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1. Bon G, Folgiero V, Bossi G, Felicioni L, Marchetti A, Sacchi A, Falcioni R: Loss of beta4 integrin subunit reduces the tumorigenicity of MCF7 mammary cells and causes apoptosis upon hormone deprivation. Clin Cancer Res; 2006 Jun 1;12(11 Pt 1):3280-7
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  • [Title] Loss of beta4 integrin subunit reduces the tumorigenicity of MCF7 mammary cells and causes apoptosis upon hormone deprivation.
  • We showed that the beta4 integrin subunit associates with the ErbB-2 tyrosine kinase in human mammary carcinoma cell lines and that its overexpression in NIH3T3/ErbB-2-transformed cells causes a constitutive activation of phosphatidylinositol 3-kinase (PI3K), inducing a strong increase of their invasive capacity.
  • EXPERIMENTAL DESIGN: In vitro and in vivo tumor growth and the biochemical consequences of beta4 integrin inactivation were studied in mammary tumor cells by using short hairpin RNA approach.
  • RESULTS: Our data show that tumor growth of mammary tumor cells strictly depends on beta4 expression, confirming the relevance of beta4 protein in these cells.
  • Accordingly, with these results and considering that PI3K activity in mammary tumor plays a relevant role in hormone resistance, we asked whether beta4 expression might be relevant for hormone responsiveness in these cells.
  • Data reported indicate that the interference with endogenous beta4 expression, upon hormone deprivation, induces caspase-9 and cytochrome c-mediated apoptosis, which is enhanced upon tamoxifen treatment.
  • On the other hand, the expression of myr-AKT in MCF7 beta4-short hairpin RNA cells rescues the cells from apoptosis in the absence of hormones and upon tamoxifen treatment.
  • CONCLUSIONS: Overall, these results confirm the relevance of beta4 expression in mammary tumors and indicate this integrin as a relevant target for tumor therapy.
  • [MeSH-minor] Animals. Cell Line, Tumor. Cell Proliferation / drug effects. Female. Gene Expression Profiling. Humans. Mice. Mice, Nude. Phosphatidylinositol 3-Kinases / drug effects. Phosphatidylinositol 3-Kinases / metabolism. Phosphorylation. Protein Kinases / drug effects. Protein Kinases / metabolism. Protein Subunits / drug effects. Protein Subunits / genetics. Protein Subunits / metabolism. Proto-Oncogene Proteins c-akt / antagonists & inhibitors. Proto-Oncogene Proteins c-akt / metabolism. RNA, Small Interfering / metabolism. RNA, Small Interfering / pharmacology. Reverse Transcriptase Polymerase Chain Reaction / methods. Signal Transduction / drug effects. Structure-Activity Relationship. TOR Serine-Threonine Kinases. Tamoxifen / pharmacology. Xenograft Model Antitumor Assays

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  • (PMID = 16740748.001).
  • [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 / Integrin beta4; 0 / Protein Subunits; 0 / RNA, Small Interfering; 094ZI81Y45 / Tamoxifen; EC 2.7.- / Protein Kinases; EC 2.7.1.- / Phosphatidylinositol 3-Kinases; EC 2.7.1.1 / MTOR protein, human; EC 2.7.1.1 / TOR Serine-Threonine Kinases; EC 2.7.1.1 / mTOR protein, mouse; EC 2.7.11.1 / Proto-Oncogene Proteins c-akt
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2. Toneff MJ, Du Z, Dong J, Huang J, Sinai P, Forman J, Hilsenbeck S, Schiff R, Huang S, Li Y: Somatic expression of PyMT or activated ErbB2 induces estrogen-independent mammary tumorigenesis. Neoplasia; 2010 Sep;12(9):718-26
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  • [Title] Somatic expression of PyMT or activated ErbB2 induces estrogen-independent mammary tumorigenesis.
  • Here, we report that in a retrovirus-based somatic mouse model (replication-competent ALV-LTR splice acceptor/tumor virus A) that closely mimics the evolution of sporadic human breast cancers, mammary epithelial cells harboring PyMT or activated ErbB2 evolve into tumors independent of estrogen or other ovarian functions in contrast to previous observations of estrogen-dependent cancer formation in germ line mouse models of ErbB2 activation.
  • Importantly, ErbB2 activation in normal mammary cells causes estrogen-independent proliferation in both estrogen receptor (ER)-negative cells as well as in normally quiescent ER-positive cells.
  • Therefore, aberrant activation of growth factor signaling contributes to estrogen-independent proliferation of both preneoplastic and cancerous mammary cells, and prophylactic therapy against both growth factor signaling and estrogen signaling may need to be considered in women with increased risk of breast cancer.

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  • (PMID = 20824048.001).
  • [ISSN] 1476-5586
  • [Journal-full-title] Neoplasia (New York, N.Y.)
  • [ISO-abbreviation] Neoplasia
  • [Language] ENG
  • [Grant] United States / NIAID NIH HHS / AI / AI45764; United States / NCI NIH HHS / CA / R01 CA113869; United States / NCI NIH HHS / CA / CA113869; United States / NIAID NIH HHS / AI / R01 AI045764; United States / NCI NIH HHS / CA / CA124820; United States / NCI NIH HHS / CA / R01 CA124820
  • [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 / Antigens, Viral, Tumor; 0 / Estrogens; EC 2.7.10.1 / Erbb2 protein, mouse; EC 2.7.10.1 / Receptor, ErbB-2
  • [Other-IDs] NLM/ PMC2933692
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3. Namba R, Young LJ, Maglione JE, McGoldrick ET, Liu S, Wurz GT, DeGregorio MW, Borowsky AD, MacLeod CL, Cardiff RD, Gregg JP: Selective estrogen receptor modulators inhibit growth and progression of premalignant lesions in a mouse model of ductal carcinoma in situ. Breast Cancer Res; 2005;7(6):R881-9
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  • [Title] Selective estrogen receptor modulators inhibit growth and progression of premalignant lesions in a mouse model of ductal carcinoma in situ.
  • INTRODUCTION: Ductal carcinoma in situ (DCIS) is a noninvasive premalignant lesion and is considered a precursor to invasive carcinoma.
  • DCIS accounts for nearly 20% of newly diagnosed breast cancer, but the lack of experimentally amenable in vivo DCIS models hinders the development of treatment strategies.
  • Here, we demonstrate the utility of a mouse transplantation model of DCIS for chemoprevention studies using selective estrogen receptor modulators (SERMs).
  • This model consists of a set of serially transplanted lines of genetically engineered mouse mammary intraepithelial neoplasia (MIN) outgrowth (MIN-O) tissue that have stable characteristics.
  • METHODS: The estrogen receptor (ER) status and ovarian-hormone-dependence of the mouse MIN outgrowth tissue were determined by immunohistochemistry and ovarian ablation.
  • Likewise, tamoxifen and ospemifene treatments decreased the MIN growth and tumor incidence in comparison with the control (P < 0.01).
  • Between the two SERM treatment groups, there were no statistically significant differences in MIN-O size, tumor latency, or proliferation rate.
  • In contrast, the ospemifene treatment significantly increased ER levels while tamoxifen significantly decreased them.
  • CONCLUSION: Tamoxifen and ospemifene inhibit the growth of premalignant mammary lesions and the progression to invasive carcinoma in a transplantable mouse model of DCIS.
  • These data demonstrate the value of this model system for preclinical testing of antiestrogen or other therapies designed to prevent or delay the malignant transformation of premalignant mammary lesions in chemoprevention.

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  • (PMID = 16280035.001).
  • [ISSN] 1465-542X
  • [Journal-full-title] Breast cancer research : BCR
  • [ISO-abbreviation] Breast Cancer Res.
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / CA89140-01; United States / NCI NIH HHS / CA / R01 CA089140; United States / NCRR NIH HHS / RR / U42 RR014905; United States / NCRR NIH HHS / RR / U42RR14905; United States / NCI NIH HHS / CA / R01CA81376
  • [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 / Receptors, Estrogen; 0 / Selective Estrogen Receptor Modulators; 094ZI81Y45 / Tamoxifen; B0P231ILBK / Ospemifene
  • [Other-IDs] NLM/ PMC1410776
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4. Walt H, Nap M, Dorward AM, Leers MP, Tennent BJ, Varga Z, Stallmach T, Björklund V, Beamer WG: Early apoptotic responses in transgenic mouse mammary carcinoma for photodynamic therapy. Photodiagnosis Photodyn Ther; 2006 Dec;3(4):227-33

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  • [Title] Early apoptotic responses in transgenic mouse mammary carcinoma for photodynamic therapy.
  • We have utilized this mammary tumour model to investigate apoptotic responses following photodynamic therapy (PDT) with a chlorin-based, water-soluble photosensitizer.
  • METHODS: Detection of apoptosis was accomplished by use of the antibody M30 against a neo-epitope of caspase-cleaved cytokeratin 18 that becomes available at an early stage of the apoptotic cascade.
  • Mice bearing multiple tumours were injected with the photosensitizer intraperitoneally, and following a drug-light interval of 96h, 40J/cm(2) of 652nm laser light was applied to one tumour per animal, while the other tumours were protected from light to serve as host controls.
  • The M30 antibody was used for standard immunohistochemistry of tumour sections and flow cytometric detection of epitope expression coupled to cell cycle analysis in tumour cell populations retrieved from paraffin blocks.
  • RESULTS: M30 staining was significantly increased within 2h following light treatment and persisted until 96h after treatment.
  • Calculating the M30/SPF ratio at both 2h and 96h suggested distinct cellular dynamics at early and late time points, and we propose the M30/SPF ratio as a tumour dynamic index (TDI) to monitor events post PDT.

