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1. Hinz AK, Wang Y, Smerdon MJ: Base excision repair in a glucocorticoid response element: effect of glucocorticoid receptor binding. J Biol Chem; 2010 Sep 10;285(37):28683-90
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  • Five substrates were designed, each containing a unique C-->U substitution within the mouse mammary tumor virus promoter, one located within each GRE half-site and the others located outside the GRE.

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  • (PMID = 20628060.001).
  • [ISSN] 1083-351X
  • [Journal-full-title] The Journal of biological chemistry
  • [ISO-abbreviation] J. Biol. Chem.
  • [Language] ENG
  • [Grant] United States / NIEHS NIH HHS / ES / R01 ES004106; United States / NIEHS NIH HHS / ES / ES004106
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / DNA, Viral; 0 / Receptors, Glucocorticoid; EC 2.7.7.- / DNA Polymerase beta; EC 3.2.2.- / Uracil-DNA Glycosidase; EC 4.2.99.18 / APEX1 protein, human; EC 4.2.99.18 / Apex1 protein, mouse; EC 4.2.99.18 / DNA-(Apurinic or Apyrimidinic Site) Lyase
  • [Other-IDs] NLM/ PMC2937895
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2. Khalid S, Hwang D, Babichev Y, Kolli R, Altamentova S, Koren S, Goodwin PJ, Ennis M, Pollak M, Sonenberg N, Fantus IG: Evidence for a tumor promoting effect of high-fat diet independent of insulin resistance in HER2/Neu mammary carcinogenesis. Breast Cancer Res Treat; 2010 Aug;122(3):647-59
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  • [Title] Evidence for a tumor promoting effect of high-fat diet independent of insulin resistance in HER2/Neu mammary carcinogenesis.
  • To investigate this mice over-expressing HER2/Neu in the mammary gland (MMTV-HER2/Neu) were fed either a high-fat diet (45% of calories) (HFD) or low-fat diet (10%) (LFD) from 4 weeks of age and followed for up to 1 year, or sacrificed when a mammary tumor reached 1.5 cm.
  • Mild glucose intolerance was observed from 3 months of age on HFD, but insulin levels were not elevated.
  • While the time of onset of a first tumor and tumor growth rates were not altered, mice on HFD had an earlier onset of a second tumor and a twofold greater incidence (LFD 25%, HFD 54%) and a greater absolute number of multiple tumors (tumors/mouse, LFD 1.5 +/- 0.25 vs. HFD 2.7 +/- 0.23, P < 0.01).
  • Similarly, there was no difference in basal or maximum insulin-stimulated phosphorylation of IRS-1/2, Akt/PKB, or p70 S6K in tumor cell lysates from HFD and LFD groups.
  • Immunohistochemistry revealed no difference in tumor tissue staining for the proliferative marker, Ki67, between diets.
  • These data indicate that HFD, in the absence of significant insulin resistance, mediates a tumor promoting, but not a tumor growth effect in this model of mammary carcinogenesis.
  • [MeSH-major] Dietary Fats / administration & dosage. Insulin Resistance. Mammary Neoplasms, Experimental / metabolism. Mammary Tumor Virus, Mouse / physiology. Receptor, ErbB-2 / metabolism


3. Fox KE, Colton LA, Erickson PF, Friedman JE, Cha HC, Keller P, MacDougald OA, Klemm DJ: Regulation of cyclin D1 and Wnt10b gene expression by cAMP-responsive element-binding protein during early adipogenesis involves differential promoter methylation. J Biol Chem; 2008 Dec 12;283(50):35096-105
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  • Here we tested the impact of CREB on expression of cyclin D1 and wingless-related mouse mammary tumor virus integration site 10b (Wnt10b) in 3T3-L1 cells.
  • Chromatin immunoprecipitation revealed CREB bound to the Wnt10b promoter in untreated preadipocytes but not following treatment with Bt(2)cAMP.

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  • (PMID = 18957421.001).
  • [ISSN] 0021-9258
  • [Journal-full-title] The Journal of biological chemistry
  • [ISO-abbreviation] J. Biol. Chem.
  • [Language] ENG
  • [Grant] United States / NIDDK NIH HHS / DK / DK053969; United States / NIDDK NIH HHS / DK / DK51563
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Wnt Proteins; 0 / Wnt10b protein, mouse; 136601-57-5 / Cyclin D1; EC 2.3.1.48 / CREB-Binding Protein
  • [Other-IDs] NLM/ PMC2596384
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4. Rose AA, Siegel PM: Breast cancer-derived factors facilitate osteolytic bone metastasis. Bull Cancer; 2006 Sep;93(9):931-43
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  • Skeletal metastases resulting from breast cancer are most often osteolytic, and contribute to the morbidity and mortality associated with this disease.
  • To accomplish this task, animal model systems have been generated to study the process of breast cancer metastasis to bone.
  • These include: intraosseous injection that models tumor growth in the bone marrow, cardiac injections that permit cancer cell dissemination to the bone marrow from the bloodstream, and spontaneous bone metastasis originating from the mammary gland.
  • Importantly, these various model systems have been combined with gene expression profiling to compare breast cancer populations with distinct bone metastatic potentials in the hopes of finding the genes that facilitate this process.
  • In this review we will address new developments that underscore the importance of secreted proteins and cell surface receptors expressed on breast cancer cells that play key roles in promoting bone resorption and tumor growth.
  • [MeSH-major] Bone Neoplasms / secondary. Breast Neoplasms. Membrane Proteins / physiology. Neoplasm Proteins / physiology
  • [MeSH-minor] Adaptation, Physiological. Animals. Bone Development / physiology. Bone Resorption / etiology. Cell Adhesion. Cell Communication / physiology. Cell Line, Tumor / metabolism. Female. Gene Expression. Gene Expression Profiling. Humans. Mice. Neoplasm Metastasis / pathology. Neoplasm Metastasis / physiopathology. Osteoblasts / physiology. Osteoclasts / physiology. Osteolysis / etiology


5. Laust AK, Sur BW, Wang K, Hubby B, Smith JF, Nelson EL: VRP immunotherapy targeting neu: treatment efficacy and evidence for immunoediting in a stringent rat mammary tumor model. Breast Cancer Res Treat; 2007 Dec;106(3):371-82
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  • [Title] VRP immunotherapy targeting neu: treatment efficacy and evidence for immunoediting in a stringent rat mammary tumor model.
  • The ability to overcome intrinsic tolerance to a strict "self" tumor-associated antigen (TAA) and successfully treat pre-existing tumor is the most stringent test for anti-tumor immunotherapeutic strategies.
  • Although this capacity has been demonstrated in various models using complicated strategies that may not be readily translated into the clinical arena, straightforward antigen-specific immunotherapeutic strategies in the most stringent models of common epithelial cancers have largely failed to meet this standard.
  • We employed an immunotherapeutic strategy using an alphavirus-based, virus-like replicon particle (VRP), which has in vivo tropism for dendritic cells, to elicit immune responses to the non-mutated TAA rat neu in an aggressive rat mammary tumor model.
  • Using this VRP-based immunotherapeutic strategy targeting a single TAA, we generated effective anti-tumor immunity in the setting of pre-existing tumor resulting in the cure of 36% of rats over multiple experiments, P = 0.002.
  • We also observed down-regulation of rat neu expression in tumors that showed initial responses followed by tumor escape with resumption of rapid tumor growth.
  • These responses were accompanied by significant anti-tumor proliferative responses and CD8+ cellular tumor infiltrates, all of which were restricted to animals receiving the anti-neu immunotherapy.
  • Together these data, obtained in a stringent "self" TAA model, indicate that the VRP-based antigen-specific immunotherapy elicits sufficiently potent immune responses to exert immunologic pressure, selection, and editing of the growing tumors, thus supporting the activity of this straightforward immunotherapy and suggesting that it is a promising platform upon which to build even more potent strategies.
  • [MeSH-major] Antigens, Neoplasm / immunology. Encephalitis Virus, Venezuelan Equine / genetics. Immunotherapy / methods. Mammary Neoplasms, Experimental / therapy. Replicon / immunology

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  • (PMID = 17351745.001).
  • [ISSN] 0167-6806
  • [Journal-full-title] Breast cancer research and treatment
  • [ISO-abbreviation] Breast Cancer Res. Treat.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Netherlands
  • [Chemical-registry-number] 0 / Antigens, Neoplasm; 0 / Histocompatibility Antigens Class I
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6. Yasmeen A, Bismar TA, Dekhil H, Ricciardi R, Kassab A, Gambacorti-Passerini C, Al Moustafa AE: ErbB-2 receptor cooperates with E6/E7 oncoproteins of HPV type 16 in breast tumorigenesis. Cell Cycle; 2007 Dec 1;6(23):2939-43
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  • In order to investigate the effect of ErbB-2/E6/E7 cooperation in breast carcinogenesis, we generated double transgenic mice carrying ErbB-2 and E6/E7 of HPV type 16 under mouse mammary tumor virus (MMTV) and human keratin 14 promoters, respectively.
  • Histological analysis of ErbB-2/E6/E7 transgenic mice tumors showed the presence of invasive breast carcinomas.
  • However, the breast tissues from ErbB-2 and E6/E7 transgenic mice showed only in-situ cancer and normal mammary phenotype, respectively.
  • [MeSH-major] Breast Neoplasms / virology. Human papillomavirus 16 / pathogenicity. Oncogene Proteins, Viral / physiology. Papillomavirus E7 Proteins / physiology. Receptor, ErbB-2 / physiology. Repressor Proteins / physiology. beta Catenin / metabolism

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  • (PMID = 18156804.001).
  • [ISSN] 1551-4005
  • [Journal-full-title] Cell cycle (Georgetown, Tex.)
  • [ISO-abbreviation] Cell Cycle
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / E6 protein, Human papillomavirus type 16; 0 / Oncogene Proteins, Viral; 0 / Papillomavirus E7 Proteins; 0 / Repressor Proteins; 0 / beta Catenin; EC 2.7.10.1 / Receptor, ErbB-2
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7. Mortara L, Castellani P, Meazza R, Tosi G, De Lerma Barbaro A, Procopio FA, Comes A, Zardi L, Ferrini S, Accolla RS: CIITA-induced MHC class II expression in mammary adenocarcinoma leads to a Th1 polarization of the tumor microenvironment, tumor rejection, and specific antitumor memory. Clin Cancer Res; 2006 Jun 1;12(11 Pt 1):3435-43
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  • [Title] CIITA-induced MHC class II expression in mammary adenocarcinoma leads to a Th1 polarization of the tumor microenvironment, tumor rejection, and specific antitumor memory.
  • In this study, we explored the immunologic basis of tumor rejection and the correlation between histopathology of tumor tissue and immune rejection.
  • In vivo cell depletion, immunohistochemistry of tumor tissues, and immune functional assays were done to assess the cellular and immunologic basis of rejection.
  • RESULTS: Ninety-two percent of mice injected with TS/A-CIITA rejected the tumor and were completely resistant to challenge with parental TS/A.
  • The tumor microenvironment in TS/A-CIITA-injected mice changed dramatically when compared with the TS/A parental-injected mice.
  • Tumor-specific CD4+ T cells of TS/A-CIITA-injected mice had the functional characteristics of Th1 cells and produced IFN-gamma and this was relevant for generation and maintenance of protective antitumor response, because IFN-gamma knockout mice were no longer rejecting TS/A-CIITA tumor cells.
  • CONCLUSION: CIITA-dependent MHC class II expression confers to TS/A tumor cells the capacity to act as a protective vaccine against the tumor by triggering tumor antigen presentation to T helper cells, antitumor polarization of cellular and soluble components of the tumor microenvironment, and establishment of antitumor immune memory.
  • [MeSH-major] Adenocarcinoma / immunology. Graft Rejection / immunology. Histocompatibility Antigens Class II / biosynthesis. Immunologic Memory / immunology. Mammary Neoplasms, Animal / immunology. Nuclear Proteins / immunology. Th1 Cells / immunology. Trans-Activators / immunology
  • [MeSH-minor] Animals. CD4-Positive T-Lymphocytes / immunology. CD8-Positive T-Lymphocytes / immunology. Cell Line, Tumor. Cell Polarity / immunology. Disease Models, Animal. Female. Mice. Mice, Inbred BALB C. Mice, Knockout. Neoplasm Transplantation. Phenotype. Transgenes

