen Antagonists; 0 / Estrogen Receptor alpha; 0 / Estrogen Receptor beta; 0 / RNA, Messenger; 0 / Recombinant Proteins; 4TI98Z838E / Estradiol; 99WUK5D0Y8 / Stigmasterol; EC 3.1.3.1 / Alkaline Phosphatase
  •  go-up   go-down


7. Temple JL, Laing E, Sunder A, Wray S: Direct action of estradiol on gonadotropin-releasing hormone-1 neuronal activity via a transcription-dependent mechanism. J Neurosci; 2004 Jul 14;24(28):6326-33
PDF icon [Fulltext service] Download fulltext PDF of this article and others, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • Consistent with previous studies, TTX reduced the activity of individual GnRH-1 neurons to a basal level, while the population of cells maintained synchronized calcium oscillations.
  • Exposure of GnRH-1 cells to TTX plus E2 increased the number of calcium peaks/cell, percentage of cells with > or =10 peaks, mean peak amplitude, and percentage of cells that contributed to each calcium pulse in explants maintained in vitro for 7 d (7 div) compared with TTX alone.
  • [MeSH-major] Estradiol / analogs & derivatives. Estradiol / pharmacology. Gonadotropin-Releasing Hormone / secretion. Neurons / drug effects
  • [MeSH-minor] Adenocarcinoma / pathology. Animals. Breast Neoplasms / pathology. Calcium / analysis. Calcium Signaling. Estrogen Receptor Modulators / pharmacology. Estrogen Receptor beta / drug effects. Female. Fluorescent Dyes / analysis. Humans. Mice. Nasal Mucosa / cytology. Organ Culture Techniques. Organic Chemicals. Secretory Rate. Sodium Channel Blockers / pharmacology. Tetrodotoxin / pharmacology. Transcription, Genetic / drug effects

  • COS Scholar Universe. author profiles.
  • Hazardous Substances Data Bank. FULVESTRANT .
  • Hazardous Substances Data Bank. TETRODOTOXIN .
  • Hazardous Substances Data Bank. ESTRADIOL .
  • Hazardous Substances Data Bank. CALCIUM, ELEMENTAL .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 15254088.001).
  • [ISSN] 1529-2401
  • [Journal-full-title] The Journal of neuroscience : the official journal of the Society for Neuroscience
  • [ISO-abbreviation] J. Neurosci.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Estrogen Receptor Modulators; 0 / Estrogen Receptor beta; 0 / Fluorescent Dyes; 0 / Organic Chemicals; 0 / Sodium Channel Blockers; 138067-55-7 / calcium green; 22X328QOC4 / fulvestrant; 33515-09-2 / Gonadotropin-Releasing Hormone; 4368-28-9 / Tetrodotoxin; 4TI98Z838E / Estradiol; SY7Q814VUP / Calcium
  •  go-up   go-down


8. Tan KP, Kosuge K, Yang M, Ito S: NRF2 as a determinant of cellular resistance in retinoic acid cytotoxicity. Free Radic Biol Med; 2008 Dec 15;45(12):1663-73
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • Clinical use of retinoic acids (RA) is hindered by toxicity possibly related to oxidative stress.
  • Using in vitro cell and in vivo mouse models, we report that RA, specifically all-trans-RA (atRA) at concentrations implicated in toxicity, can activate NRF2 and induce NRF2 target genes, particularly the subunits of the rate-limiting enzyme of glutathione biosynthesis, glutamate cysteine ligase (GCLM/GCLC).
  • RNA interference-mediated silencing of NRF2, but not of retinoid X receptor-alpha and -beta, reduced basal and atRA-induced GCLM/GCLC gene expression.
  • 4-Hydroxynonenal, a lipid peroxidation product, was increased by RA.
  • Inhibition of MEK1/ERK mitogen-activated protein kinases significantly suppressed atRA-induced NRF2 activation and ARE-regulated gene expression, reducing cell resistance against toxic concentrations of RA.
  • [MeSH-major] Antineoplastic Agents / pharmacology. Apoptosis / drug effects. Gene Expression Regulation / drug effects. NF-E2-Related Factor 2 / metabolism. Tretinoin / pharmacology
  • [MeSH-minor] Adenocarcinoma / metabolism. Aldehydes / metabolism. Animals. Antioxidants / metabolism. Breast Neoplasms / metabolism. Carcinoma, Hepatocellular / metabolism. Cells, Cultured. Glutamate-Cysteine Ligase / genetics. Glutamate-Cysteine Ligase / metabolism. Humans. Kidney / cytology. Kidney / drug effects. Kidney / metabolism. Lipid Peroxidation. Liver Neoplasms / metabolism. MAP Kinase Kinase 1 / antagonists & inhibitors. MAP Kinase Kinase 1 / metabolism. Male. Mice. Mitochondria / drug effects. Mitochondria / metabolism. Mitogen-Activated Protein Kinase 1 / antagonists & inhibitors. Mitogen-Activated Protein Kinase 1 / metabolism. Mitogen-Activated Protein Kinase 3 / antagonists & inhibitors. Mitogen-Activated Protein Kinase 3 / metabolism. RNA, Small Interfering / pharmacology. Response Elements. Retinoid X Receptor alpha / metabolism. Retinoid X Receptor beta / metabolism

  • COS Scholar Universe. author profiles.
  • Hazardous Substances Data Bank. ALL-TRANS-RETINOIC ACID .
  • NCI CPTAC Assay Portal. NCI CPTAC Assay Portal .
  • NCI CPTAC Assay Portal. NCI CPTAC Assay Portal .
  • NCI CPTC Antibody Characterization Program. NCI CPTC Antibody Characterization Program .
  • NCI CPTC Antibody Characterization Program. NCI CPTC Antibody Characterization Program .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 18845239.001).
  • [ISSN] 0891-5849
  • [Journal-full-title] Free radical biology & medicine
  • [ISO-abbreviation] Free Radic. Biol. Med.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Aldehydes; 0 / Antineoplastic Agents; 0 / Antioxidants; 0 / NF-E2-Related Factor 2; 0 / RNA, Small Interfering; 0 / Retinoid X Receptor alpha; 0 / Retinoid X Receptor beta; 29343-52-0 / 4-hydroxy-2-nonenal; 5688UTC01R / Tretinoin; EC 2.7.1.- / MAP2K1 protein, human; EC 2.7.11.24 / Mitogen-Activated Protein Kinase 1; EC 2.7.11.24 / Mitogen-Activated Protein Kinase 3; EC 2.7.12.2 / MAP Kinase Kinase 1; EC 6.3.2.2 / Glutamate-Cysteine Ligase
  •  go-up   go-down


9. Wang-Rodriguez J, Dreilinger AD, Alsharabi GM, Rearden A: The signaling adapter protein PINCH is up-regulated in the stroma of common cancers, notably at invasive edges. Cancer; 2002 Sep 15;95(6):1387-95
PDF icon [Fulltext service] Download fulltext PDF of this article and others, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • Because no information is available regarding its expression in vivo in human tissues, this study evaluated the distribution and abundance of PINCH in patients with breast, prostate, lung, colon, and skin carcinomas.
  • METHODS: A polyclonal antibody was raised to a purified 6-histidine PINCH fusion protein and used to evaluate 74 cases comprising 33 breast carcinomas (21 ductal carcinomas, 6 lobular carcinomas, 4 ductal carcinomas in situ, 2 lobular carcinomas in situ), 22 prostate carcinomas, 5 colon carcinomas, 6 lung carcinomas (3 adenocarcinomas and 3 squamous carcinomas), and 8 skin carcinomas (4 basal cell carcinomas and 4 squamous cell carcinomas) by immunoperoxidase histochemistry of formalin-fixed, paraffin-embedded tissues.
  • Lysates of frozen tissue from the epithelium of two normal breasts and six breast carcinomas were evaluated by immunoblotting.
  • The most intense stromal immunostaining for PINCH was noted at invasive edges, particularly in breast carcinomatous tissue.
  • Immunoblotting of lysates from normal breast and breast carcinomatous tissue confirmed that PINCH protein expression was markedly increased in breast carcinomatous tissues.
  • Because of this and because PINCH functions as a "molecular switch" in signal transduction, PINCH may be a new target for drug discovery aimed at the tumor-associated stroma.
  • [MeSH-major] DNA-Binding Proteins / metabolism. Neoplasms / metabolism
  • [MeSH-minor] Adaptor Proteins, Signal Transducing. Adenocarcinoma / metabolism. Breast Neoplasms / metabolism. Carcinoma in Situ / metabolism. Carcinoma, Basal Cell / metabolism. Carcinoma, Ductal, Breast / metabolism. Carcinoma, Lobular / metabolism. Carcinoma, Squamous Cell / metabolism. Colonic Neoplasms / metabolism. Female. Humans. Immunoblotting. Immunohistochemistry. LIM Domain Proteins. Lung Neoplasms / metabolism. Male. Membrane Proteins. Neoplasm Invasiveness. Paraffin Embedding. Prostatic Neoplasms / metabolism. Skin Neoplasms / metabolism. Tissue Distribution. Up-Regulation