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  • (PMID = 25046987.001).
  • [ISSN] 1572-1000
  • [Journal-full-title] Photodiagnosis and photodynamic therapy
  • [ISO-abbreviation] Photodiagnosis Photodyn Ther
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Netherlands
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5. Yin Y, Russell RG, Dettin LE, Bai R, Wei ZL, Kozikowski AP, Kopelovich L, Glazer RI: Peroxisome proliferator-activated receptor delta and gamma agonists differentially alter tumor differentiation and progression during mammary carcinogenesis. Cancer Res; 2005 May 1;65(9):3950-7
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  • [Title] Peroxisome proliferator-activated receptor delta and gamma agonists differentially alter tumor differentiation and progression during mammary carcinogenesis.
  • These and other receptor-mediated actions pertain to their role in hypolipidemic and antidiabetic therapies and as potential targets for cancer chemopreventive agents.
  • The present study evaluated the chemopreventive activity of two highly potent and selective PPARgamma and PPARdelta agonists in a progestin- and carcinogen-induced mouse mammary tumorigenesis model.
  • Gene expression analysis of tumors arising from GW7845- and GW501516-treated mice identified expression profiles that were distinct from each other and from untreated control tumors of the same histopathology.
  • Tumors from mice treated with the PPARdelta agonist exhibited increased PPARdelta levels and activated 3-phosphoinositide-dependent protein kinase-1 (PDK1), which co-associated, suggesting a link between the known oncogenic activity of PDK1 in mammary epithelium and PPARdelta activation.
  • These results indicate that PPARdelta and PPARgamma agonists produce diverse, yet profound effects on mammary tumorigenesis that give rise to distinctive histopathologic patterns of tumor differentiation and tumor development.
  • [MeSH-major] Anticarcinogenic Agents / pharmacology. Carcinoma, Ductal / prevention & control. Mammary Neoplasms, Experimental / prevention & control. Oxazoles / pharmacology. PPAR delta / agonists. PPAR gamma / agonists. Thiazoles / pharmacology. Tyrosine / analogs & derivatives. Tyrosine / pharmacology
  • [MeSH-minor] Animals. Carcinoma, Adenosquamous / chemically induced. Carcinoma, Adenosquamous / drug therapy. Carcinoma, Adenosquamous / pathology. Carcinoma, Adenosquamous / prevention & control. Carcinoma, Squamous Cell / chemically induced. Carcinoma, Squamous Cell / drug therapy. Carcinoma, Squamous Cell / pathology. Carcinoma, Squamous Cell / prevention & control. Cell Differentiation / drug effects. Disease Progression. Female. Gene Expression Profiling. Mice

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  • [ErratumIn] Cancer Res. 2005 Jul 1;65(13):5989
  • [ErratumIn] Cancer Res. 2005 Oct 1;65(19):9108. Kopleovich, Levy [corrected to Kopelovich, Levy]
  • (PMID = 15867396.001).
  • [ISSN] 0008-5472
  • [Journal-full-title] Cancer research
  • [ISO-abbreviation] Cancer Res.
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CN / N01-CN-25101
  • [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 / Anticarcinogenic Agents; 0 / GW 501516; 0 / GW 7845; 0 / Oxazoles; 0 / PPAR delta; 0 / PPAR gamma; 0 / Thiazoles; 42HK56048U / Tyrosine
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6. Janát-Amsbury MM, Yockman JW, Lee M, Kern S, Furgeson DY, Bikram M, Kim SW: Combination of local, nonviral IL12 gene therapy and systemic paclitaxel treatment in a metastatic breast cancer model. Mol Ther; 2004 Jun;9(6):829-36
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  • [Title] Combination of local, nonviral IL12 gene therapy and systemic paclitaxel treatment in a metastatic breast cancer model.
  • We combined our IL12 gene delivery with systemic paclitaxel chemotherapy as a treatment for paclitaxel (PCT)-resistant 4T1 subcutaneous mouse mammary carcinomas and PCT-sensitive, immunogenic/nonimmunogenic tumors.
  • We mixed PCT with either a biodegradable polymeric solubilizer, HySolv, or Cremophor EL for bimonthly systemic treatments and injected water-soluble lipopolymer (WSLP)/p2CMVmIL-12 (plasmid encoding IL12 gene) complexes locally every week.
  • In parallel experiments we also demonstrated additive responses for tumor growth and number of lung metastases within other PCT-sensitive mammary tumor models using this combination strategy.
  • Our combination therapy provides evidence for the efficacy and feasibility of improved drug delivery systems.
  • Local cytokine gene delivery can augment local and systemic chemotherapy without placing the host at risk for further systemic toxicity.
  • [MeSH-major] Antineoplastic Agents, Phytogenic / therapeutic use. Carcinoma / therapy. Genetic Therapy / methods. Glycerol / analogs & derivatives. Interleukin-12 / genetics. Mammary Neoplasms, Experimental / therapy. Paclitaxel / therapeutic use. Polyethyleneimine / analogs & derivatives
  • [MeSH-minor] Animals. Cell Line, Tumor. Combined Modality Therapy / methods. Female. Lipids / therapeutic use. Lung Neoplasms / secondary. Lung Neoplasms / therapy. Mice. Mice, Inbred BALB C. Plasmids / genetics

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  • (PMID = 15194049.001).
  • [ISSN] 1525-0016
  • [Journal-full-title] Molecular therapy : the journal of the American Society of Gene Therapy
  • [ISO-abbreviation] Mol. Ther.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antineoplastic Agents, Phytogenic; 0 / Lipids; 0 / poly(ethylenimine)-co-(N-(2-aminoethyl) ethyleneimin)-co-N-(N-cholesteryloxycarbonyl-(2-aminoethyl)ethylenimine); 187348-17-0 / Interleukin-12; 6D4M1DAL6O / cremophor EL; 9002-98-6 / Polyethyleneimine; P88XT4IS4D / Paclitaxel; PDC6A3C0OX / Glycerol
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7. Brantley-Sieders DM, Zhuang G, Hicks D, Fang WB, Hwang Y, Cates JM, Coffman K, Jackson D, Bruckheimer E, Muraoka-Cook RS, Chen J: The receptor tyrosine kinase EphA2 promotes mammary adenocarcinoma tumorigenesis and metastatic progression in mice by amplifying ErbB2 signaling. J Clin Invest; 2008 Jan;118(1):64-78
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  • [Title] The receptor tyrosine kinase EphA2 promotes mammary adenocarcinoma tumorigenesis and metastatic progression in mice by amplifying ErbB2 signaling.
  • However, while EphA2 has been reported to enhance tumorigenesis, proliferation, and MAPK activation in several model systems, other studies suggest that EphA2 activation diminishes these processes and inhibits the activity of MAPK upon ligand stimulation.
  • In this study, we eliminated EphA2 expression in 2 transgenic mouse models of mammary carcinoma.
  • EphA2 deficiency impaired tumor initiation and metastatic progression in mice overexpressing ErbB2 (also known as Neu) in the mammary epithelium (MMTV-Neu mice), but not in mice overexpressing the polyomavirus middle T antigen in mammary epithelium (MMTV-PyV-mT mice).
  • Histologic and ex vivo analyses of MMTV-Neu mouse mammary epithelium indicated that EphA2 enhanced tumor proliferation and motility.
  • Biochemical analyses revealed that EphA2 formed a complex with ErbB2 in human and murine breast carcinoma cells, resulting in enhanced activation of Ras-MAPK signaling and RhoA GTPase.
  • Additionally, MMTV-Neu, but not MMTV-PyV-mT, tumors were sensitive to therapeutic inhibition of EphA2.
  • These data suggest that EphA2 cooperates with ErbB2 to promote tumor progression in mice and may provide a novel therapeutic target for ErbB2-dependent tumors in humans.
  • Moreover, EphA2 function in tumor progression appeared to depend on oncogene context, an important consideration for the application of therapies targeting EphA2.