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  • (PMID = 16740768.001).
  • [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 / Histocompatibility Antigens Class II; 0 / MHC class II transactivator protein; 0 / Nuclear Proteins; 0 / Trans-Activators
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8. McNamara E, Archer MC: Ezetimibe reverses the inhibitory effects of dietary cholesterol on mammary tumorigenesis in rats. Int J Cancer; 2010 Aug 15;127(4):791-5
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  • [Title] Ezetimibe reverses the inhibitory effects of dietary cholesterol on mammary tumorigenesis in rats.
  • Here we tested the hypothesis that ezetimibe will accelerate mammary tumorigenesis in rats.
  • Tumor multiplicity was significantly smaller in rats fed cholesterol than those fed no cholesterol (1.84 +/- 0.42 vs. 3.86 +/- 0.86 respectively, P < 0.05), but was significantly greater in the cholesterol/ezetimibe group than the group fed only cholesterol (3.48 +/- 0.59 vs. 1.84 +/- 0.42 respectively, P < 0.04).
  • The average weight of tumors/rat was also significantly larger in the cholesterol/ezetimibe group than those fed cholesterol alone (5.67 +/- 1.15 vs. 2.56 +/- 0.71 respectively, P < 0.04).
  • These results show that ezetimibe reverses the inhibitory effect of dietary cholesterol on the development of rat mammary tumors.
  • [MeSH-major] Anticholesteremic Agents / administration & dosage. Azetidines / administration & dosage. Cholesterol, Dietary / administration & dosage. Mammary Neoplasms, Experimental / prevention & control

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  • (PMID = 19957328.001).
  • [ISSN] 1097-0215
  • [Journal-full-title] International journal of cancer
  • [ISO-abbreviation] Int. J. Cancer
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Anticholesteremic Agents; 0 / Azetidines; 0 / Carcinogens; 0 / Cholesterol, Dietary; 684-93-5 / Methylnitrosourea; EOR26LQQ24 / Ezetimibe
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9. Shir A, Ogris M, Wagner E, Levitzki A: EGF receptor-targeted synthetic double-stranded RNA eliminates glioblastoma, breast cancer, and adenocarcinoma tumors in mice. PLoS Med; 2006 Jan;3(1):e6
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  • [Title] EGF receptor-targeted synthetic double-stranded RNA eliminates glioblastoma, breast cancer, and adenocarcinoma tumors in mice.
  • With the available treatments, survival does not exceed 12-14 mo from the time of diagnosis.
  • Expression of several cytokines and "bystander killing" of untransfected tumor cells was detected in vitro and in vivo.
  • Intra-tumoral delivery of the EGFR-targeted poly IC induced the complete regression of pre-established intracranial tumors in nude mice, with no obvious adverse toxic effects on normal brain tissue.
  • Similarly, non-viral delivery of poly IC completely eliminated pre-established breast cancer and adenocarcinoma xenografts derived from EGFR over-expressing cancer cell lines, suggesting that the strategy is applicable to other EGFR-over-expressing tumors.
  • CONCLUSION: The strategy described has yielded an effective treatment of EGFR over-expressing GBM in an animal model.
  • If this strategy is translated successfully to the clinical setting, it may actually offer help to GBM patients.
  • Moreover the elimination of two additional EGFR over-expressing cancers in vivo suggests that in principle this strategy can be applied to treat other tumors that over-express EGFR.
  • [MeSH-major] Adenocarcinoma / metabolism. Glioblastoma / metabolism. Mammary Neoplasms, Experimental / metabolism. Poly I-C / metabolism. RNA, Double-Stranded / metabolism. Receptor, Epidermal Growth Factor / metabolism. Transfection
  • [MeSH-minor] Animals. Apoptosis. Bystander Effect. Cell Line, Tumor. Epidermal Growth Factor / metabolism. Humans. Imines. Mice. Neoplasm Transplantation. Polyethylene Glycols. Polyethylenes. Time Factors. Transplantation, Heterologous. eIF-2 Kinase / metabolism

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  • (PMID = 16318410.001).
  • [ISSN] 1549-1676
  • [Journal-full-title] PLoS medicine
  • [ISO-abbreviation] PLoS Med.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Imines; 0 / Polyethylenes; 0 / RNA, Double-Stranded; 0 / poly(ethylene imine); 24939-03-5 / Poly I-C; 30IQX730WE / Polyethylene Glycols; 62229-50-9 / Epidermal Growth Factor; EC 2.7.10.1 / Receptor, Epidermal Growth Factor; EC 2.7.11.1 / eIF-2 Kinase
  • [Other-IDs] NLM/ PMC1298941
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10. Manhès C, Kayser C, Bertheau P, Kelder B, Kopchick JJ, Kelly PA, Touraine P, Goffin V: Local over-expression of prolactin in differentiating mouse mammary gland induces functional defects and benign lesions, but no carcinoma. J Endocrinol; 2006 Aug;190(2):271-85
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  • [Title] Local over-expression of prolactin in differentiating mouse mammary gland induces functional defects and benign lesions, but no carcinoma.
  • Experimental, clinical, and epidemiological data support the growth-promoting role of endocrine prolactin (PRL) in mammary tumors.
  • Recent transgenic (Tg) mouse models have revealed the pro-oncogenic effect of PRL over-expression in virgin mammary glands.
  • To address the question whether PRL tumorigenicity was maintained on differentiated mammary glands, we generated mammary-specific Tg mice expressing human (h)PRL under the control of the milk whey acidic protein promoter, which directs autocrine hPRL over-expression in late gestation throughout lactation.
  • Minimal levels of transgene expression were detected in the mammary glands of virgin animals, which at best induced partial ductal branching and lobulo-alveolar structures in older nulliparous females.
  • As expected, expression of mammary hPRL dramatically increased at the end of first pregnancy, and from this point it never returned to baseline, although it peaked at each gestation/lactation cycle.
  • Over-expression of hPRL that starts when the gland is already well into the differentiation process led to various morphological mammary alterations, including abnormally differentiated epithelium, atropy of the myoepithelial layer, dilated ducts, cysts, and lymphocytic infiltrates.
  • Although some older, multiparous females developed benign tumors (papillomas and metaplasias), none of the animals studied developed mammary carcinomas.
  • In summary, these data show that over-expression of autocrine hPRL in a differentiating mammary gland induces dramatic functional and morphological defects, but not carcinoma.
  • This deserves further investigations on the emerging concept that autocrine PRL may have different effects on pathological development of the mammary gland depending on the differentiation state of the latter.
  • [MeSH-major] Autocrine Communication. Lactation. Mammary Glands, Animal / metabolism. Mammary Neoplasms, Animal / metabolism. Prolactin / metabolism

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  • (PMID = 16899561.001).
  • [ISSN] 0022-0795
  • [Journal-full-title] The Journal of endocrinology
  • [ISO-abbreviation] J. Endocrinol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Milk Proteins; 0 / whey acidic proteins; 9002-62-4 / Prolactin
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11. Wang L, Liu R, Ribick M, Zheng P, Liu Y: FOXP3 as an X-linked tumor suppressor. Discov Med; 2010 Oct;10(53):322-8
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  • [Title] FOXP3 as an X-linked tumor suppressor.
  • Mice with heterozygous mutations of FoxP3 (mouse version of the FOXP3 gene) succumb to mammary tumors spontaneously, while those with prostate-specific deletions develop prostate intraepithelial neoplasia.
  • Unlike autosomal tumor suppressor genes that are usually inactivated by mutations in both alleles, X-linked FOXP3 mutations in cancer samples are usually heterozygous, with the wildtype allele selectively inactivated in cancer.
  • [MeSH-major] Forkhead Transcription Factors / physiology. Tumor Suppressor Proteins / physiology
  • [MeSH-minor] Animals. Breast Neoplasms / genetics. Breast Neoplasms / therapy. Carcinoma / genetics. Carcinoma / therapy. Female. Gene Silencing / physiology. Humans. Male. Mice. Models, Biological. Prostatic Neoplasms / genetics. Prostatic Neoplasms / therapy

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  • (PMID = 21034673.001).
  • [ISSN] 1944-7930
  • [Journal-full-title] Discovery medicine
  • [ISO-abbreviation] Discov Med
  • [Language] eng
  • [Grant] United States / NIGMS NIH HHS / GM / RC1 GM091648
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, U.S. Gov't, Non-P.H.S.; Review
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / FOXP3 protein, human; 0 / Forkhead Transcription Factors; 0 / Tumor Suppressor Proteins
  • [Other-IDs] NLM/ NIHMS536835; NLM/ PMC4500105
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12. O'Brien J, Schedin P: Macrophages in breast cancer: do involution macrophages account for the poor prognosis of pregnancy-associated breast cancer? J Mammary Gland Biol Neoplasia; 2009 Jun;14(2):145-57
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  • Macrophage influx is associated with negative outcomes for women with breast cancer and has been demonstrated to be required for metastasis of mammary tumors in mouse models.
  • Recently, post-pregnancy mammary involution has been characterized as having a wound healing signature.
  • We have proposed the involution-hypothesis, which states that the wound healing microenvironment of the involuting gland is tumor promotional.
  • Macrophage influx is one of the prominent features of the involuting gland, identifying the macrophage a potential instigator of tumor progression and a novel target for breast cancer treatment and prevention.

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  • (PMID = 19350209.001).
  • [ISSN] 1573-7039
  • [Journal-full-title] Journal of mammary gland biology and neoplasia
  • [ISO-abbreviation] J Mammary Gland Biol Neoplasia
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / BC / BC060531; United States / NCI NIH HHS / BC / BC073482
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't; Research Support, U.S. Gov't, P.H.S.; Review
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Extracellular Matrix Proteins; 0 / Neoplasm Proteins; EC 3.4.24.- / Matrix Metalloproteinases
  • [Number-of-references] 117
  • [Other-IDs] NLM/ PMC2693782
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13. Itano N, Kimata K: Altered hyaluronan biosynthesis in cancer progression. Semin Cancer Biol; 2008 Aug;18(4):268-74
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  • The discovery of hyaluronan synthase (HAS) genes, which encode the key enzymes in hyaluronan biosynthesis, has enabled great strides in understanding the mechanism underlying altered hyaluronan production in cancer and the involvement of this polysaccharide in tumor progression.
  • Recent studies using HAS transgenic mice have provided evidence that overproduction of hyaluronan in mammary tumors accelerates tumor growth through the recruitment of stromal cells and vasculature, revealing further insight into how increased hyaluronan influences the malignant behaviors of cancer cells.
  • [MeSH-major] Hyaluronic Acid / biosynthesis. Neoplasms / metabolism
  • [MeSH-minor] Animals. Disease Progression. Extracellular Matrix / metabolism. Extracellular Matrix / pathology. Glucuronosyltransferase / metabolism. Humans. Stromal Cells / metabolism. Stromal Cells / pathology

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  • (PMID = 18450474.001).
  • [ISSN] 1096-3650
  • [Journal-full-title] Seminars in cancer biology
  • [ISO-abbreviation] Semin. Cancer Biol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't; Review
  • [Publication-country] England
  • [Chemical-registry-number] 9004-61-9 / Hyaluronic Acid; EC 2.4.1.17 / Glucuronosyltransferase; EC 2.4.1.212 / hyaluronan synthase
  • [Number-of-references] 66
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14. Ma LH, Liu H, Xiong H, Chen B, Zhang XW, Wang YY, Le HY, Huang QH, Zhang QH, Li BL, Chen Z, Chen SJ: Aberrant transcriptional regulation of the MLL fusion partner EEN by AML1-ETO and its implication in leukemogenesis. Blood; 2007 Jan 15;109(2):769-77
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  • [MeSH-minor] Acute Disease. Animals. Cell Transformation, Neoplastic. HL-60 Cells. Humans. K562 Cells. Mammary Neoplasms, Animal. Mice. Mice, Nude. Neoplasm Transplantation. Reverse Transcriptase Polymerase Chain Reaction / methods. Sensitivity and Specificity. Transcription Factors / metabolism. U937 Cells