  • The Lens. Cited by Patents in .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [Copyright] Copyright 2002 American Cancer Society.
  • (PMID = 12216108.001).
  • [ISSN] 0008-543X
  • [Journal-full-title] Cancer
  • [ISO-abbreviation] Cancer
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Adaptor Proteins, Signal Transducing; 0 / DNA-Binding Proteins; 0 / LIM Domain Proteins; 0 / LIMS1 protein, human; 0 / Membrane Proteins
  •  go-up   go-down


10. Graziani G, Tentori L, Muzi A, Vergati M, Tringali G, Pozzoli G, Navarra P: Evidence that corticotropin-releasing hormone inhibits cell growth of human breast cancer cells via the activation of CRH-R1 receptor subtype. Mol Cell Endocrinol; 2007 Jan 29;264(1-2):44-9
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Evidence that corticotropin-releasing hormone inhibits cell growth of human breast cancer cells via the activation of CRH-R1 receptor subtype.
  • It has been previously shown that corticotropin-releasing hormone (CRH) exerts antiproliferative activity on an estrogen-dependent tumor cell line, i.e. human endometrial adenocarcinoma Ishikawa (IK) cells.
  • Here we have investigated the effects of CRH on another estrogen-dependent tumor cell line, human breast cancer MCF7 cells.
  • In this paradigm, CRH given at a fixed concentration of 100 nM significantly inhibited cell growth induced by 100 nM estradiol (E2) after 48 and 72 h of incubation.
  • CRH inhibition of cell proliferation was counteracted in a concentration-dependent manner by the non-selective CRH receptor antagonist, astressin, as well as by a CRH-R1 selective receptor antagonist, antalarmin.
  • RNase protection assays carried out on MCF7 under basal conditions showed that these cells express in a constitutive manner the CRH-R1 receptor subtype.
  • We have also investigated the putative source of CRH acting on breast cancer cells; we found that MCF7 cells express CRH mRNA under basal conditions and secrete sizable amounts of immunoreactive CRH, which leads to postulate the existence of paracrine-autocrine inhibitory mechanism operated by CRH in breast cancer cells.
  • [MeSH-major] Autocrine Communication / drug effects. Cell Proliferation / drug effects. Corticotropin-Releasing Hormone / pharmacology. Hormones / pharmacology. Paracrine Communication / drug effects. Receptors, Corticotropin-Releasing Hormone / agonists
  • [MeSH-minor] Breast Neoplasms. Cell Line, Tumor. Dose-Response Relationship, Drug. Estradiol / pharmacology. Female. Humans. Pyrimidines / pharmacology. Pyrroles / pharmacology

  • Genetic Alliance. consumer health - Breast Cancer.
  • MedlinePlus Health Information. consumer health - Hormones.
  • Hazardous Substances Data Bank. ESTRADIOL .
  • The Lens. Cited by Patents in .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 17097220.001).
  • [ISSN] 0303-7207
  • [Journal-full-title] Molecular and cellular endocrinology
  • [ISO-abbreviation] Mol. Cell. Endocrinol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Ireland
  • [Chemical-registry-number] 0 / CRF receptor type 1; 0 / Hormones; 0 / Pyrimidines; 0 / Pyrroles; 0 / Receptors, Corticotropin-Releasing Hormone; 0 / antalarmin; 4TI98Z838E / Estradiol; 9015-71-8 / Corticotropin-Releasing Hormone
  •  go-up   go-down


11. Sengupta K, Banerjee S, Saxena N, Banerjee SK: Estradiol-induced vascular endothelial growth factor-A expression in breast tumor cells is biphasic and regulated by estrogen receptor-alpha dependent pathway. Int J Oncol; 2003 Mar;22(3):609-14
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Estradiol-induced vascular endothelial growth factor-A expression in breast tumor cells is biphasic and regulated by estrogen receptor-alpha dependent pathway.
  • We have identified two phases of activation of VEGF-A mRNA transcription, one early and one late response, induced by 17beta-estradiol (17beta-E2) in ER+ MCF-7 breast tumor cells, depending upon the length of exposure.
  • In contrast VEGF-A mRNA expression was back at basal level in MCF-7 cells exposed to 17beta-E2 for 6 h.
  • However, expression levels were again significantly augmented after 24 h of exposure, and this induction was unaltered by cycloheximide indicating that de novo protein synthesis was not required and like early response, it was a direct effect of estrogen.
  • [MeSH-major] Breast Neoplasms / metabolism. Estradiol / analogs & derivatives. Estradiol / pharmacology. Gene Expression Regulation, Neoplastic / drug effects. Neoplasm Proteins / physiology. Neoplasms, Hormone-Dependent / metabolism. Receptors, Estrogen / physiology. Vascular Endothelial Growth Factor A / biosynthesis
  • [MeSH-minor] Adenocarcinoma / genetics. Adenocarcinoma / metabolism. Adenocarcinoma / pathology. Cell Line, Tumor / drug effects. Cell Line, Tumor / metabolism. Cycloheximide / pharmacology. Estrogen Antagonists / pharmacology. Estrogen Receptor alpha. Female. Humans. Protein Synthesis Inhibitors / pharmacology. RNA, Messenger / biosynthesis. RNA, Messenger / genetics. RNA, Neoplasm / biosynthesis. RNA, Neoplasm / genetics. Transfection

  • MedlinePlus Health Information. consumer health - Breast Cancer.
  • COS Scholar Universe. author profiles.
  • Hazardous Substances Data Bank. FULVESTRANT .
  • Hazardous Substances Data Bank. ESTRADIOL .
  • Hazardous Substances Data Bank. CYCLOHEXIMIDE .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 12579315.001).
  • [ISSN] 1019-6439
  • [Journal-full-title] International journal of oncology
  • [ISO-abbreviation] Int. J. Oncol.
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / CA87680
  • [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] Greece
  • [Chemical-registry-number] 0 / Estrogen Antagonists; 0 / Estrogen Receptor alpha; 0 / Neoplasm Proteins; 0 / Protein Synthesis Inhibitors; 0 / RNA, Messenger; 0 / RNA, Neoplasm; 0 / Receptors, Estrogen; 0 / Vascular Endothelial Growth Factor A; 22X328QOC4 / fulvestrant; 4TI98Z838E / Estradiol; 98600C0908 / Cycloheximide
  •  go-up   go-down


12. Johansen P, Berg K, Selbo PK, Hofbauer GF: [Photochemical internalisation (PCI): a further development of photodynamic therapy for the treatment of skin cancer]. Praxis (Bern 1994); 2010 Nov 17;99(23):1423-8
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • Topical creams using the immune modulator imiquimod or the COX inhibitor diclofenac (with hyaluronic acid) are now registered for use against neoplasms such as basal or squamous cell carcinoma.
  • A refined version of PDT, namely photochemical internalisation, is currently subject to a first clinical trial in patients with osteosarcoma, squamous cell carcinoma, head and neck cancer as well as adenocarcinoma of the breast.
  • [MeSH-major] Carcinoma, Basal Cell / drug therapy. Carcinoma, Squamous Cell / drug therapy. Melanoma / drug therapy. Photochemotherapy / methods. Skin Neoplasms / drug therapy
  • [MeSH-minor] Animals. Antineoplastic Agents / pharmacokinetics. Antineoplastic Agents / therapeutic use. Cytosol / drug effects. Endocytosis. Endosomes / drug effects. Humans. Melanoma, Experimental / drug therapy. Mice. Neoplasm Transplantation


13. Yen L, You XL, Al Moustafa AE, Batist G, Hynes NE, Mader S, Meloche S, Alaoui-Jamali MA: Heregulin selectively upregulates vascular endothelial growth factor secretion in cancer cells and stimulates angiogenesis. Oncogene; 2000 Jul 20;19(31):3460-9
PDF icon [Fulltext service] Download fulltext PDF of this article and others, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • We report the effect of heregulin beta1, the ligand for erbB-3 and erbB-4 receptors, on the regulation of vascular endothelial growth factor (VEGF) expression, using a panel of breast and lung cancer cell lines with constitutive erbB-2 overexpression or engineered to stably overexpress the erbB-2 receptor.
  • We demonstrate that heregulin beta1 induces VEGF secretion in most cancer cell lines, while no significant effect was observed in normal human mammary and bronchial primary cells.
  • Overexpression of erbB-2 receptor results in induction of the basal level of VEGF and exposure to heregulin further enhances VEGF secretion.
  • In contrast, VEGF induction is significantly decreased in a T47D cell line where erbB-2 is functionally inactivated.
  • Conditioned media from heregulin-treated cancer cells, but not from normal cells, stimulates endothelial cell proliferation; this paracrine stimulation is inhibited by co-exposure to a specific VEGF neutralizing antibody.
  • [MeSH-major] Endothelial Growth Factors / secretion. Lymphokines / secretion. Neoplasm Proteins / physiology. Neovascularization, Pathologic. Neuregulin-1 / physiology. Receptor, Epidermal Growth Factor / physiology. Receptor, ErbB-2 / physiology. Receptor, ErbB-3 / physiology
  • [MeSH-minor] Adenocarcinoma / pathology. Animals. Breast / cytology. Breast Neoplasms / pathology. Bronchi / cytology. Carcinoma, Non-Small-Cell Lung / pathology. Cell Division. Cells, Cultured / drug effects. Chick Embryo. Culture Media, Conditioned / pharmacology. Female. Genes, erbB-2. Humans. Lung Neoplasms / pathology. Neovascularization, Physiologic. Phosphorylation. Protein Processing, Post-Translational. RNA, Messenger / biosynthesis. RNA, Neoplasm / biosynthesis. Receptor, ErbB-4. Recombinant Fusion Proteins / physiology. Transfection. Tumor Cells, Cultured / drug effects. Tumor Cells, Cultured / secretion. Umbilical Veins / cytology. Vascular Endothelial Growth Factor A. Vascular Endothelial Growth Factors