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  • (PMID = 18079969.001).
  • [ISSN] 0021-9738
  • [Journal-full-title] The Journal of clinical investigation
  • [ISO-abbreviation] J. Clin. Invest.
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / CA95004; United States / NCI NIH HHS / CA / R01 CA095004; United States / NCI NIH HHS / CA / R01 CA114301; United States / NCI NIH HHS / CA / CA1179151-02; United States / NCI NIH HHS / CA / CA114301
  • [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 / Antigens, Polyomavirus Transforming; EC 2.7.10.1 / ERBB2 protein, human; EC 2.7.10.1 / Erbb2 protein, mouse; EC 2.7.10.1 / Receptor, EphA2; EC 2.7.10.1 / Receptor, ErbB-2; EC 3.6.5.2 / RhoA protein, mouse; EC 3.6.5.2 / rho GTP-Binding Proteins
  • [Other-IDs] NLM/ PMC2129239
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8. Wietrzyk J, Mazurkiewicz M, Madej J, Dzimira S, Grynkiewicz G, Radzikowski C, Opolski A: Genistein alone or combined with cyclophosphamide may stimulate 16/C transplantable mouse mammary cancer growth. Med Sci Monit; 2004 Nov;10(11):BR414-9
Hazardous Substances Data Bank. CYCLOPHOSPHAMIDE .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Genistein alone or combined with cyclophosphamide may stimulate 16/C transplantable mouse mammary cancer growth.
  • In this paper the in vivo effects of GEN applied either alone or together with cyclophosphamide on the growth of mouse transplantable mammary carcinoma (16/C) transplanted either orthotopically or ectopically is presented.
  • The growth of 16/C mouse mammary cancer transplanted subcutaneously (s.c.) or into the mammary gland (orthotopically-orth.) was stimulated by GEN administered from day 4 after tumor cell inoculation.
  • Such stimulation was not observed when the treatment with GEN was started at day 12 after cell inoculation.
  • In the case of subcutaneously growing tumors, treatment with GEN lowered (2-fold) the expression of both ER and PgR.
  • It seems rather reasonable to exclude breast and, perhaps, other hormone-dependent cancers from the treatment and chemoprevention with soy-derived phytoestrogens until its mechanism(s) of action on various cancer cells is completely understood.
  • [MeSH-major] Antineoplastic Agents / pharmacology. Carcinoma / pathology. Cyclophosphamide / pharmacology. Genistein / pharmacology. Mammary Neoplasms, Experimental / pathology
  • [MeSH-minor] Animals. Biological Assay. Cell Proliferation / drug effects. Female. Mice. Mice, Inbred C3H. Neoplasm Metastasis. Neoplasm Transplantation. Receptors, Estrogen / metabolism. Receptors, Progesterone / metabolism

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  • (PMID = 15507846.001).
  • [ISSN] 1234-1010
  • [Journal-full-title] Medical science monitor : international medical journal of experimental and clinical research
  • [ISO-abbreviation] Med. Sci. Monit.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Poland
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / Receptors, Estrogen; 0 / Receptors, Progesterone; 8N3DW7272P / Cyclophosphamide; DH2M523P0H / Genistein
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9. Zhang J, Sun Y, Liu Y, Sun Y, Liao DJ: Synergistic effects of androgen and estrogen on the mouse uterus and mammary gland. Oncol Rep; 2004 Oct;12(4):709-16
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Synergistic effects of androgen and estrogen on the mouse uterus and mammary gland.
  • We and other investigators have previously shown that estrogen and androgen are synergistic in the induction of mammary carcinogenesis in the Noble rat.
  • However, the mechanisms behind the synergy is unknown, and it is unclear whether such synergy is unique for the Noble rat and for the mammary gland.
  • Combined treatment with E2+DHT-B caused an even more severe hyperplasia of endometrial epithelium and myometrial muscle cells, compared with the treatment with each hormone alone.
  • Uterine leiomyomas were observed in 2 of 6 mice at 7 months of combined treatment but not in any of 6 or 7 mice receiving each single hormone.
  • DHT-B alone induced growth and secretion of mammary ductal cells, as well as growth of mammary stroma.
  • E2 alone stimulated much more pronounced growth of both ductal cells and alveolar cells and secretion of alveolar cells, but had no effect on mammary stroma.
  • Treatment with both E2 and DHT-B caused more severe hyperplasia of mammary ducts and alveoli, compared to the treatment with each hormone alone.
  • Intraductal hyperplasia occurred early and frequently in the E2+DHT-B- treated mice, but no mammary tumors were observed.
  • These results suggest that E2 and DHT-B have synergistic effects on the growth of uterine endometrial epithelium and myometrial muscle cells, as well as mammary epithelial ducts and alveoli.
  • [MeSH-major] Androgens / toxicity. Dihydrotestosterone / toxicity. Estradiol / toxicity. Leiomyoma / chemically induced. Mammary Neoplasms, Experimental / chemically induced. Uterine Neoplasms / chemically induced
  • [MeSH-minor] Animals. Carcinoma, Intraductal, Noninfiltrating / chemically induced. Carcinoma, Intraductal, Noninfiltrating / drug therapy. Carcinoma, Intraductal, Noninfiltrating / pathology. Cell Proliferation / drug effects. Drug Synergism. Endometrium / drug effects. Epithelium / drug effects. Female. Hyperplasia / chemically induced. Hyperplasia / drug therapy. Hyperplasia / pathology. Mammary Glands, Animal / drug effects. Mice. Mice, Inbred Strains. Muscle, Smooth / drug effects. Myometrium / drug effects. Stromal Cells / drug effects. Uterus / drug effects

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  • (PMID = 15375489.001).
  • [ISSN] 1021-335X
  • [Journal-full-title] Oncology reports
  • [ISO-abbreviation] Oncol. Rep.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Greece
  • [Chemical-registry-number] 0 / Androgens; 08J2K08A3Y / Dihydrotestosterone; 4TI98Z838E / Estradiol
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10. Kriukova IN, Lushnikova AA, Makhov PB: [Effect of 5-azacytidine on expression of DNA sequences homologous to ENV gene of murine mammary tumor virus in normal human lymphocytes]. Mol Gen Mikrobiol Virusol; 2002;(2):36-9
Hazardous Substances Data Bank. AZACITIDINE .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] [Effect of 5-azacytidine on expression of DNA sequences homologous to ENV gene of murine mammary tumor virus in normal human lymphocytes].
  • Expression of DNA sequences, related to MMTV env gene, in peripheral blood lymphocytes, which was strictly specific for human mammary carcinoma, has been previously reported.
  • In order to elucidate the possible routes of env MMTV-homologous sequences expression, we tried to induced it in donot T lymphocytes by various methods: hormone and virus treatment (related genome "saving" at the expense of the added virus envelope), T cell culturing with conA, interferon-2, and 5-azacytidine.
  • Indirect immunofluorescence with monospecific serum to MMTV gp52 detected gp52 analogous genes only in cultures with 5-azacytidine but not other agents.
  • Expression of these sequences in T cells, specific for human mammary carcinoma, can be due to demethylation of the promoter and induction of env-homologous sequences to the level of translation of gp52 analogous antigens or by initial location of some of the expressed sequences in the demethylated zone of the genome.
  • [MeSH-major] Azacitidine / pharmacology. Genes, env / drug effects. Mammary Tumor Virus, Mouse / genetics. T-Lymphocytes / drug effects
  • [MeSH-minor] Animals. Antigens, Viral, Tumor. Cells, Cultured. Female. Gene Expression / drug effects. Humans. Interferons / pharmacology. Male. Mammary Neoplasms, Experimental / drug therapy. Mammary Neoplasms, Experimental / genetics. Mice. Polymerase Chain Reaction. Sequence Homology, Nucleic Acid. Tumor Cells, Cultured