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  • (PMID = 16990610.001).
  • [ISSN] 0006-4971
  • [Journal-full-title] Blood
  • [ISO-abbreviation] Blood
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / AML1-ETO fusion protein, human; 0 / Core Binding Factor Alpha 2 Subunit; 0 / Intracellular Signaling Peptides and Proteins; 0 / Oncogene Proteins, Fusion; 0 / SH3GL1 protein, human; 0 / Transcription Factors; 149025-06-9 / Myeloid-Lymphoid Leukemia Protein
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15. Johal H, Faedo M, Faltas J, Lau A, Mousina R, Cozzi P, Defazio A, Rawlinson WD: DNA of mouse mammary tumor virus-like virus is present in human tumors influenced by hormones. J Med Virol; 2010 May;82(6):1044-50
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  • [Title] DNA of mouse mammary tumor virus-like virus is present in human tumors influenced by hormones.
  • Mouse mammary tumor virus (MMTV) is a hormonally regulated, oncogenic virus of mice.
  • MMTV-like virus DNA has previously been detected in human breast cancers, liver disease, and liver cancers.
  • It is hypothesized that local hormonal effects might be of primary importance in determining MMTV-like virus detection in human tumors.
  • Immunohistochemistry for estrogen receptor (ER-alpha) and progesterone receptor (PgR) was performed on a subset of tumors.
  • MMTV-like virus env DNA was detected in ovarian cancers (14/89; 16%), prostate cancers (53/147; 36%), endometrial cancers (5/50; 10%), skin cancers (13/141; 9%) but not in lung cancers (0/51).
  • Therefore, unlike the mouse model, the detection of MMTV-like env sequences in human cancers in addition to breast indicates that MMTV-like viral expression is not breast cancer-specific and may relate to hormone-dependent viral expression.
  • [MeSH-major] Hormones / pharmacology. Neoplasms / virology. Retroviridae / isolation & purification
  • [MeSH-minor] DNA, Viral / chemistry. DNA, Viral / genetics. Endometrial Neoplasms / pathology. Endometrial Neoplasms / virology. Estrogen Receptor alpha / analysis. Female. Humans. Immunohistochemistry. Lung Neoplasms / pathology. Lung Neoplasms / virology. Male. Mammary Tumor Virus, Mouse / genetics. Molecular Sequence Data. Ovarian Neoplasms / pathology. Ovarian Neoplasms / virology. Polymerase Chain Reaction. Prostatic Neoplasms / pathology. Prostatic Neoplasms / virology. Receptors, Progesterone / analysis. Skin Neoplasms / pathology. Skin Neoplasms / virology. Viral Envelope Proteins / genetics

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  • [Copyright] (c) 2010 Wiley-Liss, Inc.
  • (PMID = 20419820.001).
  • [ISSN] 1096-9071
  • [Journal-full-title] Journal of medical virology
  • [ISO-abbreviation] J. Med. Virol.
  • [Language] eng
  • [Databank-accession-numbers] GENBANK/ GU109493/ GU109494/ GU109495/ GU109496/ GU109497/ GU109498/ GU109499/ GU109500/ GU109501/ GU109502/ GU109503/ GU109504/ GU109505/ GU109506/ GU109507/ GU109508/ GU109509/ GU109510/ GU109511/ GU109512/ GU109513/ GU109514/ GU109515/ GU109516
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / DNA, Viral; 0 / Estrogen Receptor alpha; 0 / Hormones; 0 / Receptors, Progesterone; 0 / Viral Envelope Proteins
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16. You S, Zuo L, Li W: Optimizing the time of Doxil injection to increase the drug retention in transplanted murine mammary tumors. Int J Nanomedicine; 2010;5:221-9
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  • [Title] Optimizing the time of Doxil injection to increase the drug retention in transplanted murine mammary tumors.
  • Sex hormonal milieus during the female fertility cycle modulate the tumor vascular permeability of breast cancer.
  • It has been proposed that the liposomal formulated doxorubicin (ie, Doxil), given at the menstrual/estrous stage with the predicted highest tumor vascular permeability, allows significantly increased drug retention in the breast tumor.
  • In the current study, syngeneic murine 4T1 mammary tumors were established on the backs of female BALB/c mice and Doxil was administered at particular mouse estrous cycle stages.
  • The results indicated that Doxil administration during certain times in the mouse estrous cycle was crucial for drug retention in 4T1 tumor tissues.
  • Significantly higher drug concentrations were detected in the tumor tissues when Doxil was administered during the diestrus stage, as compared to when the drug injection was given at all other estrous stages.
  • Our study also showed that the tumor-bearing mice exhibited nearly normal rhythmicity of the estrous cycle post drug injection, indicating the feasibility of continual injection of Doxil at the same estrous cycle stage.
  • By using 4T1 cells cultured in vitro, we showed that progesterone (P4) significantly inhibited cell proliferation and the production of six tumor-derived cytokines, eg, sTNF-RI, CXCL-16, GM-CSF, MIP-1alpha, MIP-1gamma, and Flt3-L.
  • In this report, we demonstrated that the concentration of P4 in the plasma and/or estrous cycle stage of 4T1 tumor-bearing mice can be used to select the best time for administrating the liposomal anticancer drugs.
  • [MeSH-major] Doxorubicin / administration & dosage. Mammary Neoplasms, Experimental / drug therapy. Mammary Neoplasms, Experimental / metabolism

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  • (PMID = 20463938.001).
  • [ISSN] 1178-2013
  • [Journal-full-title] International journal of nanomedicine
  • [ISO-abbreviation] Int J Nanomedicine
  • [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] New Zealand
  • [Chemical-registry-number] 0 / Antibiotics, Antineoplastic; 80168379AG / Doxorubicin
  • [Other-IDs] NLM/ PMC2865017
  • [Keywords] NOTNLM ; Doxil / breast cancer therapy / menstrual cycle / mouse mammary tumor / progesterone
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17. Shanker A, Brooks AD, Tristan CA, Wine JW, Elliott PJ, Yagita H, Takeda K, Smyth MJ, Murphy WJ, Sayers TJ: Treating metastatic solid tumors with bortezomib and a tumor necrosis factor-related apoptosis-inducing ligand receptor agonist antibody. J Natl Cancer Inst; 2008 May 7;100(9):649-62
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  • [Title] Treating metastatic solid tumors with bortezomib and a tumor necrosis factor-related apoptosis-inducing ligand receptor agonist antibody.
  • BACKGROUND: Resistance of tumors to cell death signals poses a complex clinical problem.
  • We explored the therapeutic potential and in vivo toxicity of a combination of bortezomib, a proteasome inhibitor, and MD5-1, a tumor necrosis factor-related apoptosis-inducing ligand (TRAIL) receptor (DR5) agonist monoclonal antibody, in mouse carcinomas.
  • METHODS; Mice bearing Renca-FLAG (renal) or 4T1 (mammary) tumors were treated with bortezomib and/or MD5-1 and examined for lung metastases (Renca-FLAG: n = 93; 4T1: n = 40) or monitored for survival (Renca-FLAG: n = 143).
  • Sensitization involved activation of caspase-8 and caspase-3 but not mitochondrial membrane depolarization, suggesting an amplified signaling of the extrinsic cell death pathway.
  • Treatment with bortezomib and MD5-1 reduced lung metastases in mice carrying Renca and 4T1 tumors (mean number of metastases, bortezomib + MD5-1 vs MD5-1: Renca-FLAG, 1 vs 8, difference = 7, 95% CI = 5 to 9, P < .001; 4T1, 1 vs 12, difference = 11, 95% CI = 9 to 12, P < .001) and increased median survival of mice bearing Renca-FLAG tumors (bortezomib + MD5-1 vs bortezomib + control isotype antibody: 22 of 30 [73%] were still alive at day 180 vs median survival of 42 days [95% CI = 41 to 44 days, P < .001]) in the absence of obvious toxicity.
  • CONCLUSION: Bortezomib combined with DR5 agonist monoclonal antibody may be a useful treatment for metastatic solid tumors.

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  • (PMID = 18445820.001).
  • [ISSN] 1460-2105
  • [Journal-full-title] Journal of the National Cancer Institute
  • [ISO-abbreviation] J. Natl. Cancer Inst.
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CO / N01 CO012400; United States / NCI NIH HHS / CA / N01CO12400; United States / NCI NIH HHS / CO / N01-CO-12400; United States / Intramural NIH HHS / /
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, N.I.H., Intramural; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antibodies, Monoclonal; 0 / Antineoplastic Agents; 0 / Boronic Acids; 0 / Protease Inhibitors; 0 / Proto-Oncogene Proteins c-bcl-2; 0 / Pyrazines; 0 / Receptors, TNF-Related Apoptosis-Inducing Ligand; 0 / TNF-Related Apoptosis-Inducing Ligand; 69G8BD63PP / Bortezomib; EC 3.4.22.- / Caspase 3; EC 3.4.22.- / Caspase 8
  • [Other-IDs] NLM/ NIHMS118537; NLM/ PMC2753966
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18. Raafat A, Lawson S, Bargo S, Klauzinska M, Strizzi L, Goldhar AS, Buono K, Salomon D, Vonderhaar BK, Callahan R: Rbpj conditional knockout reveals distinct functions of Notch4/Int3 in mammary gland development and tumorigenesis. Oncogene; 2009 Jan 15;28(2):219-30
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  • [Title] Rbpj conditional knockout reveals distinct functions of Notch4/Int3 in mammary gland development and tumorigenesis.
  • Transgenic mice expressing the Notch 4 intracellular domain (ICD) (Int3) in the mammary gland have two phenotypes: arrest of mammary alveolar/lobular development and mammary tumorigenesis.
  • We have conditionally ablated the Rbpj gene in the mammary glands of mice expressing whey acidic protein (Wap)-Int3.
  • Interestingly, Rbpj knockout mice (Wap-Cre(+)/Rbpj(-/-)/Wap-Int3) have normal mammary gland development, suggesting that the effect of endogenous Notch signaling on mammary gland development is complete by day 15 of pregnancy.
  • RBP-J heterozygous (Wap-Cre(+)/Rbpj(-/+)/Wap-Int3) and Rbpj control (Rbpj(flox/flox)/Wap-Int3) mice are phenotypically the same as Wap-Int3 mice with respect to mammary gland development and tumorigenesis.
  • In addition, the Wap-Cre(+)/Rbpj(-/-)/Wap-Int3-knockout mice also developed mammary tumors at a frequency similar to Rbpj heterozygous and Wap-Int3 control mice but with a slightly longer latency.
  • Thus, the effect on mammary gland development is dependent on the interaction of the Notch ICD with the transcription repressor/activator Rbpj, and Notch-induced mammary tumor development is independent of this interaction.
  • [MeSH-major] Mammary Glands, Animal / embryology. Mammary Neoplasms, Experimental / genetics. Neoplasm Proteins / physiology. Proto-Oncogene Proteins / physiology. Receptors, Notch / physiology
  • [MeSH-minor] Adenocarcinoma, Papillary / genetics. Adenocarcinoma, Papillary / pathology. Agar. Animals. Basic Helix-Loop-Helix Transcription Factors / genetics. Basic Helix-Loop-Helix Transcription Factors / metabolism. Cell Cycle Proteins / metabolism. Cell Transformation, Viral / genetics. Female. Homeodomain Proteins / metabolism. Mammary Tumor Virus, Mouse / genetics. Mice. Mice, Knockout. Mice, Nude. Milk Proteins / genetics. Pregnancy. Protein Structure, Tertiary. Recombinant Fusion Proteins / physiology. Repressor Proteins / genetics. Terminal Repeat Sequences / genetics. Tumor Cells, Cultured / cytology