  • ClinicalTrials.gov. clinical trials - ClinicalTrials.gov .
  • NCI CPTAC Assay Portal. NCI CPTAC Assay Portal .
  • NCI CPTC Antibody Characterization Program. NCI CPTC Antibody Characterization Program .
  • NCI CPTC Antibody Characterization Program. NCI CPTC Antibody Characterization Program .
  • The Lens. Cited by Patents in .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 10918604.001).
  • [ISSN] 0950-9232
  • [Journal-full-title] Oncogene
  • [ISO-abbreviation] Oncogene
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] ENGLAND
  • [Chemical-registry-number] 0 / Culture Media, Conditioned; 0 / Endothelial Growth Factors; 0 / Lymphokines; 0 / Neoplasm Proteins; 0 / Neuregulin-1; 0 / RNA, Messenger; 0 / RNA, Neoplasm; 0 / Recombinant Fusion Proteins; 0 / Vascular Endothelial Growth Factor A; 0 / Vascular Endothelial Growth Factors; EC 2.7.10.1 / ERBB4 protein, human; EC 2.7.10.1 / Receptor, Epidermal Growth Factor; EC 2.7.10.1 / Receptor, ErbB-2; EC 2.7.10.1 / Receptor, ErbB-3; EC 2.7.10.1 / Receptor, ErbB-4
  •  go-up   go-down


14. Wu XM, Liu X, Bu YQ, Sengupta J, Cui HJ, Yi FP, Liu T, Yuan CF, Shi YY, Song FZ: RNAi-mediated silencing of the Bmi-1 gene causes growth inhibition and enhances doxorubicin-induced apoptosis in MCF-7 cells. Genet Mol Biol; 2009 Oct;32(4):697-703
PDF icon [Fulltext service] Download fulltext PDF of this article and others, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • Its expression is found to be greatly increased in a number of malignant tumors including breast cancer.
  • In this study, RNAi was introduced to down-regulate the expression of Bmi-1 in a highly malignant breast adenocarcinoma cell line, MCF-7.
  • A thorough study of the biological behavior and chemosensitivity changes of the MCF-7 cells was carried out in context to the therapeutic potential of Bmi-1.
  • The number of target cells was found to increase in phase G (0) /G (1) and decrease in the S phase, but no increase in the basal level of apoptosis was noticed.
  • Silencing of Bmi-1 made the MCF-7 cells more sensitive to the chemotherapeutic agent doxorubicin and induced a significantly higher percentage of apoptotic cells.
  • Here, we report on a study regarding the RNAi-mediated silencing of the Bmi-1 gene in breast cancer.

  • NCI CPTC Antibody Characterization Program. NCI CPTC Antibody Characterization Program .
  • NCI CPTC Antibody Characterization Program. NCI CPTC Antibody Characterization Program .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [Cites] Nat Rev Mol Cell Biol. 2001 Oct;2(10):731-7 [11584300.001]
  • [Cites] Br J Cancer. 2001 May 18;84(10):1372-6 [11355949.001]
  • [Cites] Nature. 2003 May 15;423(6937):255-60 [12714970.001]
  • [Cites] Nature. 2003 May 15;423(6937):302-5 [12714971.001]
  • [Cites] Cancer Lett. 2004 Jan 20;203(2):217-24 [14732230.001]
  • [Cites] Cell. 2004 Aug 20;118(4):409-18 [15315754.001]
  • [Cites] Breast. 2004 Oct;13(5):383-8 [15454193.001]
  • [Cites] Cancer Cell. 2005 Jun;7(6):505-12 [15950900.001]
  • [Cites] Genes Dev. 2005 Jun 15;19(12):1432-7 [15964994.001]
  • [Cites] Breast Cancer Res. 2005;7(3):86-95 [15987436.001]
  • [Cites] Chin Med J (Engl). 2005 Aug 20;118(16):1346-50 [16157028.001]
  • [Cites] Oncogene. 2006 Jul 20;25(31):4370-5 [16501599.001]
  • [Cites] Cancer Res. 2006 Jun 15;66(12):6063-71 [16778178.001]
  • [Cites] Cancer Res. 2006 Jun 15;66(12):6225-32 [16778197.001]
  • [Cites] J Biol Chem. 2006 Nov 10;281(45):34696-704 [16982619.001]
  • [Cites] Br J Cancer. 2007 Jan 15;96(1):126-33 [17179983.001]
  • [Cites] Am J Pathol. 2007 Apr;170(4):1370-8 [17392175.001]
  • [Cites] Breast Cancer Res. 2007;9(4):R55 [17711569.001]
  • [Cites] Oligonucleotides. 2007 Fall;17(3):327-35 [17854272.001]
  • [Cites] Biochem Biophys Res Commun. 2008 Jul 4;371(3):531-5 [18452707.001]
  • [Cites] Cell. 1991 May 31;65(5):737-52 [1904008.001]
  • [Cites] Oncogene. 1993 Nov;8(11):3161-4 [8414519.001]
  • [Cites] Nature. 1999 Jan 14;397(6715):164-8 [9923679.001]
  • [Cites] Mol Cell Biol. 2000 Jan;20(1):273-85 [10594030.001]
  • [Cites] Cancer Res. 2002 Aug 15;62(16):4736-45 [12183433.001]
  • (PMID = 21637439.001).
  • [ISSN] 1678-4685
  • [Journal-full-title] Genetics and molecular biology
  • [ISO-abbreviation] Genet. Mol. Biol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Brazil
  • [Other-IDs] NLM/ PMC3036904
  • [Keywords] NOTNLM ; Bmi-1 / RNA interference / breast cancer / doxorubicin / retrovirus vector
  •  go-up   go-down


15. Müller I, Wischnewski F, Pantel K, Schwarzenbach H: Promoter- and cell-specific epigenetic regulation of CD44, Cyclin D2, GLIPR1 and PTEN by methyl-CpG binding proteins and histone modifications. BMC Cancer; 2010;10:297
PDF icon [Fulltext service] Download fulltext PDF of this article and others, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Promoter- and cell-specific epigenetic regulation of CD44, Cyclin D2, GLIPR1 and PTEN by methyl-CpG binding proteins and histone modifications.
  • BACKGROUND: The aim of the current study was to analyze the involvement of methyl-CpG binding proteins (MBDs) and histone modifications on the regulation of CD44, Cyclin D2, GLIPR1 and PTEN in different cellular contexts such as the prostate cancer cells DU145 and LNCaP, and the breast cancer cells MCF-7.
  • METHODS: In DU145, LNCaP and MCF-7 cells mRNA expression levels of CD44, Cyclin D2, GLIPR1 and PTEN were determined by quantitative RT-PCR at the basal status as well as after treatment with demethylating agent 5-aza-2'-deoxycytidine and/or histone deacetylase inhibitor Trichostatin A.
  • RESULTS: Comparison of the different promoters showed that MeCP2 and MBD2a repressed promoter-specifically Cyclin D2 in all cell lines, whereas in MCF-7 cells MeCP2 repressed cell-specifically all methylated promoters.
  • Treatment of the cells by the demethylating agent 5-aza-2'-deoxycytidine (5-aza-CdR) caused dissociation of the MBDs from the promoters.
  • [MeSH-major] Antigens, CD44 / genetics. Cyclin D2 / genetics. Gene Expression Regulation, Neoplastic. Histones / metabolism. Methyl-CpG-Binding Protein 2 / metabolism. Neoplasm Proteins / genetics. Nerve Tissue Proteins / genetics. PTEN Phosphohydrolase / genetics. Promoter Regions, Genetic / genetics
  • [MeSH-minor] Adenocarcinoma / genetics. Adenocarcinoma / pathology. Breast Neoplasms / genetics. Breast Neoplasms / pathology. Chromatin / genetics. Chromatin Immunoprecipitation. CpG Islands. DNA Methylation / drug effects. Enzyme Inhibitors / pharmacology. Epigenesis, Genetic. Female. Gene Silencing. Humans. Male. Prostatic Neoplasms / genetics. Prostatic Neoplasms / pathology. RNA, Messenger / genetics. Reverse Transcriptase Polymerase Chain Reaction. Tumor Cells, Cultured