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  • (PMID = 12180024.001).
  • [ISSN] 0208-0613
  • [Journal-full-title] Molekuliarnaia genetika, mikrobiologiia i virusologiia
  • [ISO-abbreviation] Mol. Gen. Mikrobiol. Virusol.
  • [Language] rus
  • [Publication-type] English Abstract; Journal Article
  • [Publication-country] Russia
  • [Chemical-registry-number] 0 / Antigens, Viral, Tumor; 0 / glycoprotein 52 antigen, Mouse mammary tumor virus; 9008-11-1 / Interferons; M801H13NRU / Azacitidine
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11. Darro F, Decaestecker C, Gaussin JF, Mortier S, Van Ginckel R, Kiss R: Are syngeneic mouse tumor models still valuable experimental models in the field of anti-cancer drug discovery? Int J Oncol; 2005 Sep;27(3):607-16
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Are syngeneic mouse tumor models still valuable experimental models in the field of anti-cancer drug discovery?
  • To establish the pharmacological profile of a molecule with anti-cancer potential, it seems essential to add an in vivo approach to the first pharmacological experiments carried out in vitro.
  • We also used some of these models to investigate whether the molecular effects on the extent of growth in a subcutaneously grafted experimental model correlate with the effects of the same drug on the survival of the animals so grafted.
  • Our data show that all the molecules demonstrated significant anti-tumor activities in two mouse leukemia models (with some discrepancies between the two).
  • Two lymphoma models displayed weaker chemosensitivity profiles than the two leukemia models from which they were developed.
  • Two other models, namely the MXT-HS mammary carcinoma and the B16 melanoma, appeared to be rather chemoresistant.
  • However, a direct relationship was evident between the drug-induced decrease in the tumor growth rate and the increase observed in the survival periods of the MXT tumor-bearing mice.
  • Finally, our data indicated that we had developed a pair of metastasizing, as opposed to non-metastasizing, lymphoma and mammary carcinoma models.
  • In conclusion, the present study shows that syngeneic mouse tumor models can be used as valuable in vivo experimental models for the screening of potential anti-cancer agents.
  • [MeSH-major] Antineoplastic Agents / therapeutic use. Drug Screening Assays, Antitumor / methods. Neoplasms, Experimental / drug therapy
  • [MeSH-minor] Animals. Cell Line, Tumor. Female. Leukemia L1210 / drug therapy. Leukemia L1210 / pathology. Leukemia P388 / drug therapy. Leukemia P388 / pathology. Male. Mammary Neoplasms, Experimental / drug therapy. Mammary Neoplasms, Experimental / pathology. Melanoma, Experimental / drug therapy. Melanoma, Experimental / pathology. Mice. Mice, Inbred C57BL. Mice, Inbred DBA. Reproducibility of Results

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  • (PMID = 16077908.001).
  • [ISSN] 1019-6439
  • [Journal-full-title] International journal of oncology
  • [ISO-abbreviation] Int. J. Oncol.
  • [Language] eng
  • [Publication-type] Comparative Study; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Greece
  • [Chemical-registry-number] 0 / Antineoplastic Agents
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12. Mundy GR, Yoneda T, Hiraga T: Preclinical studies with zoledronic acid and other bisphosphonates: impact on the bone microenvironment. Semin Oncol; 2001 Apr;28(2 Suppl 6):35-44
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] Preclinical studies with zoledronic acid and other bisphosphonates: impact on the bone microenvironment.
  • Breast cancer cells and other tumor types influence osteoclastic bone resorption by increasing the number of osteoclasts and enhancing their resorptive activity.
  • A single 3 microg intravenous injection of zoledronic acid (Zometa; Novartis Pharmaceuticals Corp, East Hanover, NJ), a new highly potent bisphosphonate, prevented destruction of trabecular bone in an orthotopic mouse mammary tumor model.
  • Tumor volume in bone was decreased by zoledronic acid in a dose-dependent manner in the same model, and tumor cell apoptosis was increased by zoledronic acid in bone metastases in the 4T1 murine model of mammary carcinoma metastasis.
  • Zoledronic acid at a dose of 1.0 microg/d for 10 days also reduced bone lesion area in a nude mouse model with existing bone metastases.
  • [MeSH-major] Bone Neoplasms / drug therapy. Bone Neoplasms / secondary. Bone and Bones / drug effects. Diphosphonates / pharmacology. Imidazoles / pharmacology
  • [MeSH-minor] Animals. Drug Evaluation, Preclinical. Mammary Neoplasms, Experimental. Mice. Models, Animal. Neoplasm Metastasis / pathology. Rats

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  • (PMID = 11346863.001).
  • [ISSN] 0093-7754
  • [Journal-full-title] Seminars in oncology
  • [ISO-abbreviation] Semin. Oncol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't; Review
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Diphosphonates; 0 / Imidazoles; 6XC1PAD3KF / zoledronic acid
  • [Number-of-references] 75
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13. Bucking M, Gudgin Dickson EF, Farahani M, Fischer F, Holmes D, Jori G, Kennedy JC, Kenney ME, Peng X, Pottier RH, Weagle G: Quantification of the selective retention of palladium octabutoxynaphthalocyanine, a potential photothermal drug, in mouse tissues. J Photochem Photobiol B; 2000 Nov;58(2-3):87-93
Hazardous Substances Data Bank. PALLADIUM, ELEMENTAL .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Quantification of the selective retention of palladium octabutoxynaphthalocyanine, a potential photothermal drug, in mouse tissues.
  • Palladium octabutoxynaphthalocyanine (PdNc(OBu)8) is a potential photothermal therapy (PTT) agent, absorbing strongly in the near-infrared region with no ability to induce photodynamic-type sensitisation (unlike many related napthalocyanines).
  • We report here on the application of high pressure liquid chromatography (HPLC) with near-infrared absorption detection for the determination of the tissue accumulation and clearance of PdNc(OBu)8 in a tumour-bearing mouse model (Balb/c mice with EMT6 carcinoma tumour).
  • Due to its insolubility in aqueous-based solvents, the drug was delivered intraperitoneally in a Cremophor-containing vehicle.
  • Good selective accumulation of the drug into the tumour versus muscle or skin is observed, with the best combination of selectivity and tumour concentration occurring at 24-72 h after drug administration.
  • Clearance times are quite long.
  • Comparison with other similar drugs as reported in the literature indicates that the Cremophor-containing vehicle is likely in large part responsible for the observed pharmacokinetic behaviour.
  • This drug shows potential for PTT and will be investigated further for therapy in this animal model.
  • [MeSH-minor] Animals. Female. Indoles / pharmacokinetics. Mammary Neoplasms, Experimental / drug therapy. Mammary Neoplasms, Experimental / metabolism. Mice. Mice, Inbred BALB C. Photochemotherapy. Polyethylene Glycols. Tissue Distribution

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  • (PMID = 11233653.001).
  • [ISSN] 1011-1344
  • [Journal-full-title] Journal of photochemistry and photobiology. B, Biology
  • [ISO-abbreviation] J. Photochem. Photobiol. B, Biol.
  • [Language] eng
  • [Publication-type] Comparative Study; Journal Article
  • [Publication-country] Switzerland
  • [Chemical-registry-number] 0 / Indoles; 0 / Organometallic Compounds; 0 / Photosensitizing Agents; 0 / palladium 5,9,14,18,23,27,32,36-octabutoxynaphthalocyanine; 30IQX730WE / Polyethylene Glycols; 39279-69-1 / cremophor; 574-93-6 / phthalocyanine; 5TWQ1V240M / Palladium
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14. Kawashima E, Nakanishi Y, Terui Y, Tomitori H, Kashiwagi K, Ohba Y, Kamaike K: Synthesis and evaluation of 2-pyrrolepolyamide-2'-deoxyguanosine 5'-phosphate. Nucleic Acids Symp Ser (Oxf); 2007;(51):263-4

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • 2-Pyrrolepolyamide-2'-deoxyguanosine 5'-phosphate (hybrid 4) was synthesized and evaluated in terms of the inhibition of mouse mammary carcinoma FM3A cell growth.
  • Hybrid 4 exhibited the highest activity compared with the other hybrids (1, 2, and 3) and distamycin A.
  • [MeSH-minor] Animals. Carcinoma / drug therapy. Mammary Neoplasms, Experimental / drug therapy. Mice

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  • (PMID = 18029687.001).
  • [ISSN] 1746-8272
  • [Journal-full-title] Nucleic acids symposium series (2004)
  • [ISO-abbreviation] Nucleic Acids Symp Ser (Oxf)
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] England
  • [Chemical-registry-number] 0 / 2-pyrrolepolyamide-2'-deoxyguaonsine 5'-phosphate; 0 / Antineoplastic Agents; 0 / Pyrroles; 85-32-5 / Guanosine Monophosphate
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15. Masuelli L, Focaccetti C, Cereda V, Lista F, Vitolo D, Trono P, Gallo P, Amici A, Monaci P, Mattei M, Modesti M, Forni G, Kraus MH, Muraro R, Modesti A, Bei R: Gene-specific inhibition of breast carcinoma in BALB-neuT mice by active immunization with rat Neu or human ErbB receptors. Int J Oncol; 2007 Feb;30(2):381-92
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] Gene-specific inhibition of breast carcinoma in BALB-neuT mice by active immunization with rat Neu or human ErbB receptors.
  • Employing the transgenic BALB-neuT mouse tumor model, we explored the in vivo biologic relevance of immunocompetent epitopes shared among the four ErbB receptors.
  • Vaccination using rat LTR-Neu at the stage of atypical hyperplasia potently inhibited neu-mediated mammary tumorigenesis.
  • Relative increase in tumor-free survival and reduction in tumor incidence corresponded to structural similarity shared with the etiologic neu oncogene, as rat orthologue LTR-Neu proved most effective followed by the human homologue LTR-ErbB2 and the other three human ErbB receptors.
  • Our findings indicated that targeted inhibition of neu oncogene-mediated mammary carcinogenesis is conditional upon the immunization schedule and discrete immunogenic epitopes shared to a variable extent by different ErbB receptors.
  • [MeSH-major] Breast Neoplasms / drug therapy. Breast Neoplasms / genetics. Gene Expression Regulation, Neoplastic. Genes, erbB-2. Receptor, ErbB-2 / biosynthesis
  • [MeSH-minor] Animals. Apoptosis. Cancer Vaccines. Disease-Free Survival. Epitopes / chemistry. Humans. Lymphocytes, Tumor-Infiltrating / cytology. Mice. Mice, Inbred BALB C. Mice, Transgenic. NIH 3T3 Cells. Rats. Time Factors. Transgenes


16. Wietrzyk J, Opolski A, Madej J, Radzikowski C: The antitumor effect of postoperative treatment with genistein alone or combined with cyclophosphamide in mice bearing transplantable tumors. Acta Pol Pharm; 2000 Nov;57 Suppl:5-8
Hazardous Substances Data Bank. CYCLOPHOSPHAMIDE .