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  • (PMID = 18836481.001).
  • [ISSN] 1476-5594
  • [Journal-full-title] Oncogene
  • [ISO-abbreviation] Oncogene
  • [Language] eng
  • [Grant] United States / Intramural NIH HHS / / Z01 BC005148-28
  • [Publication-type] Journal Article; Research Support, N.I.H., Intramural
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Basic Helix-Loop-Helix Transcription Factors; 0 / Cell Cycle Proteins; 0 / Hes1 protein, mouse; 0 / Hey1 protein, mouse; 0 / Hey2 protein, mouse; 0 / Homeodomain Proteins; 0 / Milk Proteins; 0 / Neoplasm Proteins; 0 / Proto-Oncogene Proteins; 0 / Receptors, Notch; 0 / Recombinant Fusion Proteins; 0 / Repressor Proteins; 0 / whey acidic proteins; 146991-60-8 / Notch4 protein, mouse; 9002-18-0 / Agar
  • [Other-IDs] NLM/ NIHMS162074; NLM/ PMC2794555
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19. Toullec A, Gerald D, Despouy G, Bourachot B, Cardon M, Lefort S, Richardson M, Rigaill G, Parrini MC, Lucchesi C, Bellanger D, Stern MH, Dubois T, Sastre-Garau X, Delattre O, Vincent-Salomon A, Mechta-Grigoriou F: Oxidative stress promotes myofibroblast differentiation and tumour spreading. EMBO Mol Med; 2010 Jun;2(6):211-30
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  • In a model of mammary carcinogenesis, junD inactivation increased tumour incidence and revealed an associated reactive stroma. junD-inactivation in the stroma was sufficient to shorten tumour-free survival rate and enhance metastatic spread.
  • [MeSH-major] Breast Neoplasms / secondary. Fibroblasts / drug effects. Mammary Neoplasms, Animal / secondary. Neoplasm Metastasis / pathology. Oxidative Stress. Proto-Oncogene Proteins / deficiency. Reactive Oxygen Species / toxicity

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  • (PMID = 20535745.001).
  • [ISSN] 1757-4684
  • [Journal-full-title] EMBO molecular medicine
  • [ISO-abbreviation] EMBO Mol Med
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Chemokine CXCL12; 0 / Cxcl12 protein, mouse; 0 / Hif1a protein, mouse; 0 / Hypoxia-Inducible Factor 1, alpha Subunit; 0 / Proto-Oncogene Proteins; 0 / Proto-Oncogene Proteins c-jun; 0 / Reactive Oxygen Species; 0 / junD protein, mouse
  • [Other-IDs] NLM/ PMC3377319
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20. Zinser GM, Leonis MA, Toney K, Pathrose P, Thobe M, Kader SA, Peace BE, Beauman SR, Collins MH, Waltz SE: Mammary-specific Ron receptor overexpression induces highly metastatic mammary tumors associated with beta-catenin activation. Cancer Res; 2006 Dec 15;66(24):11967-74
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  • [Title] Mammary-specific Ron receptor overexpression induces highly metastatic mammary tumors associated with beta-catenin activation.
  • To define the significance of Ron overexpression and activation in vivo, we generated transgenic mice that overexpress a wild-type or constitutively active Ron receptor in the mammary epithelium.
  • In these animals, Ron expression is significantly elevated in mammary glands and leads to a hyperplastic phenotype by 12 weeks of age.
  • Ron overexpression is sufficient to induce mammary transformation in all transgenic animals and is associated with a high degree of metastasis, with metastatic foci detected in liver and lungs of >86% of all transgenic animals.
  • [MeSH-major] Gene Expression Regulation, Neoplastic. Mammary Neoplasms, Animal / genetics. Receptor Protein-Tyrosine Kinases / genetics
  • [MeSH-minor] Animals. Cloning, Molecular. Female. Humans. Hyperplasia. Mammary Glands, Animal / pathology. Mammary Glands, Animal / physiology. Mice. Mice, Transgenic. Neoplasm Metastasis


21. Wang YA, Shen K, Ishida Y, Wang Y, Kakizuka A, Brooks SC: Induction of murine leukemia and lymphoma by dominant negative retinoic acid receptor alpha. Mol Carcinog; 2005 Dec;44(4):252-61
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  • In an attempt to study the physiological role of retinoic acid in mammary gland development, we created a transgenic model system expressing a dominant negative RARalpha under the regulation of murine mammary tumor viral promoter.
  • We found that the transgene was also targeted to the lymphoid system in addition to mammary gland.
  • Retinoic acid blocked tumor development ex vivo through induction of apoptosis.
  • [MeSH-minor] Acute Disease. Animals. Apoptosis. Cell Proliferation. Female. Humans. Male. Mammary Tumor Virus, Mouse / genetics. Mice. Mice, Transgenic. Survival Rate. Tretinoin / pharmacology. Tumor Cells, Cultured

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  • (PMID = 16273555.001).
  • [ISSN] 0899-1987
  • [Journal-full-title] Molecular carcinogenesis
  • [ISO-abbreviation] Mol. Carcinog.
  • [Language] eng
  • [Grant] United States / NIEHS NIH HHS / ES / P30 ES06639; United States / NCI NIH HHS / CA / R01 CA89526
  • [Publication-type] Comparative Study; 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 / Receptors, Retinoic Acid; 0 / retinoic acid receptor alpha; 5688UTC01R / Tretinoin
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22. Que HF, Chen HF, Gao SP, Lu DM, Tang HJ, Jia XH, Xu JN: Effect of runing II on the growth and metastasis of transplanted tumor in mammary cancer-bearing mice and its mechanism. J Tradit Chin Med; 2008 Dec;28(4):293-8
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  • [Title] Effect of runing II on the growth and metastasis of transplanted tumor in mammary cancer-bearing mice and its mechanism.
  • OBJECTIVE: To study the effect of Runing II (a Chinese herbal preparation for mammary cancer) on the growth and metastasis of transplanted tumor of mammary cancer MA-891-bearing TA2 mice and its mechanism.
  • METHODS: The model of mammary cancer MA-891 cell strain transplanted tumor of TA2 mice with lung metastasis were developed to observe the effect of Runing II on the growth and metastasis of the transplanted tumor.
  • RESULTS: In the Runing II group, the tumor weight inhibition rate and the lung metastasis inhibition rate were 37.3% and 65.4% respectively, the tumor growth and lung metastasis were obviously inhibited; And the levels of VEGF and VEGFR, MVC and MVA were significantly decreased as compared with those in the tumor-bearing control group (P<0.05).
  • CONCLUSION: The Chinese herbal preparation Running II can inhibit the metastasis of tumor through inhibiting the angiogenesis, and the mechanism is possibly related with down-regulation of VEGF and VEGFR expression.

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  • (PMID = 19226903.001).
  • [ISSN] 0255-2922
  • [Journal-full-title] Journal of traditional Chinese medicine = Chung i tsa chih ying wen pan
  • [ISO-abbreviation] J Tradit Chin Med
  • [Language] ENG
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] China
  • [Chemical-registry-number] 0 / Drugs, Chinese Herbal; 0 / Vascular Endothelial Growth Factor A; EC 2.7.10.1 / Receptors, Vascular Endothelial Growth Factor
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23. Wang W, Mouneimne G, Sidani M, Wyckoff J, Chen X, Makris A, Goswami S, Bresnick AR, Condeelis JS: The activity status of cofilin is directly related to invasion, intravasation, and metastasis of mammary tumors. J Cell Biol; 2006 May 8;173(3):395-404
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  • [Title] The activity status of cofilin is directly related to invasion, intravasation, and metastasis of mammary tumors.
  • Previous studies have made opposite conclusions as to the role of LIMK1 in tumor cell motility and metastasis, claiming either an increase or decrease in cell motility and metastasis as a result of LIMK1 over expression (Zebda, N., O.
  • LIMK1-mediated decreases or increases in the activity of the cofilin pathway are shown to cause proportional decreases or increases in motility, intravasation, and metastasis of tumor cells.

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  • (PMID = 16651380.001).
  • [ISSN] 0021-9525
  • [Journal-full-title] The Journal of cell biology
  • [ISO-abbreviation] J. Cell Biol.
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / P01 CA100324; United States / NIGMS NIH HHS / GM / R01 GM038511; United States / NCI NIH HHS / CA / CA 100324; United States / NIGMS NIH HHS / GM / GM38511
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Cfl1 protein, rat; 0 / Cofilin 1; 0 / RNA, Small Interfering; 147336-22-9 / Green Fluorescent Proteins; 62229-50-9 / Epidermal Growth Factor; EC 2.7.- / Protein Kinases; EC 2.7.11.1 / Lim Kinases; EC 2.7.11.1 / Limk1 protein, rat
  • [Other-IDs] NLM/ PMC2063840
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24. Vicent GP, Ballaré C, Zaurin R, Saragüeta P, Beato M: Chromatin remodeling and control of cell proliferation by progestins via cross talk of progesterone receptor with the estrogen receptors and kinase signaling pathways. Ann N Y Acad Sci; 2006 Nov;1089:59-72
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  • Transcription from the mouse mammary tumor virus (MMTV) promoter can be induced by glucocorticoids or progestins.
  • In nucleosomes assembled on promoter sequences, SWI/SNF displaces histones H2A and H2B from MMTV nucleosome B, but not from other MMTV nucleosomes or from an rDNA promoter nucleosome.
  • [MeSH-major] Cell Proliferation / drug effects. Chromatin Assembly and Disassembly. Gene Expression Regulation. Mammary Tumor Virus, Mouse / drug effects. Progestins / pharmacology. Receptors, Estrogen / metabolism. Receptors, Progesterone / metabolism

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  • (PMID = 17261755.001).
  • [ISSN] 0077-8923
  • [Journal-full-title] Annals of the New York Academy of Sciences
  • [ISO-abbreviation] Ann. N. Y. Acad. Sci.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't; Review
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Progestins; 0 / Receptors, Estrogen; 0 / Receptors, Progesterone; EC 2.7.- / Protein Kinases
  • [Number-of-references] 39
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25. Eberhardt W, Kilz T, Akool el-S, Müller R, Pfeilschifter J: Dissociated glucocorticoids equipotently inhibit cytokine- and cAMP-induced matrix degrading proteases in rat mesangial cells. Biochem Pharmacol; 2005 Aug 1;70(3):433-45
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  • Along with these transrepressive activities RU 24858, RU 24782 and RU 40066 displayed similar transactivation potentials as indicated by induction of the glucocorticoid-inducible mouse mammary tumor virus (MMTV) reporter gene and by induced expression level of plasminogen activator inhibitor 1 (PAI-1).

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  • (PMID = 15963473.001).
  • [ISSN] 0006-2952
  • [Journal-full-title] Biochemical pharmacology
  • [ISO-abbreviation] Biochem. Pharmacol.
  • [Language] eng
  • [Publication-type] Comparative Study; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Cytokines; 0 / Glucocorticoids; 0 / Matrix Metalloproteinase Inhibitors; 0 / Protease Inhibitors; E0399OZS9N / Cyclic AMP; EC 3.4.24.- / Matrix Metalloproteinases
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26. Stakhiv TM, Mesia-Vela S, Kauffman FC: Phase II antioxidant enzyme activities in brain of male and female ACI rats treated chronically with estradiol. Brain Res; 2006 Aug 9;1104(1):80-91
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  • ACI rats were selected for study because this strain is highly responsive to treatment with low doses of E(2) as indexed by a high incidence of E(2)-induced mammary tumors compared to other strains.
  • This treatment increased activities of all four enzymes in the striatum of male but not female ACI rats.
  • Blood E(2) levels at time of sacrifice correlated closely with activities of striatal NQO1, GST, and SULT1A1, but not with striatal UGT.