  • NCI CPTAC Assay Portal. NCI CPTAC Assay Portal .
  • NCI CPTC Antibody Characterization Program. NCI CPTC Antibody Characterization Program .
  • NCI CPTC Antibody Characterization Program. NCI CPTC Antibody Characterization Program .
  • NCI CPTC Antibody Characterization Program. NCI CPTC Antibody Characterization Program .
  • NCI CPTC Antibody Characterization Program. NCI CPTC Antibody Characterization Program .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [Cites] Nature. 2000 Jan 6;403(6765):41-5 [10638745.001]
  • [Cites] Oncogene. 2010 Jan 14;29(2):305-12 [19881542.001]
  • [Cites] Prostate. 2001 Oct 1;49(2):110-5 [11582589.001]
  • [Cites] Nucleic Acids Res. 2001 Nov 1;29(21):4493-501 [11691937.001]
  • [Cites] Nucleic Acids Res. 2001 Nov 15;29(22):4598-606 [11713309.001]
  • [Cites] J Pathol. 2002 Jan;196(1):1-7 [11748635.001]
  • [Cites] Mol Cell Biol. 2002 Mar;22(6):1844-57 [11865062.001]
  • [Cites] Brain Tumor Pathol. 2001;18(2):109-14 [11908866.001]
  • [Cites] Int J Biochem Cell Biol. 2002 Jul;34(7):718-21 [11950588.001]
  • [Cites] Mol Cell Biol. 2003 Apr;23(8):2645-57 [12665568.001]
  • [Cites] Proc Natl Acad Sci U S A. 2003 Apr 1;100(7):3983-8 [12629218.001]
  • [Cites] Trends Genet. 2003 May;19(5):269-77 [12711219.001]
  • [Cites] EMBO J. 2003 Dec 1;22(23):6335-45 [14633992.001]
  • [Cites] Cancer Res. 2004 Feb 1;64(3):969-76 [14871827.001]
  • [Cites] Mol Cell Biol. 2004 Apr;24(8):3387-95 [15060159.001]
  • [Cites] Nat Rev Cancer. 2004 Jun;4(6):448-56 [15170447.001]
  • [Cites] FEBS Lett. 2004 Jul 16;570(1-3):37-40 [15251435.001]
  • [Cites] Gene. 1996 Nov 21;180(1-2):125-30 [8973356.001]
  • [Cites] Mol Cell Biol. 1998 Nov;18(11):6538-47 [9774669.001]
  • [Cites] Nat Genet. 1999 Sep;23(1):58-61 [10471499.001]
  • [Cites] Mol Cell Biol. 2005 Jun;25(11):4388-96 [15899845.001]
  • [Cites] Oncogene. 2005 Nov 14;24(50):7465-74 [16288293.001]
  • [Cites] Trends Biochem Sci. 2006 Feb;31(2):89-97 [16403636.001]
  • [Cites] Cancer Res. 2006 Apr 15;66(8):4139-48 [16618735.001]
  • [Cites] Genome Res. 2006 Jul;16(7):890-900 [16751344.001]
  • [Cites] Cancer Res. 2006 Sep 1;66(17):8342-6 [16951140.001]
  • [Cites] J Mol Med (Berl). 2006 Nov;84(11):911-8 [17016690.001]
  • [Cites] Cancer Res. 2006 Nov 1;66(21):10233-7 [17079438.001]
  • [Cites] Oncogene. 2007 Feb 26;26(9):1338-45 [17322919.001]
  • [Cites] Stem Cells. 2007 Apr;25(4):1037-46 [17272500.001]
  • [Cites] Life Sci. 2007 Apr 24;80(20):1873-81 [17383681.001]
  • [Cites] Cell. 2007 May 18;129(4):823-37 [17512414.001]
  • [Cites] Carcinogenesis. 2007 Jul;28(7):1379-86 [17341655.001]
  • [Cites] Mol Cancer Res. 2007 Jul;5(7):749-59 [17634428.001]
  • [Cites] Int J Oncol. 2007 Nov;31(5):1119-26 [17912438.001]
  • [Cites] Int J Biochem Cell Biol. 2008;40(9):1944-55 [18373939.001]
  • [Cites] Breast Cancer Res Treat. 2008 Sep;111(1):15-25 [17891453.001]
  • [Cites] Med Res Rev. 2008 Sep;28(5):645-87 [18271058.001]
  • [Cites] Curr Opin Oncol. 2008 Nov;20(6):705-10 [18841054.001]
  • [Cites] Lab Invest. 2000 Aug;80(8):1291-8 [10950120.001]
  • (PMID = 20565761.001).
  • [ISSN] 1471-2407
  • [Journal-full-title] BMC cancer
  • [ISO-abbreviation] BMC Cancer
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Antigens, CD44; 0 / CCND2 protein, human; 0 / CD44 protein, human; 0 / Chromatin; 0 / Cyclin D2; 0 / Enzyme Inhibitors; 0 / GLIPR1 protein, human; 0 / Histones; 0 / Methyl-CpG-Binding Protein 2; 0 / Neoplasm Proteins; 0 / Nerve Tissue Proteins; 0 / RNA, Messenger; EC 3.1.3.48 / PTEN protein, human; EC 3.1.3.67 / PTEN Phosphohydrolase
  • [Other-IDs] NLM/ PMC2912262
  •  go-up   go-down


16. Roy JW, Cowley EA, Blay J, Linsdell P: The intermediate conductance Ca2+-activated K+ channel inhibitor TRAM-34 stimulates proliferation of breast cancer cells via activation of oestrogen receptors. Br J Pharmacol; 2010 Feb 1;159(3):650-8
PDF icon [Fulltext service] Download fulltext PDF of this article and others, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] The intermediate conductance Ca2+-activated K+ channel inhibitor TRAM-34 stimulates proliferation of breast cancer cells via activation of oestrogen receptors.
  • We have investigated the effects of specific K(+) channel inhibitors on basal and oestrogen-stimulated proliferation of breast cancer cells.
  • EXPERIMENTAL APPROACH: Using the mammary adenocarcinoma cell line MCF-7 we assayed cell proliferation by radiolabelled thymidine incorporation in the absence or presence of various K(+) channel inhibitors with or without 17beta-oestradiol.
  • KEY RESULTS: Inhibitors of K(v)10.1 and K(Ca)3.1 K(+) channels suppressed basal proliferation of MCF-7 cells, but not oestrogen-stimulated proliferation.
  • TRAM-34, a specific inhibitor of K(Ca)3.1 channels increased or decreased cell proliferation depending on the concentration.
  • At intermediate concentrations (3-10 microM) TRAM-34 increased cell proliferation, whereas at higher concentrations (20-100 microM) TRAM-34 decreased cell proliferation.
  • The enhancement of cell proliferation caused by TRAM-34 was blocked by the oestrogen receptor antagonists ICI182,780 and tamoxifen.
  • CONCLUSIONS AND IMPLICATIONS: Our results demonstrate that K(+) channels K(v)10.1 and K(Ca)3.1 play a role in basal, but not oestrogen-stimulated MCF-7 cell proliferation.
  • TRAM-34, as well as inhibiting K(Ca)3.1, directly interacts with the oestrogen receptor and mimics the effects of 17beta-oestradiol on MCF-7 cell proliferation and gene modulation.
  • [MeSH-major] Breast Neoplasms / drug therapy. Breast Neoplasms / metabolism. Estradiol / pharmacology. Potassium Channels, Calcium-Activated. Tamoxifen / pharmacology
  • [MeSH-minor] Calcium / metabolism. Calcium / pharmacology. Calcium / therapeutic use. Cell Line, Tumor. Cells / metabolism. Cells / pathology. Cellular Structures / metabolism. Cellular Structures / pathology. Estrogen Receptor alpha / metabolism. Estrogens / metabolism. Estrogens / pharmacology. Estrogens / therapeutic use. Female. Gene Expression / drug effects. Humans. Ion Transport / drug effects. Pyrazoles. RNA, Messenger / metabolism. RNA, Messenger / pharmacology. Receptors, Estrogen / metabolism. Receptors, Progesterone / metabolism