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  • [Title] The antitumor effect of postoperative treatment with genistein alone or combined with cyclophosphamide in mice bearing transplantable tumors.
  • In this paper we described the results of our studies on the antimetastatic activity of genistein alone or combined with cyclophosphamide (CY) in mice which before this treatment were exposed to surgical excision of the primary tumor.
  • Three transplantable subcutaneously growing mouse tumors were applied: Lewis lung cancer (LL2), B16F-10 melanoma and 16/C mammary cancer.
  • Twenty days after the surgery, an average of 52 lung tumor colonies per mouse were detected in control mice bearing LL2 cancer.
  • The treatment with genistein resulted in the reduction of the lung colonies to 24 per mouse.
  • The treatment with CY reduced the number of lung colonies to 12 (p < 0.05) and combined treatment with both agents to 4 (p < 0.05).
  • Two different protocols of the treatment with genistein were applied in 16/C mammary cancer model.
  • In the first one genistein was injected before and in the other after surgical excision of tumor.
  • [MeSH-major] Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Cyclophosphamide / administration & dosage. Genistein / therapeutic use. Neoplasms, Experimental / drug therapy
  • [MeSH-minor] Animals. Carcinoma, Lewis Lung / drug therapy. Male. Mammary Neoplasms, Experimental / drug therapy. Melanoma, Experimental / drug therapy. Mice. Mice, Inbred Strains. Neoplasm Transplantation

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  • (PMID = 11293263.001).
  • [ISSN] 0001-6837
  • [Journal-full-title] Acta poloniae pharmaceutica
  • [ISO-abbreviation] Acta Pol Pharm
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Poland
  • [Chemical-registry-number] 8N3DW7272P / Cyclophosphamide; DH2M523P0H / Genistein
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17. Francia G, Green SK, Bocci G, Man S, Emmenegger U, Ebos JM, Weinerman A, Shaked Y, Kerbel RS: Down-regulation of DNA mismatch repair proteins in human and murine tumor spheroids: implications for multicellular resistance to alkylating agents. Mol Cancer Ther; 2005 Oct;4(10):1484-94
Hazardous Substances Data Bank. AZACITIDINE .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • Similar to other anticancer agents, intrinsic or acquired resistance to DNA-damaging chemotherapeutics is a major obstacle for cancer therapy.
  • Current strategies aimed at overcoming this problem are mostly based on the premise that tumor cells acquire heritable genetic mutations that contribute to drug resistance.
  • Here, we present evidence for an epigenetic, tumor cell adhesion-mediated, and reversible form of drug resistance that is associated with a reduction of DNA mismatch repair proteins PMS2 and/or MLH1 as well as other members of this DNA repair process.
  • Growth of human breast cancer, human melanoma, and murine EMT-6 breast cancer cell lines as multicellular spheroids in vitro, which is associated with increased resistance to many chemotherapeutic drugs, including alkylating agents, is shown to lead to a reproducible down-regulation of PMS2, MLH1, or, in some cases, both as well as MHS6, MSH3, and MSH2.
  • The observed down-regulation is in part reversible by treatment of tumor spheroids with the DNA-demethylating agent, 5-azacytidine.
  • Thus, treatment of EMT-6 mouse mammary carcinoma spheroids with 5-azacytidine resulted in reduced and/or disrupted cell-cell adhesion, which in turn sensitized tumor spheroids to cisplatin-mediated killing in vitro.
  • [MeSH-major] Adenosine Triphosphatases / metabolism. Antineoplastic Agents, Alkylating / pharmacology. Carrier Proteins / metabolism. DNA Repair. DNA Repair Enzymes / metabolism. DNA-Binding Proteins / metabolism. Mammary Neoplasms, Experimental / drug therapy. Nuclear Proteins / metabolism
  • [MeSH-minor] Adaptor Proteins, Signal Transducing. Animals. Azacitidine / pharmacology. Base Pair Mismatch. Blotting, Western. Cell Line, Tumor. Cisplatin / pharmacology. DNA Methylation. Drug Resistance, Neoplasm. Humans. Hydroxamic Acids / pharmacology. Mice. Promoter Regions, Genetic. Spheroids, Cellular. Tumor Cells, Cultured

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  • (PMID = 16227397.001).
  • [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 / Adaptor Proteins, Signal Transducing; 0 / Antineoplastic Agents, Alkylating; 0 / Carrier Proteins; 0 / DNA-Binding Proteins; 0 / Hydroxamic Acids; 0 / MLH1 protein, human; 0 / Mlh1 protein, mouse; 0 / Nuclear Proteins; 3X2S926L3Z / trichostatin A; EC 3.6.1.- / Adenosine Triphosphatases; EC 3.6.1.- / PMS2 protein, human; EC 3.6.1.- / Pms2 protein, mouse; EC 6.5.1.- / DNA Repair Enzymes; M801H13NRU / Azacitidine; Q20Q21Q62J / Cisplatin
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18. Gali-Muhtasib H, Sidani M, Geara F, Mona AD, Al-Hmaira J, Haddadin MJ, Zaatari G: Quinoxaline 1,4-dioxides are novel angiogenesis inhibitors that potentiate antitumor effects of ionizing radiation. Int J Oncol; 2004 May;24(5):1121-31
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  • Clonogenic survival, Matrigel, and radiosensitization assays were performed in vitro and in vivo using Lewis lung carcinoma (LLC) and EMT-6 mammary adenocarcinoma cells.
  • Treatment with either drug inhibited HIF-1alpha and VEGF secretion, with DCQ being more potent than BPQ.
  • Using the C57BL/6 mouse model, combined treatment with DCQ and radiation delayed the growth of LLC tumors for 17 days and reduced mean tumor volume by 80% at day 20.
  • Histological analyses revealed a significant increase in tissue necrosis in tumors treated by DCQ and radiation.
  • These findings should stimulate further research in other tumor models as these compounds could have potential clinical applications in cancer therapy.
  • [MeSH-major] Adenocarcinoma / blood supply. Angiogenesis Inhibitors / therapeutic use. Carcinoma, Lewis Lung / blood supply. Mammary Neoplasms, Experimental / blood supply. Neovascularization, Pathologic / prevention & control. Quinoxalines / therapeutic use
  • [MeSH-minor] Animals. Blotting, Western. Cell Hypoxia / drug effects. Cell Survival / drug effects. Collagen / chemistry. Collagen / metabolism. Combined Modality Therapy. Drug Combinations. Female. Hypoxia-Inducible Factor 1, alpha Subunit. Laminin / chemistry. Laminin / metabolism. Mice. Mice, Inbred C57BL. Necrosis. Proteoglycans / chemistry. Proteoglycans / metabolism. Radiation Tolerance. Radiation, Ionizing. Radiation-Sensitizing Agents. Reverse Transcriptase Polymerase Chain Reaction. Transcription Factors / genetics. Transcription Factors / metabolism. Tumor Cells, Cultured. Tumor Stem Cell Assay. Vascular Endothelial Growth Factor A / genetics. Vascular Endothelial Growth Factor A / metabolism