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  • (PMID = 16822482.001).
  • [ISSN] 0006-8993
  • [Journal-full-title] Brain research
  • [ISO-abbreviation] Brain Res.
  • [Language] eng
  • [Grant] United States / NIEHS NIH HHS / ES / ES-05022; United States / NIEHS NIH HHS / ES / ES-07148
  • [Publication-type] Comparative Study; Journal Article; Research Support, N.I.H., Extramural
  • [Publication-country] Netherlands
  • [Chemical-registry-number] 4TI98Z838E / Estradiol; EC 1.6.5.2 / NAD(P)H Dehydrogenase (Quinone); EC 1.6.5.2 / NQO1 protein, rat; EC 2.4.1.17 / Glucuronosyltransferase; EC 2.5.1.18 / Glutathione Transferase; EC 2.8.2.1 / Arylsulfotransferase
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27. Wang X, Zhou YX, Qiao W, Tominaga Y, Ouchi M, Ouchi T, Deng CX: Overexpression of aurora kinase A in mouse mammary epithelium induces genetic instability preceding mammary tumor formation. Oncogene; 2006 Nov 16;25(54):7148-58
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  • [Title] Overexpression of aurora kinase A in mouse mammary epithelium induces genetic instability preceding mammary tumor formation.
  • Aurora-A/STK15/BTAK, which encodes a centrosome-associated kinase, is amplified and overexpressed in multiple types of human tumors, including breast cancer.
  • However, the causal relationship between overexpression of Aurora-A and tumorigenesis has not been fully established due to contradictory data obtained from different experimental systems.
  • We showed that all the MMTV-Aurora-A mice displayed enhanced branch morphogenesis in the mammary gland and about 40% developed mammary tumors at 20 months of age.
  • The tumor incidence was significantly increased in a p53(+/-) mutation background with about 70% MMTV-Aurora-A;p53(+/-) animals developed tumors at 18 months of age.
  • Of note, overexpression of Aurora-A led to genetic instability, characterized by centrosome amplification, chromosome tetraploidization and premature sister chromatid segregation, at stages prior to tumor formation.
  • Most notably, the severe chromosomal abnormality did not cause cell death owing to the activation of AKT pathway, including elevated levels of phosphorylated AKT and mammalian target of rapamycin, and nuclear accumulation of cyclin D1, which enabled continuous proliferation of the tetraploid cells.
  • [MeSH-major] Cell Transformation, Neoplastic / genetics. Epithelium / enzymology. Mammary Glands, Animal / enzymology. Mammary Neoplasms, Experimental / genetics. Protein-Serine-Threonine Kinases / biosynthesis
  • [MeSH-minor] Animals. Aurora Kinase A. Aurora Kinases. Blotting, Western. Chromosome Aberrations. Female. Humans. Immunohistochemistry. In Situ Nick-End Labeling. Mammary Tumor Virus, Mouse. Mice. Mice, Transgenic. Mutation. Oncogene Protein v-akt / metabolism. Reverse Transcriptase Polymerase Chain Reaction. Tumor Suppressor Protein p53 / genetics


28. Lu X, Kang Y: Organotropism of breast cancer metastasis. J Mammary Gland Biol Neoplasia; 2007 Sep;12(2-3):153-62
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  • Recent studies have confirmed earlier speculations that metastasis is a non-random process and is dependent on intricate tumor-stroma interactions at the target organ.
  • Advances in animal modeling, in vivo imaging and functional genomics have accelerated the discovery of important molecular mediators of organ-specific metastasis.
  • [MeSH-major] Breast Neoplasms / pathology. Neoplasm Metastasis
  • [MeSH-minor] Animals. Bone Neoplasms / metabolism. Bone Neoplasms / pathology. Bone Neoplasms / secondary. Humans. Lung Neoplasms / genetics. Lung Neoplasms / metabolism. Lung Neoplasms / pathology. Lung Neoplasms / secondary. Neoplastic Stem Cells / metabolism. Neoplastic Stem Cells / pathology. RANK Ligand / metabolism

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  • (PMID = 17566854.001).
  • [ISSN] 1083-3021
  • [Journal-full-title] Journal of mammary gland biology and neoplasia
  • [ISO-abbreviation] J Mammary Gland Biol Neoplasia
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't; Research Support, U.S. Gov't, Non-P.H.S.; Review
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / RANK Ligand
  • [Number-of-references] 68
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29. Zabuawala T, Taffany DA, Sharma SM, Merchant A, Adair B, Srinivasan R, Rosol TJ, Fernandez S, Huang K, Leone G, Ostrowski MC: An ets2-driven transcriptional program in tumor-associated macrophages promotes tumor metastasis. Cancer Res; 2010 Feb 15;70(4):1323-33
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  • [Title] An ets2-driven transcriptional program in tumor-associated macrophages promotes tumor metastasis.
  • Tumor-associated macrophages (TAM) are implicated in breast cancer metastasis, but relatively little is known about the underlying genes and pathways that are involved.
  • We conditionally deleted Ets in TAMs to determine its function at this level on mouse mammary tumor growth and metastasis.
  • Consistent with these results, Ets2 ablation in TAMs led to decreased angiogenesis and decreased growth of tumors.
  • In summary, we identified Ets2 as a central driver of a transcriptional program in TAMs that acts to promote lung metastasis of breast tumors.

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  • (PMID = 20145133.001).
  • [ISSN] 1538-7445
  • [Journal-full-title] Cancer research
  • [ISO-abbreviation] Cancer Res.
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / P01 CA097189-04; United States / NCI NIH HHS / CA / CA053271-17A1; United States / NCI NIH HHS / CA / CA097189-01A20003; United States / NCI NIH HHS / CA / CA097189-01A2; United States / NCI NIH HHS / CA / P01 CA097189; United States / NCI NIH HHS / CA / P01 CA097189-03; United States / NCI NIH HHS / CA / P01 CA097189-01A20003; United States / NCI NIH HHS / CA / CA097189-020003; United States / NCI NIH HHS / CA / CA097189-02; United States / NCI NIH HHS / CA / P01 CA097189-020003; United States / NCI NIH HHS / CA / CA097189-03; United States / NCI NIH HHS / CA / CA053271-18; United States / NCI NIH HHS / CA / R01 CA053271-18; United States / NCI NIH HHS / CA / CA097189-030003; United States / NCI NIH HHS / CA / P01 CA097189-040003; United States / NCI NIH HHS / CA / CA097189-050003; United States / NCI NIH HHS / CA / P01 CA097189-030003; United States / NCI NIH HHS / CA / CA097189-040003; United States / NCI NIH HHS / CA / CA097189-04; United States / NCI NIH HHS / CA / R01 CA053271-19; United States / NCI NIH HHS / CA / P01 CA097189-02; United States / NCI NIH HHS / CA / P01 CA097189-050003; United States / NCI NIH HHS / CA / CA053271-19; United States / NCI NIH HHS / CA / R01 CA053271-17A1; United States / NCI NIH HHS / CA / P01 CA097189-01A2; United States / NCI NIH HHS / CA / P01 CA097189-05; United States / NCI NIH HHS / CA / R01 CA053271
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Angiogenesis Inhibitors; 0 / Ets2 protein, mouse; 0 / Proto-Oncogene Protein c-ets-2
  • [Other-IDs] NLM/ NIHMS165052; NLM/ PMC2822898
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30. Pyter LM, Cochrane SF, Ouwenga RL, Patel PN, Pineros V, Prendergast BJ: Mammary tumors induce select cognitive impairments. Brain Behav Immun; 2010 Aug;24(6):903-7
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Mammary tumors induce select cognitive impairments.
  • In humans, various factors likely contribute to cancer-associated cognitive deficits including disease awareness and chemotherapy; however, the endogenous biological factors arising from tumor development may also play a causal role.
  • In the present study, rats with mammary tumors exhibited impaired spatial reference memory on a radial arm maze and amnesia for familiar objects in an object recognition memory test.
  • These select cognitive impairments were accompanied by elevations in hippocampal interleukin-1beta mRNA expression, but were not associated with decreases in hippocampal brain-derived neurotrophic factor gene expression.
  • Together the results indicate that peripheral tumors alone are sufficient to induce increases in hippocampal cytokine expression and select deficits in hippocampal-dependent memory tasks.

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  • [Copyright] Copyright 2010 Elsevier Inc. All rights reserved.
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  • (PMID = 20188817.001).
  • [ISSN] 1090-2139
  • [Journal-full-title] Brain, behavior, and immunity
  • [ISO-abbreviation] Brain Behav. Immun.
  • [Language] ENG
  • [Grant] United States / NIAID NIH HHS / AI / AI067406-01; United States / NIAID NIH HHS / AI / R01 AI067406; United States / NIAID NIH HHS / AI / AI-67406; United States / NIAID NIH HHS / AI / R01 AI067406-01
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
  • [Publication-country] Netherlands
  • [Chemical-registry-number] 0 / Brain-Derived Neurotrophic Factor; 0 / Cytokines; 0 / Intercellular Signaling Peptides and Proteins; 0 / Interleukin-1beta
  • [Other-IDs] NLM/ NIHMS190884; NLM/ PMC2902787
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31. Coombs GS, Covey TM, Virshup DM: Wnt signaling in development, disease and translational medicine. Curr Drug Targets; 2008 Jul;9(7):513-31
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Wnt signaling in development, disease and translational medicine.
  • Subsequently, the proto-oncogene INT-1 was identified in mice in 1984 when its activation by mouse mammary tumor virus' proviral insertion was found to induce tumor formation.

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  • (PMID = 18673238.001).
  • [ISSN] 1873-5592
  • [Journal-full-title] Current drug targets
  • [ISO-abbreviation] Curr Drug Targets
  • [Language] eng
  • [Publication-type] Historical Article; Journal Article; Review
  • [Publication-country] Netherlands
  • [Chemical-registry-number] 0 / Drosophila Proteins; 0 / Wnt Proteins; 0 / Wnt1 Protein; 0 / wg protein, Drosophila
  • [Number-of-references] 205
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32. Tan H, Zhong Y, Pan Z: Autocrine regulation of cell proliferation by estrogen receptor-alpha in estrogen receptor-alpha-positive breast cancer cell lines. BMC Cancer; 2009;9:31
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  • BACKGROUND: Estrogen receptor-alpha (ERalpha) is essential for mammary gland development and is a major oncogene in breast cancer.
  • Since ERalpha is not colocalized with the cell proliferation marker Ki-67 in the normal mammary glands and the majority of primary breast tumors, it is generally believed that paracrine regulation is involved in ERalpha mediated cell proliferation.
  • In a subpopulation of cancer cells in some primary breast tumors, however, ERalpha does colocalize with the cell proliferation marker Ki-67, suggesting an autocrine regulation by ERalpha in some primary breast tumors.
  • Unlike that in the normal mammary glands and the majority of primary breast tumors, ERalpha is highly expressed throughout the cell cycle in MCF-7 cells.
  • Inhibition of EGFR signaling does not inhibit the autocrine action of ERalpha.
  • All of the three ERalpha-positive cell lines used in our study showed colocalization of ERalpha and Ki-67, indicating that these cell lines might be originated from primary tumor cells with autocrine regulation.
  • [MeSH-major] Breast Neoplasms / metabolism. Breast Neoplasms / pathology. Cell Proliferation. Estrogen Receptor alpha / metabolism. Ki-67 Antigen / metabolism. Neoplasm Proteins / metabolism
  • [MeSH-minor] Autocrine Communication / physiology. Cell Cycle / drug effects. Cell Cycle / physiology. Cell Line, Tumor. Estradiol / analogs & derivatives. Estradiol / pharmacology. Estrogen Antagonists / pharmacology. Estrogens / pharmacology. Female. Fluorescent Antibody Technique / methods. Humans. Receptor, Epidermal Growth Factor / metabolism

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  • (PMID = 19171042.001).
  • [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 / Estrogen Antagonists; 0 / Estrogen Receptor alpha; 0 / Estrogens; 0 / Ki-67 Antigen; 0 / Neoplasm Proteins; 22X328QOC4 / fulvestrant; 4TI98Z838E / Estradiol; EC 2.7.10.1 / EGFR protein, human; EC 2.7.10.1 / Receptor, Epidermal Growth Factor
  • [Other-IDs] NLM/ PMC2636826
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33. Shafirstein G, Novák P, Moros EG, Siegel E, Hennings L, Kaufmann Y, Ferguson S, Myhill J, Swaney M, Spring P: Conductive interstitial thermal therapy device for surgical margin ablation: in vivo verification of a theoretical model. Int J Hyperthermia; 2007 Sep;23(6):477-92
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  • The female pig animal model was used to test the validity of the mathematical model.
  • Thus, it can be used to secure negative margins following the resection of a primary tumor, which could impede local recurrences in the treatment of local diseases such as early staged, non-metastatic, breast cancer.
  • [MeSH-major] Breast Neoplasms / surgery. Cautery / instrumentation. Equipment Design. Hyperthermia, Induced / instrumentation. Mammary Glands, Animal / surgery
  • [MeSH-minor] Animals. Disease Models, Animal. Female. Mastectomy, Segmental / methods. Models, Biological. Neoplasm Recurrence, Local / prevention & control. Neoplasm, Residual / surgery. Sus scrofa. Tetrazolium Salts. Thermal Conductivity