  • Genetic Alliance. consumer health - Breast Cancer.
  • MedlinePlus Health Information. consumer health - Breast Cancer.
  • COS Scholar Universe. author profiles.
  • Hazardous Substances Data Bank. TAMOXIFEN .
  • Hazardous Substances Data Bank. ESTRADIOL .
  • Hazardous Substances Data Bank. CALCIUM, ELEMENTAL .
  • NCI CPTAC Assay Portal. NCI CPTAC Assay Portal .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [Cites] Proc Natl Acad Sci U S A. 2000 Jul 5;97(14):8151-6 [10884437.001]
  • [Cites] Oncogene. 2009 Apr 16;28(15):1792-806 [19270724.001]
  • [Cites] Receptors Channels. 2001;7(5):345-56 [11697078.001]
  • [Cites] Endocr Relat Cancer. 2003 Jun;10(2):179-86 [12790780.001]
  • [Cites] Mol Pharmacol. 2004 Mar;65(3):630-8 [14978241.001]
  • [Cites] Biochem Biophys Res Commun. 2004 Mar 26;316(1):244-51 [15003537.001]
  • [Cites] Pflugers Arch. 2004 Jun;448(3):274-86 [15048575.001]
  • [Cites] Am J Physiol Cell Physiol. 2004 Jul;287(1):C125-34 [14985237.001]
  • [Cites] Steroids. 2004 Jun;69(6):401-18 [15219790.001]
  • [Cites] Cancer Res. 2004 Oct 1;64(19):6996-7001 [15466192.001]
  • [Cites] J Biol Chem. 1973 Sep 10;248(17):6251-3 [4353636.001]
  • [Cites] Endocrinology. 1989 May;124(5):2577-83 [2651098.001]
  • [Cites] Proc Natl Acad Sci U S A. 1996 Jun 11;93(12):5925-30 [8650195.001]
  • [Cites] J Membr Biol. 1996 Nov;154(2):91-107 [8929284.001]
  • [Cites] Toxicol Appl Pharmacol. 1997 Jun;144(2):363-76 [9194421.001]
  • [Cites] J Membr Biol. 1999 Sep 15;171(2):107-15 [10489423.001]
  • [Cites] Arterioscler Thromb Vasc Biol. 2005 Apr;25(4):704-9 [15662023.001]
  • [Cites] FEBS Lett. 2005 Jun 6;579(14):2995-3000 [15893312.001]
  • [Cites] Eur Biophys J. 2005 Aug;34(6):515-29 [16184309.001]
  • [Cites] J Membr Biol. 2005 Jun;205(3):115-24 [16362499.001]
  • [Cites] J Membr Biol. 2005 Jun;205(3):159-73 [16362504.001]
  • [Cites] J Membr Biol. 2005 Jun;205(3):175-84 [16362505.001]
  • [Cites] J Biol Chem. 2006 May 12;281(19):13030-7 [16537547.001]
  • [Cites] FEBS Lett. 2006 May 22;580(12):2850-2 [16783874.001]
  • [Cites] Cancer Detect Prev. 2006;30(4):375-85 [16971052.001]
  • [Cites] Pflugers Arch. 2006 Nov;453(2):167-76 [17047984.001]
  • [Cites] Curr Med Chem. 2007;14(13):1437-57 [17584055.001]
  • [Cites] J Cell Physiol. 2007 Sep;212(3):690-701 [17520698.001]
  • [Cites] Oncogene. 2007 Aug 2;26(35):5107-14 [17310992.001]
  • [Cites] Pflugers Arch. 2007 Sep;454(6):945-56 [17429684.001]
  • [Cites] Am J Physiol Cell Physiol. 2007 Sep;293(3):C1010-9 [17596298.001]
  • [Cites] J Membr Biol. 2008 Jan;221(1):1-6 [18060344.001]
  • [Cites] Br J Pharmacol. 2008 Mar;153 Suppl 2:S1-209 [18347570.001]
  • [Cites] Expert Rev Mol Diagn. 2008 Mar;8(2):179-87 [18366304.001]
  • [Cites] Oncol Rep. 2008 Jun;19(6):1511-6 [18497958.001]
  • [Cites] J Clin Invest. 2008 Sep;118(9):3025-37 [18688283.001]
  • [Cites] J Biol Chem. 2000 Nov 24;275(47):37137-49 [10961988.001]
  • (PMID = 20050851.001).
  • [ISSN] 1476-5381
  • [Journal-full-title] British journal of pharmacology
  • [ISO-abbreviation] Br. J. Pharmacol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Estrogen Receptor alpha; 0 / Estrogens; 0 / Potassium Channels, Calcium-Activated; 0 / Pyrazoles; 0 / RNA, Messenger; 0 / Receptors, Estrogen; 0 / Receptors, Progesterone; 0 / TRAM 34; 0 / estrogen receptor alpha, human; 094ZI81Y45 / Tamoxifen; 4TI98Z838E / Estradiol; SY7Q814VUP / Calcium
  • [Other-IDs] NLM/ PMC2828028
  •  go-up   go-down


17. Catino A, Crucitta E, Latorre A, Sambiasi D, Calabrese P, Lorusso V: Amifostine as chemoprotectant in metastatic breast cancer patients treated with doxorubicin. Oncol Rep; 2003 Jan-Feb;10(1):163-7
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Amifostine as chemoprotectant in metastatic breast cancer patients treated with doxorubicin.
  • Amifostine has shown to selectively protect normal tissues against cytotoxic and mutagenic effects of several anti-neoplastic drugs, such as alkylating agents, organoplatinum compounds, anthracyclines, taxanes, and ionising radiation.
  • In this study we have treated 31 patients affected with inoperable or metastatic breast cancer, not previously submitted to chemotherapy for advanced disease, with amifostine 910 mg/m(2) followed by doxorubicin 75 mg/m(2).
  • Grade 3 mucositis was observed in only 1 patient, whereas 2 patients (6%) developed an asymptomatic drop of left ventricular ejection fraction (LVEF) >10% below basal value.
  • In conclusion, this study suggests that amifostine can reduce doxorubicin related toxicity, thus improving the patients' quality of life and the efficacy/toxicity ratio of this drug.
  • [MeSH-major] Adenocarcinoma / drug therapy. Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Breast Neoplasms / drug therapy
  • [MeSH-minor] Adult. Aged. Amifostine / administration & dosage. Blood Cell Count. Bone Neoplasms / drug therapy. Bone Neoplasms / secondary. Doxorubicin / administration & dosage. Female. Hematologic Diseases / chemically induced. Humans. Middle Aged. Soft Tissue Neoplasms / drug therapy. Soft Tissue Neoplasms / secondary. Survival Rate

  • Genetic Alliance. consumer health - Breast Cancer.
  • Genetic Alliance. consumer health - Metastatic cancer.
  • MedlinePlus Health Information. consumer health - Breast Cancer.
  • Hazardous Substances Data Bank. AMIFOSTINE .
  • Hazardous Substances Data Bank. DOXORUBICIN .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 12469164.001).
  • [ISSN] 1021-335X
  • [Journal-full-title] Oncology reports
  • [ISO-abbreviation] Oncol. Rep.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Greece
  • [Chemical-registry-number] 80168379AG / Doxorubicin; M487QF2F4V / Amifostine
  •  go-up   go-down


18. Sauer G, Kafka A, Grundmann R, Kreienberg R, Zeillinger R, Deissler H: Basal expression of the multidrug resistance gene 1 (MDR-1) is associated with the TT genotype at the polymorphic site C3435T in mammary and ovarian carcinoma cell lines. Cancer Lett; 2002 Nov 8;185(1):79-85
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Basal expression of the multidrug resistance gene 1 (MDR-1) is associated with the TT genotype at the polymorphic site C3435T in mammary and ovarian carcinoma cell lines.
  • Resistance to established drugs for cancer therapy is in many cases associated with overexpression of the multidrug resistance gene 1 (MDR-1).
  • Regulation of basal expression of MDR-1 and mechanisms of induction as a result of exposure to cytotoxic substances are still not completely understood.
  • We analyzed the C3435T and G2677T genotypes of 38 mammary and ovarian carcinoma cell lines and measured basal MDR-1 expression by real-time reverse transcriptase-polymerase chain reaction.
  • Cell lines were classified as non-expressing or showing weak basal expression that was found to be significantly associated (six/seven versus 13/31 expressing cell lines; P=0.0448, Fisher's exact test) with the TT genotype at position 3435 of the MDR-1 gene.
  • [MeSH-major] Adenocarcinoma / genetics. Breast Neoplasms / genetics. Genes, MDR / genetics. Ovarian Neoplasms / genetics. Polymorphism, Genetic
  • [MeSH-minor] DNA Primers / chemistry. Drug Resistance, Multiple. Drug Resistance, Neoplasm. Female. Gene Expression Regulation, Neoplastic. Genotype. Humans. Reverse Transcriptase Polymerase Chain Reaction. Thymidine / chemistry. Tumor Cells, Cultured. beta 2-Microglobulin / genetics

  • MedlinePlus Health Information. consumer health - Breast Cancer.
  • MedlinePlus Health Information. consumer health - Ovarian Cancer.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 12142082.001).
  • [ISSN] 0304-3835
  • [Journal-full-title] Cancer letters
  • [ISO-abbreviation] Cancer Lett.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Ireland
  • [Chemical-registry-number] 0 / DNA Primers; 0 / beta 2-Microglobulin; VC2W18DGKR / Thymidine
  •  go-up   go-down


19. Gooch JL, Christy B, Yee D: STAT6 mediates interleukin-4 growth inhibition in human breast cancer cells. Neoplasia; 2002 Jul-Aug;4(4):324-31
PDF icon [Fulltext service] Download fulltext PDF of this article and others, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] STAT6 mediates interleukin-4 growth inhibition in human breast cancer cells.
  • In this study, we show that insulin receptor substrate (IRS)-1, IRS-2, and signal transducer and activator of transcription 6 (STAT6) are phosphorylated following IL-4 treatment in MCF-7 breast cancer cells.
  • In STAT6-transfected cells, basal proliferation was reduced whereas apoptosis was increased.
  • These results suggest STAT6 is required for IL-4-mediated growth inhibition and induction of apoptosis in human breast cancer cells.