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  • (PMID = 15067333.001).
  • [ISSN] 1019-6439
  • [Journal-full-title] International journal of oncology
  • [ISO-abbreviation] Int. J. Oncol.
  • [Language] eng
  • [Publication-type] Comparative Study; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Greece
  • [Chemical-registry-number] 0 / Angiogenesis Inhibitors; 0 / Drug Combinations; 0 / Hypoxia-Inducible Factor 1, alpha Subunit; 0 / Laminin; 0 / Proteoglycans; 0 / Quinoxalines; 0 / Radiation-Sensitizing Agents; 0 / Transcription Factors; 0 / Vascular Endothelial Growth Factor A; 119978-18-6 / matrigel; 9007-34-5 / Collagen; AMX8J6YS1H / quindoxin
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19. Bustuoabad OD, di Gianni PD, Franco M, Kordon EC, Vanzulli SI, Meiss RP, Grion LC, Díaz GS, Nosetto SH, Hockl P, Lombardi MG, Pasqualini CD, Ruggiero RA: Embryonal mass and hormone-associated effects of pregnancy inducing a differential growth of four murine tumors. Oncol Res; 2002;13(3):147-60
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  • On the other hand, one of two tumors bearing receptors for progesterone and estrogen [medroxyprogesterone (MPA)-induced mammary adenocarcinoma (C7HI)] exhibited three phases: up to days 8-10 of gestation the tumor grew faster than in virgins, between days 8-10 and 15 it reached a plateau, and beyond day 15 a sharp reduction in tumor mass was observed.
  • The other tumor [mouse mammary tumor virus (MMTV)-induced mammary carcinoma(T2280)] behaved as a typical pregnancy-dependent tumor (i.e., it grew in pregnant but not in virgin mice, regressed soon after delivery, and reassumed its growth at the middle of a second round of pregnancy).
  • On the other hand, MPA-treated mice enhanced C7HI tumor and reciprocally C7HI tumor-bearing mice treated with estrogen strongly inhibited tumor growth.
  • As for T2280, neither MPA nor estrogen alone could promote tumor growth and, in consequence, no tumor developed.
  • When the four tumors were implanted in mice bearing grafts of embryonal tissues (teratomas), all of them were inhibited.
  • On the other hand, with tumors bearing progesterone and estrogen receptors, differences in tumor growth were detected in pregnant and teratoma-bearing mice.
  • [MeSH-major] Hormones / physiology. Neoplasms, Experimental / drug therapy. Neoplasms, Experimental / physiopathology. Pregnancy Complications, Neoplastic / physiopathology
  • [MeSH-minor] Adenocarcinoma / drug therapy. Adenocarcinoma / pathology. Adenocarcinoma / physiopathology. Animals. Anti-Inflammatory Agents, Non-Steroidal / pharmacology. Cell Division / drug effects. Cell Division / physiology. Estrogens / pharmacology. Female. Fibrosarcoma / drug therapy. Fibrosarcoma / pathology. Fibrosarcoma / physiopathology. Indomethacin / pharmacology. Leukemia, Lymphoid / drug therapy. Leukemia, Lymphoid / pathology. Leukemia, Lymphoid / physiopathology. Male. Mammary Neoplasms, Experimental / drug therapy. Mammary Neoplasms, Experimental / pathology. Mammary Neoplasms, Experimental / physiopathology. Mice. Mice, Inbred BALB C. Neoplasm Transplantation. Neovascularization, Pathologic. Pregnancy. Progesterone / metabolism. Progesterone / pharmacology. Receptors, Progesterone / metabolism. Teratoma / pathology. Teratoma / physiopathology

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  • (PMID = 12549624.001).
  • [ISSN] 0965-0407
  • [Journal-full-title] Oncology research
  • [ISO-abbreviation] Oncol. Res.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Anti-Inflammatory Agents, Non-Steroidal; 0 / Estrogens; 0 / Hormones; 0 / Receptors, Progesterone; 4G7DS2Q64Y / Progesterone; XXE1CET956 / Indomethacin
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20. Wankhede M, Dedeugd C, Siemann DW, Sorg BS: In vivo functional differences in microvascular response of 4T1 and Caki-1 tumors after treatment with OXi4503. Oncol Rep; 2010 Mar;23(3):685-92
Hazardous Substances Data Bank. OXYGEN .

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  • [Title] In vivo functional differences in microvascular response of 4T1 and Caki-1 tumors after treatment with OXi4503.
  • 4T1 mouse mammary adenocarcinomas and Caki-1 human renal cell carcinomas grown in mouse dorsal window chambers were serially treated with the vascular disrupting agent (VDA) OXi4503 and their responses compared.
  • The real-time in vivo response was assessed using spectral imaging of microvascular hemoglobin saturation.
  • Previous research showing tumor size dependence in the treatment response to VDAs suggested that for the size of tumors used in this study only a moderate response would be observed; however, the tumors unexpectedly had very different responses to treatment.
  • Caki-1 tumors showed little permanent vessel damage and experienced transient vessel collapse with time-dependent oxygenation changes followed by recovery starting at 6 h after treatment.
  • Caki-1 tumors did not manifest necrotic avascular regions even after repeated treatments.
  • These results are consistent with those obtained using other imaging modalities and histology.
  • In contrast, similarly sized 4T1 tumors showed extensive vessel disintegration, minor vascular collapse, and a drop in tumor oxygenation up to 6 h post-treatment, after which reperfusion of collapsed vessels and extensive vascular remodeling and neovascularization of the tumor rim occurred from 8-48 h.
  • The differential responses of these two tumor-types suggest that further investigation of the mechanisms of action of VDAs and individual characterization of tumor VDA-responses may be needed for optimal clinical use of these agents.

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  • (PMID = 20127007.001).
  • [ISSN] 1791-2431
  • [Journal-full-title] Oncology reports
  • [ISO-abbreviation] Oncol. Rep.
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / CA084408-11; United States / NCI NIH HHS / CA / R01 CA084408; United States / NCI NIH HHS / CA / R01 CA084408-11
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Greece
  • [Chemical-registry-number] 0 / Diphosphates; 0 / Oxi 4503; 0 / Stilbenes; S88TT14065 / Oxygen
  • [Other-IDs] NLM/ NIHMS248113; NLM/ PMC2978044
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21. Di Francesco AM, Mayalarp SP, Kim S, Butler J, Lee M: Synthesis and biological evaluation of novel diaziridinylquinone-acridine conjugates. Anticancer Drugs; 2003 Sep;14(8):601-15
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  • The cytotoxicity of compounds 9-15 was examined using a MTT assay on several human cancer cell lines, including chronic myeloid leukemia K562, the non-small cell lung cancers H596 and H460, and colon carcinoma cells BE and HT29.
  • H460 and HT29 are rich in DT-diaphorase (DTD), and H596 and BE cells have negligible amounts of functional DTD.
  • Under continuous exposure of drugs, except to the non-aziridine compound 19b, the IC50 values of all other compounds were determined to be in the range of 0.3-11.3 nM.
  • When BDF1 mice with established mouse mammary carcinoma were treated with compound 10 (2 mg/kg at day 1 and 5 mg/kg at day 7), a significant delay (9-10 days) in cancer growth was recorded when compared to untreated controls.
  • [MeSH-minor] Animals. Cell Line, Tumor. Drug Screening Assays, Antitumor. Drug Stability. Humans. Inhibitory Concentration 50. Male. Mammary Neoplasms, Animal / drug therapy. Mice. Models, Molecular. NAD(P)H Dehydrogenase (Quinone) / chemistry

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  • (PMID = 14501382.001).
  • [ISSN] 0959-4973
  • [Journal-full-title] Anti-cancer drugs
  • [ISO-abbreviation] Anticancer Drugs
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't; Research Support, U.S. Gov't, Non-P.H.S.
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Acridines; 0 / Antineoplastic Agents; 0 / Aziridines; 0 / Benzoquinones; 526-62-5 / ethylenimine quinone; EC 1.6.5.2 / NAD(P)H Dehydrogenase (Quinone)
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22. Ciocca DR, Rozados VR, Cuello Carrión FD, Gervasoni SI, Matar P, Scharovsky OG: Hsp25 and Hsp70 in rodent tumors treated with doxorubicin and lovastatin. Cell Stress Chaperones; 2003;8(1):26-36
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • Heat shock protein 27 (Hsp27) and Hsp70 have been involved in resistance to anticancer drugs in human breast cancer cells growing in vitro and in vivo.
  • In this study, we examined the expression of Hsp25 (the rodent homologue to human Hsp27) and Hsp70 in 3 different rodent tumors (a mouse breast carcinoma, a rat sarcoma, and a rat lymphoma maintained by subcutaneous passages) treated in vivo with doxorubicin (DOX) and lovastatin (LOV).
  • All tumors showed massive cell death under control untreated conditions, and this massive death increased after cytotoxic drug administration.
  • The tumor type that was more resistant to cell death was the sarcoma, and this was found in sarcomas growing both under control conditions and after cytotoxic drug administration.
  • After drug treatment, only sarcoma tumor cells showed a significant increase in Hsp70.
  • In other words, sarcomas were the tumors with lower cell death, displayed a competent Hsp70 and Hsp25 response with nuclear translocation, and had the highest levels of Hsp25.
  • In sarcomas, Hsp25 and Hsp70 were found in viable tumor cells located around the blood vessels, and these areas showed the most resistant tumor cell phenotype after chemotherapy.
  • In conclusion, our study shows that each tumor type has unique features regarding the expression of Hsp25 and Hsp70 and that these proteins seem to be implicated in drug resistance mainly in sarcomas, making these model systems important to perform more mechanistic studies on the role of Hsps in resistance to certain cytotoxic drugs.
  • [MeSH-major] Adenocarcinoma / metabolism. Antineoplastic Combined Chemotherapy Protocols / pharmacology. Fibrosarcoma / metabolism. HSP70 Heat-Shock Proteins / biosynthesis. Heat-Shock Proteins. Mammary Neoplasms, Animal / metabolism. Neoplasm Proteins / biosynthesis
  • [MeSH-minor] Animals. Apoptosis. Doxorubicin / administration & dosage. Drug Resistance, Neoplasm. Endothelium, Vascular / metabolism. Female. HSP27 Heat-Shock Proteins. Lovastatin / administration & dosage. Lymphoma, B-Cell / metabolism. Lymphoma, B-Cell / pathology. Mice. Mice, Inbred Strains. Rats. Rats, Inbred Strains