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  • (PMID = 17852514.001).
  • [ISSN] 0265-6736
  • [Journal-full-title] International journal of hyperthermia : the official journal of European Society for Hyperthermic Oncology, North American Hyperthermia Group
  • [ISO-abbreviation] Int J Hyperthermia
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / CA108678-01
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't; Validation Studies
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Tetrazolium Salts; 7OL20RET2I / triphenyltetrazolium
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34. Hickey J, Bartke A, Winters T, Henry N, Banz W: Effects of soy protein and soy phytochemicals on mammary tumor development in female transgenic mice overexpressing human pituitary growth hormone. J Med Food; 2005;8(4):556-9
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  • [Title] Effects of soy protein and soy phytochemicals on mammary tumor development in female transgenic mice overexpressing human pituitary growth hormone.
  • The objective of this study was to determine the effect of soy-based diets on mammary tumors in female cancer- prone mice.
  • Indices of tumor development were measured throughout the study.
  • Days from birth to first tumor were increased by 7% (P < .05), as was days on diet to first tumor by 5% (P < .05), in the LIS group when compared with the C group.
  • First-onset number of tumors was decreased (P = .02) by 41% and 34% in the LIS and C groups, respectively, when compared with the HIS group.
  • Final onset of tumors was decreased (P < .05) by 44% and 9% in the LIS and HIS groups, respectively, when compared with the C group.
  • Total area of final tumors was decreased (P < .05) by 30% in the LIS group when compared with the C group.
  • Taken cumulatively, these data suggest that a diet rich in soy protein may provide protective benefits regarding tumor development in female cancer-prone mice.
  • [MeSH-major] Gene Expression. Growth Hormone / genetics. Isoflavones / administration & dosage. Mammary Neoplasms, Experimental / prevention & control. Soybean Proteins / pharmacology. Soybeans / chemistry
  • [MeSH-minor] Animals. Diet. Female. Genetic Predisposition to Disease. Mice. Mice, Transgenic

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  • (PMID = 16379573.001).
  • [ISSN] 1096-620X
  • [Journal-full-title] Journal of medicinal food
  • [ISO-abbreviation] J Med Food
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Isoflavones; 0 / Soybean Proteins; 9002-72-6 / Growth Hormone
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35. Pylayeva Y, Guo W, Giancotti FG: Analysis of integrin signaling in genetically engineered mouse models of mammary tumor progression. Methods Enzymol; 2007;426:439-61
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  • [Title] Analysis of integrin signaling in genetically engineered mouse models of mammary tumor progression.
  • Cancer progression-the evolution of malignant tumors towards metastatic dissemination-is a complex, multistep process orchestrated by neoplastic cells but aided by elements of the tumor microenvironment such as macrophages, activated fibroblasts, and endothelial cells.
  • During tumor progression, cancer cells acquire a number of traits, such as the ability to undergo unrestrained proliferation, to resist pro-apoptotic insults, and to invade through tissue boundaries.
  • It is becoming increasingly clear that certain integrins and integrin-signaling components amplify oncogenic signaling to promote tumor progression.
  • Mouse models of cancer provide useful, if not necessary, experimental systems to study tumor initiation and progression in vivo and to test novel therapeutic approaches.
  • We have utilized mouse models of mammary tumorigenesis to examine the role of integrin alpha6beta4 signaling in tumor progression in vivo.
  • In this chapter, we describe a collection of cell biological and genetic methods that may aid in characterizing the roles of integrin signals in mammary tumorigenesis.
  • [MeSH-major] Genetic Engineering / methods. Integrins / physiology. Mammary Neoplasms, Animal / genetics. Mammary Neoplasms, Animal / pathology. Signal Transduction
  • [MeSH-minor] Animals. Disease Models, Animal. Disease Progression. Female. Immunohistochemistry. Mice. Neoplasms, Experimental / genetics. Neoplasms, Experimental / pathology

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  • (PMID = 17697895.001).
  • [ISSN] 0076-6879
  • [Journal-full-title] Methods in enzymology
  • [ISO-abbreviation] Meth. Enzymol.
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / P30 CA08748; United States / NCI NIH HHS / CA / R01 CA113996; United States / NCI NIH HHS / CA / R37 CA58976
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Review
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Integrins
  • [Number-of-references] 35
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36. Motoyama J, Yamashita N, Morino T, Tanaka M, Kobayashi T, Honda H: Hyperthermic treatment of DMBA-induced rat mammary cancer using magnetic nanoparticles. Biomagn Res Technol; 2008;6:2
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  • [Title] Hyperthermic treatment of DMBA-induced rat mammary cancer using magnetic nanoparticles.
  • In this study, the in vivo effect of hyperthermia mediated by MCLs was examined using 7,12-dimethylbenz(a)anthracene (DMBA)-induced rat mammary cancer as a spontaneous cancer model.
  • METHOD: MCLs were injected into the mammary cancer and then subjected to an AMF.
  • RESULTS: Four rats in 20 developed mammary tumors at more than 1 site in the body.
  • The first-developed tumor in each of these 4 rats was selected and heated to over 43 degrees C following administration of MCLs by an infusion pump.
  • After a series of 3 hyperthermia treatments, treated tumors in 3 of the 4 rats were well controlled over a 30-day observation period.
  • In this rat, there were 3 sites of tumor regrowth.

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  • (PMID = 18298831.001).
  • [ISSN] 1477-044X
  • [Journal-full-title] Biomagnetic research and technology
  • [ISO-abbreviation] Biomagn Res Technol
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] England
  • [Other-IDs] NLM/ PMC2266920
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37. Snedeker SM: Chemical exposures in the workplace: effect on breast cancer risk among women. AAOHN J; 2006 Jun;54(6):270-9; quiz 280-1
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  • Animal cancer bioassays conducted by the National Toxicology Program indicate more than 40 chemicals can induce mammary tumors, and most of these are still in production.
  • Although some chemical exposures are suspected to affect breast cancer risk, estimates of or actual exposures to these chemicals in the workplace often have not been determined.
  • [MeSH-major] Breast Neoplasms. Hazardous Substances / adverse effects. Occupational Exposure / adverse effects
  • [MeSH-minor] Age Distribution. Carcinogenicity Tests. Cocarcinogenesis. Epidemiologic Studies. Female. Genetic Predisposition to Disease / epidemiology. Health Education. Humans. Incidence. Life Style. Nurse's Role. Occupational Health. Occupational Health Nursing. Reproductive History. Risk Factors. Socioeconomic Factors. United States / epidemiology. Women's Health. Workplace

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  • (PMID = 16800404.001).
  • [ISSN] 0891-0162
  • [Journal-full-title] AAOHN journal : official journal of the American Association of Occupational Health Nurses
  • [ISO-abbreviation] AAOHN J
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Hazardous Substances
  • [Number-of-references] 79
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38. Toniti W, Buranasinsup S, Kongcharoen A, Charoonrut P, Puchadapirom P, Kasorndorkbua C: Immunohistochemical determination of estrogen and progesterone receptors in canine mammary tumors. Asian Pac J Cancer Prev; 2009;10(5):907-11
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  • [Title] Immunohistochemical determination of estrogen and progesterone receptors in canine mammary tumors.
  • Mammary gland tumors are by far the most commonly found tumors in domestic dogs.
  • Effective therapeutic procedures with prompt accurate diagnoses are of prime importance for this life threatening neoplasm.
  • Although immunohistochemical methods provide valuable information such as the location and semi-quantitative data of the interested antigens in particular tumors, conventional methods like histopathological diagnosis remain useful and necessary for identification and classification of tumors.
  • In the present study, we combined histopathology with immunohistochemical staining of estrogen receptors (ER) and progesterone receptors (PR) in canine mammary gland tumors.
  • Fifty dogs with primary mammary tumors underwent surgery at the Veterinary Teaching Hospital of Mahidol University during 2005 to 2007.
  • Twenty-one were diagnosed with benign tumors classified as adenomas and benign mixed mammary gland tumors.
  • PR positively stained, both PR and ER stained and ER stained tumors accounted for 19%, 19% and 5%, respectively.
  • Of the malignant tumors, eighty-six percent were adenocarcinomas and 14% were malignant mixed mammary gland tumors.
  • In summary, more than half of of our benign and malignant canine mammary tumors were negatively stained for ER and PR.
  • [MeSH-major] Adenocarcinoma / metabolism. Adenoma / metabolism. Carcinoma, Ductal, Breast / metabolism. Mammary Neoplasms, Experimental / metabolism. Receptors, Estrogen / metabolism. Receptors, Progesterone / metabolism
  • [MeSH-minor] Animals. Dogs. Female. Immunoenzyme Techniques. Mammary Glands, Animal / metabolism. Mammary Glands, Animal / pathology. Prospective Studies

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  • (PMID = 20104988.001).
  • [ISSN] 2476-762X
  • [Journal-full-title] Asian Pacific journal of cancer prevention : APJCP
  • [ISO-abbreviation] Asian Pac. J. Cancer Prev.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Thailand
  • [Chemical-registry-number] 0 / Receptors, Estrogen; 0 / Receptors, Progesterone
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39. Rajkumar L, Canada A, Esparza D, Collins K, Moreno E, Duong H: Decreasing hormonal promotion is key to breast cancer prevention. Endocrine; 2009 Apr;35(2):220-6
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  • We determined the effect of long-term hormonal promotion following the protective short-term estradiol and progesterone treatment that mimics parity protection against mammary tumors.
  • Mammary tumor incidence in all the short-term estradiol- plus progesterone-treated rats was significantly lower compared with controls.
  • Short-term hormone treatment followed by long-term promotion resulted in an increased mammary tumor incidence compared with animals that received only the short-term treatment.
  • Overall, the results demonstrate the importance of the promotional environment in mammary carcinogenesis indicating that the decreased promotional environment could be the reason for protection against mammary carcinogenesis.
  • [MeSH-major] Estradiol / administration & dosage. Mammary Neoplasms, Animal / prevention & control. Progesterone / administration & dosage

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  • (PMID = 19214806.001).
  • [ISSN] 1355-008X
  • [Journal-full-title] Endocrine
  • [ISO-abbreviation] Endocrine
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Carcinogens; 4G7DS2Q64Y / Progesterone; 4TI98Z838E / Estradiol; 684-93-5 / Methylnitrosourea
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40. Liu B, Ordonez-Ercan D, Fan Z, Huang X, Edgerton SM, Yang X, Thor AD: Estrogenic promotion of ErbB2 tyrosine kinase activity in mammary tumor cells requires activation of ErbB3 signaling. Mol Cancer Res; 2009 Nov;7(11):1882-92
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  • [Title] Estrogenic promotion of ErbB2 tyrosine kinase activity in mammary tumor cells requires activation of ErbB3 signaling.
  • Interactions were studied using mammary/breast cancer cell lines from wild-type rat c-neu gene transgenic mice and humans.
  • Estradiol promoted cell proliferation and activated erbB2/neu tyrosine kinase, Akt, and mitogen-activated protein kinase signaling exclusively in mammary and breast epithelial cell lines with coexpression of both erbB2 and erbB3.
  • [MeSH-major] Breast Neoplasms / enzymology. Estradiol / pharmacology. Mammary Neoplasms, Experimental / enzymology. Receptor, ErbB-2 / metabolism. Receptor, ErbB-3 / metabolism
  • [MeSH-minor] Animals. Cell Line, Tumor. Disease Models, Animal. Enzyme Activation. Female. Humans. Mice. Mice, Transgenic. Rats. Signal Transduction / drug effects


41. Peace BE, Toney-Earley K, Collins MH, Waltz SE: Ron receptor signaling augments mammary tumor formation and metastasis in a murine model of breast cancer. Cancer Res; 2005 Feb 15;65(4):1285-93
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  • [Title] Ron receptor signaling augments mammary tumor formation and metastasis in a murine model of breast cancer.
  • Mice with a targeted deletion of the Ron tyrosine kinase signaling domain (TK-/-) were crossed to mice expressing the polyoma virus middle T antigen (pMT) under the control of the mouse mammary tumor virus promoter.
  • Both pMT-expressing wild-type control (pMT+/- TK+/+) and pMT+/- TK-/- mice developed mammary tumors and lung metastases.
  • However, a significant decrease in mammary tumor initiation and growth was found in the pMT+/- TK-/- mice compared with controls.
  • An examination of mammary tumors showed that there was a significant decrease in microvessel density, significantly decreased cellular proliferation, and a significant increase in terminal deoxynucleotidyl transferase-mediated nick end labeling-positive staining in mammary tumor cells from the pMT+/- TK-/- mice compared with the pMT+/- TK+/+ mice.
  • Biochemical analyses on mammary tumor lysates showed that whereas both the pMT-expressing TK+/+ and TK-/- tumors have increased Ron expression compared with normal mammary glands, the pMT-expressing TK-/- tumors have deficits in mitogen-activated protein kinase and AKT activation.
  • These results indicate that Ron signaling synergizes with pMT signaling to induce mammary tumor formation, growth, and metastasis.