  • Genetic Alliance. consumer health - Breast Cancer.
  • MedlinePlus Health Information. consumer health - Breast Cancer.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [Cites] J Biol Chem. 1998 Apr 17;273(16):9994-10003 [9545345.001]
  • [Cites] Cancer Res. 1998 Sep 15;58(18):4199-205 [9751635.001]
  • [Cites] J Biol Chem. 1999 Feb 26;274(9):5333-8 [10026141.001]
  • [Cites] Mol Endocrinol. 1999 Apr;13(4):555-65 [10194762.001]
  • [Cites] J Immunol. 1999 Apr 15;162(8):4472-81 [10201984.001]
  • [Cites] Mol Endocrinol. 1999 May;13(5):787-96 [10319328.001]
  • [Cites] Mol Cell Biol. 2000 Mar;20(5):1489-96 [10669726.001]
  • [Cites] Mol Endocrinol. 2000 Feb;14(2):229-40 [10674396.001]
  • [Cites] J Biol Chem. 2000 Apr 7;275(14):10212-7 [10744706.001]
  • [Cites] Cell Growth Differ. 2000 Jun;11(6):335-42 [10910100.001]
  • [Cites] Mol Immunol. 2000 Aug;37(11):641-52 [11164892.001]
  • [Cites] Cell. 1989 May 5;57(3):503-12 [2785856.001]
  • [Cites] Br J Cancer Suppl. 1990 Jul;10:96-8 [2200499.001]
  • [Cites] Cancer Res. 1990 Nov 1;50(21):6931-5 [2170011.001]
  • [Cites] Cancer Res. 1991 Jan 1;51(1):261-4 [1846310.001]
  • [Cites] Blood. 1991 May 1;77(9):1859-70 [2018830.001]
  • [Cites] Cancer Res. 1991 Jun 1;51(11):3011-7 [2032239.001]
  • [Cites] Science. 1991 Nov 1;254(5032):713-6 [1948050.001]
  • [Cites] Cancer Res. 1992 Jan 15;52(2):275-9 [1728401.001]
  • [Cites] Br J Cancer. 1992 Jul;66(1):204-10 [1637669.001]
  • [Cites] Biotechniques. 1992 Nov;13(5):700-1 [1418966.001]
  • [Cites] J Clin Invest. 1993 Jan;91(1):88-93 [8423237.001]
  • [Cites] Clin Exp Immunol. 1994 Jan;95(1):148-55 [8287600.001]
  • [Cites] Res Immunol. 1993 Oct;144(8):579-83 [8303076.001]
  • [Cites] J Biol Chem. 1994 Feb 18;269(7):5403-12 [7508938.001]
  • [Cites] Proc Natl Acad Sci U S A. 1994 May 24;91(11):4915-9 [8197157.001]
  • [Cites] Cancer Res. 1995 May 15;55(10):2173-6 [7743520.001]
  • [Cites] J Biol Chem. 1995 Aug 18;270(33):19481-6 [7642632.001]
  • [Cites] Proc Natl Acad Sci U S A. 1995 Aug 15;92(17):7971-5 [7544011.001]
  • [Cites] Nature. 1995 Oct 19;377(6550):591-4 [7566171.001]
  • [Cites] Behring Inst Mitt. 1995 Jun;(96):97-102 [7575358.001]
  • [Cites] J Immunol. 1995 Dec 15;155(12):5637-46 [7499848.001]
  • [Cites] J Biol Chem. 1996 Mar 1;271(9):5112-7 [8617790.001]
  • [Cites] Biochem J. 1996 May 1;315 ( Pt 3):767-74 [8645156.001]
  • [Cites] Mol Cell Biol. 1996 Oct;16(10):5811-20 [8816495.001]
  • [Cites] Mol Cell Endocrinol. 1996 Jul 23;121(1):11-8 [8865161.001]
  • [Cites] J Immunol. 1996 Dec 1;157(11):4926-34 [8943397.001]
  • [Cites] J Biol Chem. 1997 Jan 10;272(2):1377-81 [8995447.001]
  • [Cites] J Immunol. 1997 Aug 1;159(3):1255-64 [9233621.001]
  • [Cites] Cancer Res. 1998 Feb 1;58(3):570-6 [9458107.001]
  • [Cites] Cancer J Sci Am. 1998 Jan-Feb;4(1):46-51 [9467046.001]
  • [Cites] Mol Cell Biol. 1998 Apr;18(4):1996-2003 [9528771.001]
  • (PMID = 12082548.001).
  • [ISSN] 1522-8002
  • [Journal-full-title] Neoplasia (New York, N.Y.)
  • [ISO-abbreviation] Neoplasia
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / P30 CA054174; United States / NCI NIH HHS / CA / R01 CA074285; United States / NCI NIH HHS / CA / P30 CA 54174; United States / NCI NIH HHS / CA / R01 CA 74285
  • [Publication-type] Journal Article; Research Support, U.S. Gov't, P.H.S.
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / DNA, Complementary; 0 / Growth Inhibitors; 0 / IRS1 protein, human; 0 / IRS2 protein, human; 0 / Insulin Receptor Substrate Proteins; 0 / Intracellular Signaling Peptides and Proteins; 0 / Neoplasm Proteins; 0 / Phosphoproteins; 0 / Recombinant Fusion Proteins; 0 / STAT6 Transcription Factor; 0 / STAT6 protein, human; 0 / Trans-Activators; 207137-56-2 / Interleukin-4
  • [Other-IDs] NLM/ PMC1531710
  •  go-up   go-down


20. Ullerås E, Miller SJ, Adam GI, Kanduri C, Wilcock AC, Franklin GC: Inhibition of histone deacetylase activity causes cell type-specific induction of the PDGF-B promoter only in the absence of activation by its enhancer. Exp Cell Res; 2001 Nov 1;270(2):188-98
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Inhibition of histone deacetylase activity causes cell type-specific induction of the PDGF-B promoter only in the absence of activation by its enhancer.
  • This activation showed an inverse correlation with the cell type-specific transcriptional activities of the promoter.
  • The TSA response was minimal in three tumor cell lines that exhibit high-level promoter activity.
  • In JEG-3 choriocarcinoma cells, however, where the basal promoter activity is considerably lower, there was a strong response to TSA.
  • TSA treatment of JEG-3 cells, either alone or in combination with the demethylating agent 5-azacytidine, failed to activate the silenced endogenous PDGF-B transcript, however, which appears to be repressed by additional mechanisms.
  • [MeSH-major] Enhancer Elements, Genetic / physiology. Histone Deacetylase Inhibitors. Promoter Regions, Genetic / physiology. Proto-Oncogene Proteins c-sis / genetics
  • [MeSH-minor] Adenocarcinoma. Breast Neoplasms. Carcinoma, Hepatocellular. Choriocarcinoma. Chromosomes. DNA Methylation. Enzyme Inhibitors / pharmacology. Female. Gene Expression Regulation, Neoplastic / drug effects. Gene Expression Regulation, Neoplastic / physiology. Histone Deacetylases / metabolism. Humans. Hydroxamic Acids / pharmacology. Introns. Liver Neoplasms. Mutagenesis / physiology. Rhabdomyosarcoma. Transcription, Genetic / drug effects. Transcription, Genetic / physiology. Tumor Cells, Cultured

  • COS Scholar Universe. author profiles.
  • NCI CPTC Antibody Characterization Program. NCI CPTC Antibody Characterization Program .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [Copyright] Copyright 2001 Academic Press.
  • (PMID = 11640883.001).
  • [ISSN] 0014-4827
  • [Journal-full-title] Experimental cell research
  • [ISO-abbreviation] Exp. Cell Res.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Enzyme Inhibitors; 0 / Histone Deacetylase Inhibitors; 0 / Hydroxamic Acids; 0 / Proto-Oncogene Proteins c-sis; 3X2S926L3Z / trichostatin A; EC 3.5.1.98 / Histone Deacetylases
  •  go-up   go-down


21. Pires MM, Emmert D, Hrycyna CA, Chmielewski J: Inhibition of P-glycoprotein-mediated paclitaxel resistance by reversibly linked quinine homodimers. Mol Pharmacol; 2009 Jan;75(1):92-100
PDF icon [Fulltext service] Download fulltext PDF of this article and others, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • P-glycoprotein (P-gp), an ATP-dependent drug efflux pump, has been implicated in multidrug resistance of several cancers as a result of its overexpression.
  • These dimeric agents include reversible tethers with a built-in clearance mechanism.
  • The designed agents were potent inhibitors of rhodamine 123 efflux in cultured cancer cell lines that display high levels of P-gp expression at the cell surface and in transfected cells expressing P-gp.
  • The reversibility of the tether was confirmed in experiments showing that Q2 was readily hydrolyzed by esterases in vitro (t(1/2) approximately 20 h) while demonstrating high resistance to nonenzymatic hydrolysis in cell culture media (t(1/2) approximately 21 days).
  • Specific inhibition of [(125)I]iodoarylazidoprazosin binding to P-gp by Q2 verified that the bivalent agent interacted specifically with the drug binding site(s) of P-gp.
  • In addition, low concentrations of Q2 stimulated basal P-gp ATPase levels.