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  • (PMID = 12820652.001).
  • [ISSN] 1355-8145
  • [Journal-full-title] Cell stress & chaperones
  • [ISO-abbreviation] Cell Stress Chaperones
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / HSP27 Heat-Shock Proteins; 0 / HSP70 Heat-Shock Proteins; 0 / Heat-Shock Proteins; 0 / Hspb1 protein, mouse; 0 / Hspb1 protein, rat; 0 / Neoplasm Proteins; 80168379AG / Doxorubicin; 9LHU78OQFD / Lovastatin
  • [Other-IDs] NLM/ PMC514851
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23. Prat A, Parker JS, Karginova O, Fan C, Livasy C, Herschkowitz JI, He X, Perou CM: Phenotypic and molecular characterization of the claudin-low intrinsic subtype of breast cancer. Breast Cancer Res; 2010;12(5):R68
The Lens. Cited by Patents in .

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  • METHODS: The clinical, pathological and biological features of claudin-low tumors were compared to the other tumor subtypes using an updated human tumor database and multiple independent data sets.
  • These main features of claudin-low tumors were also evaluated in a panel of breast cancer cell lines and genetically engineered mouse models.
  • They also have a response rate to standard preoperative chemotherapy that is intermediate between that of basal-like and luminal tumors.
  • Interestingly, we show that a group of highly utilized breast cancer cell lines, and several genetically engineered mouse models, express the claudin-low phenotype.
  • Finally, we confirm that a prognostically relevant differentiation hierarchy exists across all breast cancers in which the claudin-low subtype most closely resembles the mammary epithelial stem cell.

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  • (PMID = 20813035.001).
  • [ISSN] 1465-542X
  • [Journal-full-title] Breast cancer research : BCR
  • [ISO-abbreviation] Breast Cancer Res.
  • [Language] ENG
  • [Grant] United States / NIEHS NIH HHS / ES / P30 ES010126; United States / NCI NIH HHS / CA / P50-CA58223-09A1; United States / NCI NIH HHS / CA / R01 CA138255; United States / NCI NIH HHS / CN / N01-CN43308; United States / NCI NIH HHS / CA / P50 CA058223; United States / NCI NIH HHS / CA / R01-CA-138255
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Biomarkers, Tumor; 0 / Claudins; 0 / Receptors, Estrogen; 0 / Receptors, Progesterone; EC 2.7.10.1 / Receptor, Epidermal Growth Factor
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24. Mason KA, Hunter NR, Raju U, Ariga H, Husain A, Valdecanas D, Neal R, Ang KK, Milas L: Flavopiridol increases therapeutic ratio of radiotherapy by preferentially enhancing tumor radioresponse. Int J Radiat Oncol Biol Phys; 2004 Jul 15;59(4):1181-9
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  • [Title] Flavopiridol increases therapeutic ratio of radiotherapy by preferentially enhancing tumor radioresponse.
  • PURPOSE: Recently we reported that inhibition of cyclin-dependent kinases (cdks) by flavopiridol enhanced the radiation response of murine ovarian carcinoma cells in culture.
  • The purpose of this investigation was to extend these studies to in vivo tumor models and test whether flavopiridol increases the therapeutic ratio of radiotherapy.
  • METHODS AND MATERIALS: Three transplantable syngeneic mouse tumors were used: mammary carcinoma (MCa-29), ovarian carcinoma (OCa-I), and a lymphoma (Ly-TH).
  • Tumor treatment endpoints included growth delay, cure, and spontaneous lung metastases (OCa-I tumor).
  • The normal tissue endpoint was survival of jejunal crypt cells quantified microscopically.
  • Combined therapy flavopiridol treatments were initiated either several days before or shortly after the start of single dose or daily fractionated radiotherapy.
  • Two of the tumors (MCa-29 and Ly-TH) responded in a schedule-dependent manner with larger radiation enhancement factors when flavopiridol treatment was started a few hours after irradiation (radioenhancement factors [EF] Ly-TH = 2.04, EF MCa-29 = 1.50 for single dose irradiation).
  • When combined with fractionated irradiation (2.6 Gy daily for 10 or 20 days), flavopiridol enhanced the response of the MCa-29 tumor by a factor of 1.25-1.46.
  • A fractional radiation dose of 6 Gy in combination with flavopiridol produced a 62.5% cure rate compared with 25% tumor cure for radiation alone.
  • CONCLUSIONS: Therapeutic gain was achieved when flavopiridol treatment was initiated either before or after the start of radiotherapy.
  • Flavopiridol shows promising clinical potential administered alone or in combination with other cytotoxic agents, including both chemotherapy and radiotherapy.
  • [MeSH-major] Antineoplastic Agents / therapeutic use. Cyclin-Dependent Kinases / antagonists & inhibitors. Flavonoids / therapeutic use. Lung Neoplasms / drug therapy. Ovarian Neoplasms / radiotherapy. Piperidines / therapeutic use. Radiation-Sensitizing Agents / therapeutic use
  • [MeSH-minor] Animals. Cell Line, Tumor. Dose Fractionation. Drug Screening Assays, Antitumor. Enzyme Inhibitors. Female. Jejunum / pathology. Jejunum / radiation effects. Mice. Mice, Inbred C3H

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  • (PMID = 15234054.001).
  • [ISSN] 0360-3016
  • [Journal-full-title] International journal of radiation oncology, biology, physics
  • [ISO-abbreviation] Int. J. Radiat. Oncol. Biol. Phys.
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / CA 06294; United States / NCI NIH HHS / CA / CA 16672
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't; Research Support, U.S. Gov't, P.H.S.
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / Enzyme Inhibitors; 0 / Flavonoids; 0 / Piperidines; 0 / Radiation-Sensitizing Agents; 45AD6X575G / alvocidib; EC 2.7.11.22 / Cyclin-Dependent Kinases
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25. Lynn KD, Udugamasooriya DG, Roland CL, Castrillon DH, Kodadek TJ, Brekken RA: GU81, a VEGFR2 antagonist peptoid, enhances the anti-tumor activity of doxorubicin in the murine MMTV-PyMT transgenic model of breast cancer. BMC Cancer; 2010 Jul 30;10:397
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  • Anti-VEGF therapy is a clinically proven strategy for the treatment of a variety of cancers including colon, breast, lung, and renal cell carcinoma.
  • Since VEGFR2 is the dominant angiogenic signaling receptor, it has become an important target in the development of novel anti-angiogenic therapies.
  • METHODS: In the current study, we utilize a derivative of GU40C4, termed GU81 in therapy studies.
  • Single agent therapy (doxorubicin or GU81 alone) had no effect on tumor weight, histology, tumor fat content, or tumor growth index.
  • GU81 used in combination with doxorubicin significantly reduced tumor weight and growth index compared to all other treatment groups.
  • Furthermore, treatment with combination therapy significantly arrested tumor progression at the premalignant stage, resulting in increased tumor fat content.
  • Interestingly, treatment with GU81 alone increased tumor-VEGF levels and macrophage infiltration, an effect that was abrogated when used in combination with doxorubicin.