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  • (PMID = 15735014.001).
  • [ISSN] 0008-5472
  • [Journal-full-title] Cancer research
  • [ISO-abbreviation] Cancer Res.
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / R01 CA100002-04; United States / NCI NIH HHS / CA / CA100002-05; United States / NCI NIH HHS / CA / R01 CA100002-05; United States / NCI NIH HHS / CA / CA100002-02; United States / NICHD NIH HHS / HD / HD36888; United States / NCI NIH HHS / CA / CA100002-03; United States / NCI NIH HHS / CA / CA100002-01A1; United States / NCI NIH HHS / CA / R01 CA100002-01A1; United States / NHLBI NIH HHS / HL / T-32-HL07752; United States / NCI NIH HHS / CA / R01 CA100002-03; United States / NCI NIH HHS / CA / CA100002-04; United States / NCI NIH HHS / CA / R01 CA100002; United States / NCI NIH HHS / CA / CA100002; United States / NCI NIH HHS / CA / R01 CA100002-02
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't; Research Support, U.S. Gov't, Non-P.H.S.; Research Support, U.S. Gov't, P.H.S.
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Proto-Oncogene Proteins; EC 2.7.1.- / RON protein; EC 2.7.10.1 / Receptor Protein-Tyrosine Kinases; EC 2.7.11.1 / Protein-Serine-Threonine Kinases; EC 2.7.11.1 / Proto-Oncogene Proteins c-akt
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42. Vallejos M, Ramdohr P, Valiente-Echeverría F, Tapia K, Rodriguez FE, Lowy F, Huidobro-Toro JP, Dangerfield JA, López-Lastra M: The 5'-untranslated region of the mouse mammary tumor virus mRNA exhibits cap-independent translation initiation. Nucleic Acids Res; 2010 Jan;38(2):618-32
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  • [Title] The 5'-untranslated region of the mouse mammary tumor virus mRNA exhibits cap-independent translation initiation.
  • In this study, we demonstrate the identification of an internal ribosome entry site (IRES) within the 5'-untranslated region (5'-UTR) of the mouse mammary tumor virus (MMTV).
  • In vitro translational activity from the MMTV 5'-UTR was resistant to the addition of m(7)GpppG cap-analog and cleavage of eIF4G by foot-and-mouth disease virus (FMDV) L-protease.
  • [MeSH-major] 5' Untranslated Regions. Mammary Tumor Virus, Mouse / genetics. Peptide Chain Initiation, Translational. RNA, Viral / chemistry

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  • (PMID = 19889724.001).
  • [ISSN] 1362-4962
  • [Journal-full-title] Nucleic acids research
  • [ISO-abbreviation] Nucleic Acids Res.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / 5' Untranslated Regions; 0 / Nucleocytoplasmic Transport Proteins; 0 / RNA Caps; 0 / RNA, Messenger; 0 / RNA, Viral; 0 / rev Gene Products, Human Immunodeficiency Virus; 0 / rev protein, Human Immunodeficiency Virus-1; EC 1.13.12.7 / Luciferases, Firefly
  • [Other-IDs] NLM/ PMC2811009
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43. Planas-Silva MD, Rutherford TM, Stone MC: Prevention of age-related spontaneous mammary tumors in outbred rats by late ovariectomy. Cancer Detect Prev; 2008;32(1):65-71
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  • [Title] Prevention of age-related spontaneous mammary tumors in outbred rats by late ovariectomy.
  • BACKGROUND: Breast cancer prevention trials have shown that the antiestrogen tamoxifen inhibits development of estrogen receptor (ER)-positive tumors.
  • In Sprague-Dawley rats, removal of ovarian function in young animals can reduce the incidence of spontaneous age-dependent mammary tumors.
  • However, it is not known whether removal of ovaries late in life, before middle age onset, can still prevent mammary tumor development.
  • METHODS: In this study we used Hsd:Sprague-Dawley SD (Hsd) rats to determine the effect of late ovariectomy on mammary tumor development.
  • In some experiments, palpable tumors were surgically removed upon presentation.
  • RESULTS: Removal of ovaries before middle age onset ( approximately 5-7 months) inhibited development of spontaneous mammary tumors by 95%.
  • Only one mammary tumor was observed in 19 late ovariectomized animals while 47 total tumors developed in 42 non-ovariectomized animals.
  • Tumor incidence was reduced from 73.8 to 5.3% (relative risk=0.05, 95% CI=0.0072-0.354).
  • The frequency of mammary carcinomas in non-ovariectomized virgin female rats was one in eight rats.
  • When palpable tumors were removed by surgical excision, tumor multiplicity increased from 0.76 to 1.61 tumors per rat.
  • CONCLUSION: Late ovariectomy prevents spontaneous mammary tumor development in Hsd rats.
  • This animal model may be useful for evaluating novel interventions in breast cancer prevention.
  • [MeSH-major] Mammary Neoplasms, Experimental / prevention & control. Mammary Neoplasms, Experimental / surgery. Ovariectomy

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  • (PMID = 18407436.001).
  • [ISSN] 1525-1500
  • [Journal-full-title] Cancer detection and prevention
  • [ISO-abbreviation] Cancer Detect. Prev.
  • [Language] eng
  • [Publication-type] Comparative Study; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
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44. Hong J, Holcomb VB, Dang F, Porampornpilas K, Núñez NP: Alcohol consumption, obesity, estrogen treatment and breast cancer. Anticancer Res; 2010 Jan;30(1):1-8
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  • The objective of the present study was to determine if the effect of alcohol on mammary cancer is modified by body weight and exogenous estrogen.
  • Ovariectomized mice of various body weights, receiving estrogen or placebo supplementation, and consuming water or alcohol were injected with mammary cancer cells.
  • Alcohol intake resulted in insulin sensitivity and increased tumor growth in obese mice.
  • Exogenous estrogen alone inhibited tumor growth.
  • The combination of estrogen and alcohol overcame the inhibitory effects of estrogen on tumor growth in obese mice.
  • In conclusion, alcohol and estrogen treatment can modify mammary tumor growth, possibly through the regulation of estrogen and leptin, especially in obese mice.
  • [MeSH-major] Alcohol Drinking / pathology. Estrogens / administration & dosage. Hormone Replacement Therapy / adverse effects. Mammary Neoplasms, Experimental / pathology
  • [MeSH-minor] Animals. Body Weight. Cell Line, Tumor. Estradiol / blood. Female. Insulin / blood. Insulin-Like Growth Factor I / metabolism. Leptin / blood. Mice. Obesity

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  • (PMID = 20150611.001).
  • [ISSN] 1791-7530
  • [Journal-full-title] Anticancer research
  • [ISO-abbreviation] Anticancer Res.
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / 1K22CA127519-01A1; United States / NIEHS NIH HHS / ES / ES007784; United States / NIEHS NIH HHS / ES / ES09145
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
  • [Publication-country] Greece
  • [Chemical-registry-number] 0 / Estrogens; 0 / Insulin; 0 / Leptin; 4TI98Z838E / Estradiol; 67763-96-6 / Insulin-Like Growth Factor I
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45. Luth JA, Hubbard GB, Dick EJ Jr, Frazier SR, Barrier BF: Characterization of spontaneous mammary gland carcinomas in female baboons. J Med Primatol; 2008 Feb;37(1):55-61
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  • [Title] Characterization of spontaneous mammary gland carcinomas in female baboons.
  • Spontaneous mammary gland carcinomas occurred in five baboons during a 13-year period at Southwest Foundation for Biomedical Research.
  • Morphologically, the tumors were characterized by neoplastic cells arranged from pseudopapillary and cribiform to more poorly differentiated solid cellular growth patterns.
  • Additional features included lack of tubule formation (4/5), marked nuclear pleomorphism (5/5), a high mitotic rate (4/5) and tumor necrosis (4/5).
  • Applying a grading system used for breast cancer in women, four tumors were graded as poorly differentiated carcinomas and one was graded as moderately differentiated.
  • Co-existent ductal carcinoma in situ (DCIS) was observed in three of the mammary tumors.
  • Metastases to the regional lymph nodes were confirmed in two animals, both with histological evidence of lymphovascular invasion in the primary tumor.
  • Distant metastases were observed in only one animal.
  • Immunohistochemical staining for human therapeutic markers revealed 2/5 tumors strongly positive for estrogen receptor, 1/5 strongly positive for progesterone receptor and 4/4 negative for HER2 expression.
  • Although the incidence appears to be low, these five cases of mammary carcinoma in female baboons suggest that when present baboon mammary carcinoma is usually of ductal origin and behaves similar to a human breast carcinoma.
  • [MeSH-major] Carcinoma, Ductal, Breast / veterinary. Mammary Neoplasms, Animal / pathology. Monkey Diseases / pathology. Papio

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  • (PMID = 18199073.001).
  • [ISSN] 0047-2565
  • [Journal-full-title] Journal of medical primatology
  • [ISO-abbreviation] J. Med. Primatol.
  • [Language] eng
  • [Publication-type] Comparative Study; Journal Article
  • [Publication-country] Denmark
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46. Sathiakumar N, Delzell E: A follow-up study of women in the synthetic rubber industry: study methods. Chem Biol Interact; 2007 Mar 20;166(1-3):25-8
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  • Experimental studies have shown that BD produces mammary tumors in female mice and rats and ovarian tumors in female mice.

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  • (PMID = 17229413.001).
  • [ISSN] 0009-2797
  • [Journal-full-title] Chemico-biological interactions
  • [ISO-abbreviation] Chem. Biol. Interact.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Ireland
  • [Chemical-registry-number] 9006-04-6 / Rubber
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47. Felicetti P, Mennecozzi M, Barucca A, Montgomery S, Orlandi F, Manova K, Houghton AN, Gregor PD, Concetti A, Venanzi FM: Tumor endothelial marker 8 enhances tumor immunity in conjunction with immnization against differentiation Ag. Cytotherapy; 2007;9(1):23-34
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  • [Title] Tumor endothelial marker 8 enhances tumor immunity in conjunction with immnization against differentiation Ag.
  • BACKGROUND: We have previously shown that xenogenic DNA vaccines encoding rat neu and melanosomal differentiation Ag induce tumor immunity.
  • Others have developed vaccines targeting tumor neovasculature.
  • Tumor endothelial marker 8 (TEM8) is expressed in the neovasculature of human tumors, and in the mouse melanoma B16, but its expression is limited in normal adult tissues.
  • We describe a DNA vaccine combining xenogeneic tumor Ag and TEM8.
  • METHODS: In-situ hybridization was used to detect TEM8 RNA in mouse tumors.
  • RESULTS: TEM8 was expressed in the stroma of transplantable mouse breast and melanoma tumors.
  • In both model systems, TEM8 DNA had no activity as a single agent but significantly enhanced the anit-tumor immunity of neu and hTYRP1/hgp75 DNA vaccines when given in concert.
  • The observed synergy was dependent upon CD8+ T cells, as depletion of this cell population just prior to tumor challenge obviated the effect of the TEM8 vaccine in both tumor models.
  • DISCUSSION: A local immune responses to TEM8 may increase inflammation or tumor necrosis within the tumor, resulting in improved Ag presentation of HER2/neu and hTYRP1/hgp75.
  • [MeSH-major] Antigens, Differentiation / immunology. Cancer Vaccines / immunology. Immune Tolerance / immunology. Membrane Proteins / immunology. Neoplasm Proteins / immunology. Receptors, Cell Surface / immunology
  • [MeSH-minor] Animals. Blotting, Western. CD8-Positive T-Lymphocytes / immunology. Cell Differentiation / immunology. Cell Line, Tumor. Female. Gene Expression Regulation, Neoplastic. Humans. Immunization. In Situ Hybridization. Mammary Neoplasms, Animal / genetics. Mammary Neoplasms, Animal / immunology. Mammary Neoplasms, Animal / pathology. Melanoma, Experimental / genetics. Melanoma, Experimental / immunology. Melanoma, Experimental / pathology. Membrane Glycoproteins / immunology. Mice. Mice, Inbred C57BL. Mice, Transgenic. Oxidoreductases / immunology. Rats. Recombinant Proteins / immunology. Survival Analysis