  • COS Scholar Universe. author profiles.
  • Hazardous Substances Data Bank. QUININE .
  • Hazardous Substances Data Bank. VERAPAMIL HYDROCHLORIDE .
  • Hazardous Substances Data Bank. PRAZOSIN HYDROCHLORIDE .
  • Hazardous Substances Data Bank. DOXORUBICIN .
  • Hazardous Substances Data Bank. TAXOL .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [Cites] Methods Enzymol. 1998;292:456-73 [9711574.001]
  • [Cites] Pharm Biotechnol. 1998;11:345-65 [9760687.001]
  • [Cites] Eur J Biochem. 1999 Feb;259(3):841-50 [10092872.001]
  • [Cites] Annu Rev Pharmacol Toxicol. 1999;39:361-98 [10331089.001]
  • [Cites] Biochemistry. 1999 Oct 19;38(42):13887-99 [10529234.001]
  • [Cites] Mol Pharmacol. 2005 Mar;67(3):902-11 [15598974.001]
  • [Cites] Nat Rev Neurosci. 2005 Aug;6(8):591-602 [16025095.001]
  • [Cites] Biochemistry. 2006 Sep 26;45(38):11695-702 [16981729.001]
  • [Cites] J Med Chem. 2006 Nov 16;49(23):6742-59 [17154505.001]
  • [Cites] Cancer Res. 1983 Sep;43(9):4413-9 [6135505.001]
  • [Cites] J Immunol Methods. 1983 Dec 16;65(1-2):55-63 [6606682.001]
  • [Cites] Cancer Res. 1987 Oct 1;47(19):5141-8 [2441861.001]
  • [Cites] Mol Pharmacol. 1988 Feb;33(2):144-7 [2893251.001]
  • [Cites] Proc Natl Acad Sci U S A. 1988 May;85(10):3580-4 [3368466.001]
  • [Cites] J Biol Chem. 1988 Sep 5;263(25):12163-6 [2900833.001]
  • [Cites] Cancer Res. 1990 Mar 15;50(6):1748-56 [1968358.001]
  • [Cites] Biochemistry. 1990 Mar 6;29(9):2295-303 [1970935.001]
  • [Cites] Annu Rev Cell Biol. 1992;8:67-113 [1282354.001]
  • [Cites] Biochem Pharmacol. 1993 Sep 14;46(6):1096-9 [8105783.001]
  • [Cites] Biochim Biophys Acta. 1994 Jan 3;1189(1):1-6 [7905747.001]
  • [Cites] J Natl Cancer Inst Monogr. 1993;(15):55-61 [7912530.001]
  • [Cites] J Biol Chem. 1995 Sep 29;270(39):22957-61 [7559432.001]
  • [Cites] Proc Natl Acad Sci U S A. 1997 Mar 4;94(5):2031-5 [9050899.001]
  • [Cites] Proc Natl Acad Sci U S A. 1997 Sep 30;94(20):10594-9 [9380680.001]
  • [Cites] N Engl J Med. 1998 Jan 1;338(1):35-45 [9414330.001]
  • [Cites] Eur J Biochem. 1997 Nov 15;250(1):130-7 [9432000.001]
  • [Cites] Biochemistry. 1998 Mar 17;37(11):3594-601 [9530286.001]
  • [Cites] Mol Pharmacol. 2000 Sep;58(3):624-32 [10953057.001]
  • [Cites] Semin Cell Dev Biol. 2001 Jun;12(3):247-56 [11428917.001]
  • [Cites] Biochem Biophys Res Commun. 2001 Nov 30;289(2):580-5 [11716514.001]
  • [Cites] Mol Pharmacol. 2002 Mar;61(3):637-48 [11854445.001]
  • [Cites] Nat Rev Cancer. 2002 Jan;2(1):48-58 [11902585.001]
  • [Cites] Adv Drug Deliv Rev. 2003 Jan 21;55(1):3-29 [12535572.001]
  • [Cites] J Exp Biol. 2003 Nov;206(Pt 21):3753-9 [14506210.001]
  • [Cites] J Biol Chem. 2003 Oct 10;278(41):39706-10 [12909621.001]
  • [Cites] J Biol Chem. 2003 Dec 12;278(50):50136-41 [14522974.001]
  • [Cites] Biochemistry. 2004 Mar 2;43(8):2262-71 [14979722.001]
  • [Cites] Leukemia. 2004 Mar;18(3):401-8 [14724652.001]
  • [Cites] J Biol Chem. 2004 Apr 30;279(18):18232-8 [14749322.001]
  • (PMID = 18945821.001).
  • [ISSN] 1521-0111
  • [Journal-full-title] Molecular pharmacology
  • [ISO-abbreviation] Mol. Pharmacol.
  • [Language] ENG
  • [Grant] United States / NEI NIH HHS / EY / R21 EY018481; United States / NCI NIH HHS / CA / 2P30-CA23168; United States / NEI NIH HHS / EY / EY018481
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Affinity Labels; 0 / Fluorescent Dyes; 0 / P-Glycoprotein; 1N3CZ14C5O / Rhodamine 123; 80168379AG / Doxorubicin; A7V27PHC7A / Quinine; CJ0O37KU29 / Verapamil; EC 3.6.1.- / Adenosine Triphosphatases; P88XT4IS4D / Paclitaxel; XM03YJ541D / Prazosin
  • [Other-IDs] NLM/ PMC2685053
  •  go-up   go-down


22. Martinez VG, Williams KJ, Stratford IJ, Clynes M, O'Connor R: Overexpression of cytochrome P450 NADPH reductase sensitises MDA 231 breast carcinoma cells to 5-fluorouracil: possible mechanisms involved. Toxicol In Vitro; 2008 Apr;22(3):582-8
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Overexpression of cytochrome P450 NADPH reductase sensitises MDA 231 breast carcinoma cells to 5-fluorouracil: possible mechanisms involved.
  • Activity of cytochromes P450 is highly dependent on cytochrome P450 NADPH reductase (P450R), but this enzyme can also metabolise drugs on its own.
  • MDA 231 breast adenocarcinoma cells transfected with human P450R (MDA R4) or an empty vector (MDA EV) were exposed to a series of commonly used chemotherapeutic drugs.
  • Overexpression of P450R did not affect cell sensitivity to cisplatin, mitoxantrone, paclitaxel, docetaxel, vincristine or etoposide.
  • Levels of NADPH were considerably decreased in MDA R4 as compared to MDA EV cells, while reactive oxygen species (ROS) production was increased in MDA R4 cells in basal conditions, showing no significant further increase after treatment with mitomycin C or 5-fluorouracil.
  • [MeSH-major] Antimetabolites, Antineoplastic / pharmacology. Breast Neoplasms / drug therapy. Fluorouracil / pharmacology. NADPH-Ferrihemoprotein Reductase / biosynthesis
  • [MeSH-minor] Antibiotics, Antineoplastic / metabolism. Antibiotics, Antineoplastic / pharmacology. Antineoplastic Agents, Phytogenic / metabolism. Antineoplastic Agents, Phytogenic / pharmacology. Blotting, Western. Cell Line, Tumor. Cell Survival. Female. Glutathione / metabolism. Humans. Microsomes / metabolism. Mitomycin / metabolism. Mitomycin / pharmacology. NADP / metabolism. Reactive Oxygen Species / metabolism. Transfection. Vincristine / metabolism. Vincristine / pharmacology

  • MedlinePlus Health Information. consumer health - Breast Cancer.
  • COS Scholar Universe. author profiles.
  • Hazardous Substances Data Bank. MITOMYCIN C .
  • Hazardous Substances Data Bank. FLUOROURACIL .
  • Hazardous Substances Data Bank. VINCRISTINE .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 18191533.001).
  • [ISSN] 0887-2333
  • [Journal-full-title] Toxicology in vitro : an international journal published in association with BIBRA
  • [ISO-abbreviation] Toxicol In Vitro
  • [Language] eng
  • [Grant] United Kingdom / Medical Research Council / / G0500366; United Kingdom / Medical Research Council / /
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Antibiotics, Antineoplastic; 0 / Antimetabolites, Antineoplastic; 0 / Antineoplastic Agents, Phytogenic; 0 / Reactive Oxygen Species; 50SG953SK6 / Mitomycin; 53-59-8 / NADP; 5J49Q6B70F / Vincristine; EC 1.6.2.4 / NADPH-Ferrihemoprotein Reductase; GAN16C9B8O / Glutathione; U3P01618RT / Fluorouracil
  •  go-up   go-down