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  • (PMID = 20673348.001).
  • [ISSN] 1471-2407
  • [Journal-full-title] BMC cancer
  • [ISO-abbreviation] BMC Cancer
  • [Language] ENG
  • [Grant] United States / NCRR NIH HHS / RR / K26RR024196; United States / NHLBI NIH HHS / HV / N01-HV-28185
  • [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 / Antineoplastic Agents; 0 / GU 81 compound; 0 / Peptides; 0 / Peptoids; 0 / Vascular Endothelial Growth Factor A; 80168379AG / Doxorubicin; EC 2.7.10.1 / Vascular Endothelial Growth Factor Receptor-2
  • [Other-IDs] NLM/ PMC2920882
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26. Choudhuri T, Pal S, Das T, Sa G: Curcumin selectively induces apoptosis in deregulated cyclin D1-expressed cells at G2 phase of cell cycle in a p53-dependent manner. J Biol Chem; 2005 May 20;280(20):20059-68
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  • In asynchronous cultures, with time-lapse video-micrography in combination with quantitative fluorescence microscopy, we have demonstrated that curcumin induces apoptosis at G(2) phase of cell cycle in deregulated cyclin D1-expressed mammary epithelial carcinoma cells, leaving its normal counterpart unaffected.
  • In our search toward delineating the molecular mechanisms behind such differential activities of curcumin, we found that it selectively increases p53 expression at G(2) phase of carcinoma cells and releases cytochrome c from mitochondria, which is an essential requirement for apoptosis.
  • Further experiments using p53-null as well as dominant-negative and wild-type p53-transfected cells have established that curcumin induces apoptosis in carcinoma cells via a p53-dependent pathway.
  • On the other hand, curcumin reversibly inhibits normal mammary epithelial cell cycle progression by down-regulating cyclin D1 expression and blocking its association with Cdk4/Cdk6 as well as by inhibiting phosphorylation and inactivation of retinoblastoma protein.
  • Interestingly, these processes remain unaffected by curcumin in carcinoma cells where cyclin D1 expression is high.
  • These observations together suggest that curcumin may have a possible therapeutic potential in breast cancer patients.
  • [MeSH-major] Apoptosis / drug effects. Curcumin / pharmacology. Cyclin D1 / metabolism. G2 Phase / drug effects. Tumor Suppressor Protein p53 / metabolism
  • [MeSH-minor] Animals. Antineoplastic Agents / pharmacology. Breast / cytology. Breast / drug effects. Breast / metabolism. Breast Neoplasms / drug therapy. Breast Neoplasms / metabolism. Breast Neoplasms / pathology. Cell Cycle Proteins / metabolism. Cell Line. Cell Line, Tumor. Cyclin-Dependent Kinase Inhibitor p21. Epithelial Cells / cytology. Epithelial Cells / drug effects. Epithelial Cells / metabolism. Female. Humans. Mice. Mice, Knockout. Microscopy, Fluorescence. Microscopy, Video. NIH 3T3 Cells

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  • (PMID = 15738001.001).
  • [ISSN] 0021-9258
  • [Journal-full-title] The Journal of biological chemistry
  • [ISO-abbreviation] J. Biol. Chem.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / CDKN1A protein, human; 0 / Cdkn1a protein, mouse; 0 / Cell Cycle Proteins; 0 / Cyclin-Dependent Kinase Inhibitor p21; 0 / Tumor Suppressor Protein p53; 136601-57-5 / Cyclin D1; IT942ZTH98 / Curcumin
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27. Ueda Y, Yamagishi T, Ikeya H, Hirayama N, Itokawa T, Aozuka Y, Samata K, Nakaike S, Tanaka M, Ono M, Saiki I: VGA1155, a novel binding antagonist of VEGF, inhibits angiogenesis in vitro and in vivo. Anticancer Res; 2004 Sep-Oct;24(5A):3009-17
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  • Since vascular endothelial growth factor (VEGF) plays a pivotal role in tumor angiogenesis, it is reasonable to expect that antagonizing VEGF binding to its receptor may be effective in cancer therapy.
  • On the other hand, VGA 1155 did not affect the proliferation of human epidermoid carcinoma (KB) cells and mouse mammary carcinoma (MM2) cells.
  • [MeSH-major] Angiogenesis Inhibitors / pharmacology. Benzoates / pharmacology. Endothelium, Vascular / drug effects. Melanoma, Experimental / blood supply. Neovascularization, Pathologic / drug therapy. Vascular Endothelial Growth Factor A / antagonists & inhibitors

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  • (PMID = 15517909.001).
  • [ISSN] 0250-7005
  • [Journal-full-title] Anticancer research
  • [ISO-abbreviation] Anticancer Res.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Greece
  • [Chemical-registry-number] 0 / Angiogenesis Inhibitors; 0 / Benzoates; 0 / VGA1155; 0 / Vascular Endothelial Growth Factor A; VC2W18DGKR / Thymidine
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28. Katano M: Hedgehog signaling pathway as a therapeutic target in breast cancer. Cancer Lett; 2005 Sep 28;227(2):99-104
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  • [Title] Hedgehog signaling pathway as a therapeutic target in breast cancer.
  • The Hedgehog (Hh) signaling pathway, which is well conserved even in mammals and other vertebrate species, has long been known to direct growth and patterning during embryonic development.
  • It has been shown that the Hh pathway also plays a critical role in mouse normal mammary gland development.
  • In addition, it has been reported that breast carcinoma cells have disruption of these genes.
  • These findings strongly indicate a contribution of the Hh pathway to development of human breast carcinoma.
  • In fact, constitutive activation of the Hh pathway was found in most of 52 surgically resected breast carcinoma specimens.
  • Interestingly, exposure to cyclopamine, a steroidal alkaroid that blocks the Hh pathway, suppressed the growth of the Hh pathway-activated breast carcinoma cells.
  • Thus, the Hh pathway may function in progression of breast carcinoma.
  • In this short review, possibilities of the Hh pathway as a new therapeutic target in breast carcinoma will be mainly discussed.
  • [MeSH-major] Breast Neoplasms / therapy. Receptors, Cell Surface / metabolism. Signal Transduction / drug effects. Trans-Activators / metabolism. Veratrum Alkaloids / pharmacology

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  • (PMID = 16112412.001).
  • [ISSN] 0304-3835
  • [Journal-full-title] Cancer letters
  • [ISO-abbreviation] Cancer Lett.
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] Ireland
  • [Chemical-registry-number] 0 / Receptors, Cell Surface; 0 / Trans-Activators; 0 / Veratrum Alkaloids; 0 / patched receptors; ZH658AJ192 / cyclopamine
  • [Number-of-references] 43
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29. Kralova J, Synytsya A, Pouckova P, Koc M, Dvorak M, Kral V: Novel porphyrin conjugates with a potent photodynamic antitumor effect: differential efficacy of mono- and bis-beta-cyclodextrin derivatives in vitro and in vivo. Photochem Photobiol; 2006 Mar-Apr;82(2):432-8
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  • In the present study we investigated the photosensitizing properties of two novel mono- and bis-cyclodextrin tetrakis (pentafluorophenyl) porphyrin derivatives in several tumor cell lines and in BALB/c mice bearing subcutaneously transplanted syngeneic mouse mammary carcinoma 4T1.
  • In 4T1 and other cell lines both apoptotic and necrotic modes of cell death occurred depending on drug and light doses.
  • Thus, P(beta-CD)2 represents a new photosensitizing drug displaying fast and selective tumor uptake, strong antitumor activity and fast elimination from the body.
  • [MeSH-major] Antineoplastic Agents / pharmacology. Photosensitizing Agents / pharmacology. Porphyrins / pharmacology. Skin / drug effects. beta-Cyclodextrins / pharmacology
  • [MeSH-minor] Animals. Cell Death / drug effects. Cell Death / radiation effects. Dermatitis, Phototoxic / drug therapy. Humans. Lysosomes / pathology. Mice. Mice, Inbred BALB C. Time Factors. Tumor Cells, Cultured

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  • (PMID = 16613522.001).
  • [ISSN] 0031-8655
  • [Journal-full-title] Photochemistry and photobiology
  • [ISO-abbreviation] Photochem. Photobiol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / Photosensitizing Agents; 0 / Porphyrins; 0 / beta-Cyclodextrins
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30. Campbell MJ, Esserman LJ, Zhou Y, Shoemaker M, Lobo M, Borman E, Baehner F, Kumar AS, Adduci K, Marx C, Petricoin EF, Liotta LA, Winters M, Benz S, Benz CC: Breast cancer growth prevention by statins. Cancer Res; 2006 Sep 1;66(17):8707-14
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  • Statins are cholesterol-lowering drugs with pleiotropic activities including inhibition of isoprenylation reactions and reduction of signals driving cell proliferation and survival responses.
  • We also examined the in vivo effect of statin administration in a mouse ErbB2(+) breast cancer model.
  • Key intermediates regulating cell survival by NF-kappaB activation, as well as cell proliferation by the mitogen activated protein kinase cascade, were among the earliest phosphoproteins influenced by statin treatment.
  • These early effects were followed by declines in activator protein-1 and NF-kappaB activation and concordant changes in other mediators of proliferation and apoptosis.
  • In vivo results showed that oral dosing of statins significantly inhibited the growth of a mouse mammary carcinoma.
  • [MeSH-major] Antineoplastic Agents / pharmacology. Breast Neoplasms / drug therapy. Breast Neoplasms / pathology. Cell Division / drug effects. Hydroxymethylglutaryl-CoA Reductase Inhibitors / pharmacology
  • [MeSH-minor] Cell Line, Tumor. DNA, Neoplasm / chemistry. DNA, Neoplasm / drug effects. Female. Humans. NF-kappa B / metabolism. Nucleic Acid Conformation






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