23. Lobenhofer EK, Huper G, Iglehart JD, Marks JR: Inhibition of mitogen-activated protein kinase and phosphatidylinositol 3-kinase activity in MCF-7 cells prevents estrogen-induced mitogenesis. Cell Growth Differ; 2000 Feb;11(2):99-110
PDF icon [Fulltext service] Download fulltext PDF of this article and others, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • Estrogen acts to promote DNA synthesis in the MCF-7 human breast cancer cell line via its interaction with high levels of estrogen receptor.
  • However, the drugs did prevent the accumulation of cyclin D1 and hyperphosphorylated retinoblastoma protein, indicating that the block occurred at, or prior to, this point in the cell cycle.
  • Although these compounds were effective in preventing estrogen-mediated mitogenesis, the downstream kinases extracellular signal-regulated kinase 1, extracellular signal-regulated kinase 2, and protein kinase B were not activated over basal levels by estrogen treatment.
  • These studies suggest that estrogen initiates mitogenesis by inducing the transcription of immediate early genes, but cytoplasmic signaling pathways play an important role in the control of subsequent events in the cell cycle.
  • [MeSH-major] Adenocarcinoma / pathology. Breast Neoplasms / pathology. Estradiol / pharmacology. Estrogens. MAP Kinase Signaling System / drug effects. Neoplasm Proteins / metabolism. Neoplasms, Hormone-Dependent / pathology. Phosphatidylinositol 3-Kinases / antagonists & inhibitors. Protein-Serine-Threonine Kinases. Sulfonamides
  • [MeSH-minor] Androstadienes / pharmacology. Butadienes / pharmacology. Chromones / pharmacology. Culture Media, Serum-Free. Cyclic AMP-Dependent Protein Kinases / antagonists & inhibitors. Cyclic AMP-Dependent Protein Kinases / metabolism. Cyclin D1 / metabolism. DNA Replication / drug effects. Depression, Chemical. Enzyme Activation. Enzyme Inhibitors / pharmacology. Estrogen Receptor Modulators / pharmacology. Female. Flavonoids / pharmacology. Humans. Isoquinolines / pharmacology. Mitogen-Activated Protein Kinase 1 / metabolism. Mitogen-Activated Protein Kinase 3. Mitogen-Activated Protein Kinases / metabolism. Mitosis / drug effects. Morpholines / pharmacology. Nitriles / pharmacology. Proto-Oncogene Proteins / antagonists & inhibitors. Proto-Oncogene Proteins / metabolism. Proto-Oncogene Proteins c-akt. Retinoblastoma Protein / metabolism

  • MedlinePlus Health Information. consumer health - Breast Cancer.
  • Hazardous Substances Data Bank. FULVESTRANT .
  • Hazardous Substances Data Bank. ESTRADIOL .
  • NCI CPTC Antibody Characterization Program. NCI CPTC Antibody Characterization Program .
  • NCI CPTC Antibody Characterization Program. NCI CPTC Antibody Characterization Program .
  • NCI CPTC Antibody Characterization Program. NCI CPTC Antibody Characterization Program .
  • NCI CPTC Antibody Characterization Program. NCI CPTC Antibody Characterization Program .
  • NCI CPTC Antibody Characterization Program. NCI CPTC Antibody Characterization Program .
  • NCI CPTC Antibody Characterization Program. NCI CPTC Antibody Characterization Program .
  • The Lens. Cited by Patents in .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 10714766.001).
  • [ISSN] 1044-9523
  • [Journal-full-title] Cell growth & differentiation : the molecular biology journal of the American Association for Cancer Research
  • [ISO-abbreviation] Cell Growth Differ.
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / CA68438; United States / NCI NIH HHS / CA / CA73802
  • [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 / 2-(2-amino-3-methoxyphenyl)-4H-1-benzopyran-4-one; 0 / Androstadienes; 0 / Butadienes; 0 / Chromones; 0 / Culture Media, Serum-Free; 0 / Enzyme Inhibitors; 0 / Estrogen Receptor Modulators; 0 / Estrogens; 0 / Flavonoids; 0 / Isoquinolines; 0 / Morpholines; 0 / Neoplasm Proteins; 0 / Nitriles; 0 / Proto-Oncogene Proteins; 0 / Retinoblastoma Protein; 0 / Sulfonamides; 0 / U 0126; 127243-85-0 / N-(2-(4-bromocinnamylamino)ethyl)-5-isoquinolinesulfonamide; 136601-57-5 / Cyclin D1; 154447-36-6 / 2-(4-morpholinyl)-8-phenyl-4H-1-benzopyran-4-one; 22X328QOC4 / fulvestrant; 4TI98Z838E / Estradiol; EC 2.7.1.- / Phosphatidylinositol 3-Kinases; EC 2.7.11.1 / Protein-Serine-Threonine Kinases; EC 2.7.11.1 / Proto-Oncogene Proteins c-akt; EC 2.7.11.11 / Cyclic AMP-Dependent Protein Kinases; EC 2.7.11.24 / Mitogen-Activated Protein Kinase 1; EC 2.7.11.24 / Mitogen-Activated Protein Kinase 3; EC 2.7.11.24 / Mitogen-Activated Protein Kinases; XVA4O219QW / wortmannin
  •  go-up   go-down


24. Richards JA, Petrel TA, Brueggemeier RW: Signaling pathways regulating aromatase and cyclooxygenases in normal and malignant breast cells. J Steroid Biochem Mol Biol; 2002 Feb;80(2):203-12
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Signaling pathways regulating aromatase and cyclooxygenases in normal and malignant breast cells.
  • Aromatase activity has been demonstrated in breast tissue in vitro, and expression of aromatase is highest in or near breast tumor sites.
  • Thus, local regulation of aromatase by both endogenous factors as well as exogenous medicinal agents will influence the levels of estrogen available for breast cancer growth.
  • The prostaglandin PGE(2) increases intracellular cAMP levels and stimulates estrogen biosynthesis, and our recent studies have shown a strong linear association between CYP19 expression and the sum of cyclooxygenase-1 (COX-1) and cyclooxygenase-2 (COX-2) expression in breast cancer specimens.
  • Knowledge of the signaling pathways that regulate the expression and enzyme activity of aromatase and cyclooxygenases (COXs) in stromal and epithelial breast cells will aid in understanding the interrelationships of these two enzyme systems and potentially identify novel targets for regulation.
  • The effects of epidermal growth factor (EGF), transforming growth factor-beta (TGFbeta), and tetradecanoyl phorbol acetate (TPA) on aromatase and COXs were studied in primary cultures of normal human adipose stromal cells and in cell cultures of normal immortalized human breast epithelial cells MCF-10F, estrogen-responsive human breast cancer cells MCF-7, and estrogen-unresponsive human breast cancer cells MDA-MB-231.
  • Levels of the constitutive COX isozyme, COX-1, were not altered by the various treatments in the cell systems studied.
  • In breast adenocarcinoma cells, EGF and TGFbeta did not alter COX-2 levels at 24h, while TPA induced COX-2 levels by 75% in MDA-MB-231 cells.
  • Untreated normal adipose stromal cells exhibited high basal levels of COX-1 but low to undetectable levels of COX-2.
  • In summary, the results of this investigation on the effects of several paracrine and/or autocrine signaling pathways in the regulation of expression of aromatase, COX-1, and COX-2 in breast cells has identified more complex relationships.
  • Overall, elevated levels of these factors in the breast cancer tissue microenvironment can result in increased aromatase activity (and subsequent increased estrogen biosynthesis) via autocrine mechanisms in breast epithelial cells and via paracrine mechanisms in breast stromal cells.
  • Furthermore, increased secretion of prostaglandins such as PGE(2) from constitutive COX-1 and inducible COX-2 isozymes present in epithelial and stromal cell compartments will result in both autocrine and paracrine actions to increase aromatase expression in the tissues.

  • MedlinePlus Health Information. consumer health - Breast Cancer.
  • COS Scholar Universe. author profiles.
  • Hazardous Substances Data Bank. 12-O-TETRADECANOYLPHORBOL-13-ACETATE .
  • NCI CPTAC Assay Portal. NCI CPTAC Assay Portal .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 11897504.001).
  • [ISSN] 0960-0760
  • [Journal-full-title] The Journal of steroid biochemistry and molecular biology
  • [ISO-abbreviation] J. Steroid Biochem. Mol. Biol.
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / R01 CA073698-03S1; United States / NCI NIH HHS / CA / R01 CA073698-03; United States / NCI NIH HHS / CA / R01 CA 73698; United States / NCI NIH HHS / CA / CA073698-03; United States / NCI NIH HHS / CA / CA073698-03S1
  • [Publication-type] Journal Article; Research Support, U.S. Gov't, Non-P.H.S.; Research Support, U.S. Gov't, P.H.S.; Review
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Isoenzymes; 0 / Membrane Proteins; 0 / Recombinant Proteins; 62229-50-9 / Epidermal Growth Factor; EC 1.14.14.1 / Aromatase; EC 1.14.99.1 / Cyclooxygenase 1; EC 1.14.99.1 / Cyclooxygenase 2; EC 1.14.99.1 / PTGS1 protein, human; EC 1.14.99.1 / PTGS2 protein, human; EC 1.14.99.1 / Prostaglandin-Endoperoxide Synthases; NI40JAQ945 / Tetradecanoylphorbol Acetate
  • [Number-of-references] 34
  •  go-up   go-down






Advertisement