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  • [ErratumIn] Cytotherapy. 2007;9(2):205
  • (PMID = 17361485.001).
  • [ISSN] 1465-3249
  • [Journal-full-title] Cytotherapy
  • [ISO-abbreviation] Cytotherapy
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / CA33049; United States / NCI NIH HHS / CA / CA59350; United States / PHS HHS / / P50 92629
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / ANTXR1 protein, human; 0 / Antigens, Differentiation; 0 / Cancer Vaccines; 0 / Membrane Glycoproteins; 0 / Membrane Proteins; 0 / Neoplasm Proteins; 0 / Receptors, Cell Surface; 0 / Recombinant Proteins; EC 1.- / Oxidoreductases; EC 1.14.18.- / TYRP1 protein, human
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48. Jiang G, Tao K, Kuperwasser C: Identification of selective inhibitors of cancer stem cells by high-throughput screening. Cell; 2009 Aug 21;138(4):645-659
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  • Screens for agents that specifically kill epithelial cancer stem cells (CSCs) have not been possible due to the rarity of these cells within tumor cell populations and their relative instability in culture.
  • Treatment of mice with salinomycin inhibits mammary tumor growth in vivo and induces increased epithelial differentiation of tumor cells.
  • [MeSH-major] Antineoplastic Agents / pharmacology. Drug Screening Assays, Antitumor / methods. Mammary Neoplasms, Experimental / drug therapy. Neoplastic Stem Cells / drug effects. Paclitaxel / pharmacology. Pyrans / pharmacology
  • [MeSH-minor] Animals. Apoptosis. Cell Line, Tumor. Drug Resistance, Neoplasm. Gene Expression Regulation, Neoplastic. Humans. Mice. Mice, Inbred BALB C. Mice, Inbred NOD. Mice, SCID. Neoplasm Metastasis / drug therapy. Neoplasm Transplantation

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  • [CommentIn] Cell. 2009 Aug 21;138(4):623-5 [19703390.001]
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  • (PMID = 19682730.001).
  • [ISSN] 1097-4172
  • [Journal-full-title] Cell
  • [ISO-abbreviation] Cell
  • [Language] eng
  • [Databank-accession-numbers] GEO/ GSE17215
  • [Grant] United States / NIMH NIH HHS / MH / R03 MH089663
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / Pyrans; 62UXS86T64 / salinomycin; P88XT4IS4D / Paclitaxel
  • [Other-IDs] NLM/ NIHMS128642; NLM/ PMC4892125
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49. Largaespada DA, Collier LS: Transposon-mediated mutagenesis in somatic cells: identification of transposon-genomic DNA junctions. Methods Mol Biol; 2008;435:95-108
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  • Understanding the genetic basis for tumor formation is crucial for treating cancer.
  • Forward genetic screens using insertional mutagenesis technologies have identified many important tumor suppressor genes and oncogenes in mouse models of human cancer.
  • Traditionally, retroviruses have been used for this purpose, allowing the identification of genes that can cause various forms of leukemia or lymphoma with murine leukemia viruses or mammary cancer with mouse mammary tumor viruses.
  • We provide an overview of some general issues related to use of Sleeping Beauty for cancer genetic studies and present here the polymerase chain reaction-based method for cloning transposon-tagged sequences from tumors.
  • [MeSH-minor] Animals. Base Sequence. Cloning, Molecular. DNA Primers / genetics. Genes, Tumor Suppressor. Humans. Mice. Neoplasms, Experimental / etiology. Neoplasms, Experimental / genetics. Oncogenes. Polymerase Chain Reaction. Transposases / genetics

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  • (PMID = 18370070.001).
  • [ISSN] 1064-3745
  • [Journal-full-title] Methods in molecular biology (Clifton, N.J.)
  • [ISO-abbreviation] Methods Mol. Biol.
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / K01 CA122183; United States / NCI NIH HHS / CA / R01 CA113636; United States / NCI NIH HHS / CA / R01 CA113636; United States / NCI NIH HHS / CA / R21 CA118600
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / DNA Primers; 0 / DNA Transposable Elements; EC 2.7.7.- / Transposases; EC 2.7.7.- / sleeping beauty transposase, human
  • [Other-IDs] NLM/ NIHMS421445; NLM/ PMC3517914
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50. Beniashvili D, Avinoach I, Baazov D, Zusman I: Household electromagnetic fields and breast cancer in elderly women. In Vivo; 2005 May-Jun;19(3):563-6
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  • The relationship between the rate of household low-frequency electromagnetic fields (EMF) and incidences of mammary tumors was studied in 1290 clinical case-records of female patients aged 60 and more over a period of 26 years, based on the materials of the Edith Wolfson Medical Center, Israel.
  • Group I included patients with mammary tumors under observation from 1978 to 1990, who rarely used EMF-generating appliances.
  • Mammary tumors were found in 2824 women (1.4%), of which 1290 cases (45.6%) were observed in elderly women.
  • Most of the observed tumors--1254 (97.2%)--were epithelial neoplasms.
  • Mammary tumors were found in 585 elderly women in Group I and 705 women in Group II.
  • There was a statistically significant influence of EMF on the formation of all observed epithelial mammary tumors in Group II.
  • [MeSH-major] Air Pollution, Indoor. Breast Neoplasms / epidemiology. Electromagnetic Fields
  • [MeSH-minor] Age Distribution. Aged. Aged, 80 and over. Carcinoma, Ductal / epidemiology. Carcinoma, Ductal / pathology. Female. Humans. Israel / epidemiology. Medical Records. Middle Aged. Neoplasm Invasiveness. Neoplasms, Radiation-Induced / epidemiology. Neoplasms, Radiation-Induced / pathology


51. Xie Z, Yuan H, Yin Y, Zeng X, Bai R, Glazer RI: 3-phosphoinositide-dependent protein kinase-1 (PDK1) promotes invasion and activation of matrix metalloproteinases. BMC Cancer; 2006 Mar 21;6:77
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  • BACKGROUND: Metastasis is a major cause of morbidity and mortality in breast cancer with tumor cell invasion playing a crucial role in the metastatic process.
  • PDK1 is a key molecule that couples PI3K to cell proliferation and survival signals in response to growth factor receptor activation, and is oncogenic when expressed in mouse mammary epithelial cells.
  • METHODS: Invasion assays in Matrigel, MMP-2 zymogram analysis, gene microarray analysis and mammary isografts were used to characterize the invasive and proliferative function of cells expressing PDK1.
  • Tissue microarray analysis of human breast cancers was used to measure PDK1 expression in invasive tumors by IHC.
  • Mammary fat pad isografts of PDK1-expressing cells produced invasive adenocarcinomas.
  • CONCLUSION: These results indicate that PDK1 serves as an important effector of mammary epithelial cell growth and invasion in the transformed phenotype.

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  • (PMID = 16551362.001).
  • [ISSN] 1471-2407
  • [Journal-full-title] BMC cancer
  • [ISO-abbreviation] BMC Cancer
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / R01CA81565
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, U.S. Gov't, Non-P.H.S.
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Drug Combinations; 0 / Laminin; 0 / Mmp14 protein, mouse; 0 / Proteoglycans; 119978-18-6 / matrigel; 9007-34-5 / Collagen; EC 1.13.12.- / Luciferases; EC 2.7.11.1 / 3-Phosphoinositide-Dependent Protein Kinases; EC 2.7.11.1 / PDPK1 protein, human; EC 2.7.11.1 / Pdpk1 protein, mouse; EC 2.7.11.1 / Protein-Serine-Threonine Kinases; EC 3.4.24.- / Matrix Metalloproteinases; EC 3.4.24.- / Matrix Metalloproteinases, Membrane-Associated; EC 3.4.24.24 / Matrix Metalloproteinase 2; EC 3.4.24.80 / Matrix Metalloproteinase 14
  • [Other-IDs] NLM/ PMC1459872
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52. Wicha MS: Breast cancer stem cells: the other side of the story. Stem Cell Rev; 2007 Jun;3(2):110-2; discussion 113
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [MeSH-major] Breast Neoplasms / genetics. Breast Neoplasms / metabolism. Mammary Neoplasms, Animal / genetics. Mammary Neoplasms, Animal / metabolism. Models, Biological. Neoplastic Stem Cells / metabolism
  • [MeSH-minor] Animals. Cell Survival. Cell Transformation, Neoplastic / genetics. Cell Transformation, Neoplastic / metabolism. Evolution, Molecular. Female. Humans. Neoplasm Metastasis

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  • [CommentOn] Stem Cell Rev. 2007 Jun;3(2):107-9 [17873341.001]
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  • (PMID = 17873342.001).
  • [ISSN] 1550-8943
  • [Journal-full-title] Stem cell reviews
  • [ISO-abbreviation] Stem Cell Rev
  • [Language] eng
  • [Publication-type] Comment; Journal Article
  • [Publication-country] United States
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53. Rodenburg W, Pennings JL, van Oostrom CT, Roodbergen M, Kuiper RV, Luijten M, de Vries A: Identification of breast cancer biomarkers in transgenic mouse models: A proteomics approach. Proteomics Clin Appl; 2010 Jul;4(6-7):603-12
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  • Multi-analyte profiling technique was used to analyze 70 proteins in individual serum samples of non-tumor and mammary tumor-bearing Tg.NK (MMTV/c-neu) mice.
  • RESULTS: A small set of proteins fully differentiated tumor samples from controls.
  • However, other biomarkers showed distinct expression in the two different breast-cancer models, indicating that different mammary tumor sub-types with respect to molecular and estrogen receptor status reveal divergent serum biomarker sets.
  • CONCLUSIONS AND CLINICAL RELEVANCE: The current study supports the concept that serum proteins can discriminate mammary tumor cases from controls, and yielded interesting biomarkers that need further testing and validation in human studies.
  • [MeSH-major] Biomarkers, Tumor / blood. Mammary Neoplasms, Experimental / blood

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  • [Copyright] Copyright © 2010 WILEY-VCH Verlag GmbH & Co. KGaA, Weinheim.
  • (PMID = 21137078.001).
  • [ISSN] 1862-8354
  • [Journal-full-title] Proteomics. Clinical applications
  • [ISO-abbreviation] Proteomics Clin Appl
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Germany
  • [Chemical-registry-number] 0 / Antigens, CD40; 0 / Biomarkers, Tumor; 0 / Cst3 protein, mouse; 0 / Cystatin C; 0 / Interleukin-18; 106441-73-0 / Osteopontin
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54. Su HM, Hsieh PH, Chen HF: A maternal high n-6 fat diet with fish oil supplementation during pregnancy and lactation in rats decreases breast cancer risk in the female offspring. J Nutr Biochem; 2010 Nov;21(11):1033-7
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  • Exposure during the perinatal period to a maternal high n-6 fat diet with fish oil supplementation significantly reduced the incidence of carcinogen-induced mammary tumors in the female offspring compared to a maternal high n-6 fat diet with no fish oil supplementation or fish oil supplementation later in life (P=.0228 by Cox proportional hazards model).
  • We found that a maternal high n-6 fat diet during pregnancy is more important in increasing the risk of mammary tumors in the female offspring than a maternal high n-6 fat diet during lactation.
  • This study suggests that fish oil supplementation during the perinatal period decreases the effect of a maternal high n-6 fat diet on subsequent carcinogen-induced mammary tumor risk, whereas fish oil supplementation during puberty or adulthood does not.
  • [MeSH-major] Breast Neoplasms / pathology. Carcinoma / pathology. Fatty Acids, Omega-6 / metabolism. Lactation. Maternal Nutritional Physiological Phenomena
  • [MeSH-minor] Animals. Body Weight. Diet. Dietary Fats / administration & dosage. Dietary Fats / adverse effects. Estradiol / blood. Fatty Acids, Omega-3 / metabolism. Female. Fish Oils / administration & dosage. Mammary Neoplasms, Experimental / etiology. Mammary Neoplasms, Experimental / pathology. Plant Oils / administration & dosage. Plant Oils / adverse effects. Pregnancy. Rats. Rats, Sprague-Dawley. Risk Factors

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  • [Copyright] Copyright © 2010 Elsevier Inc. All rights reserved.
  • (PMID = 19954943.001).
  • [ISSN] 1873-4847
  • [Journal-full-title] The Journal of nutritional biochemistry
  • [ISO-abbreviation] J. Nutr. Biochem.
  • [Language] eng
  • [Publication-type] Comparative Study; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Dietary Fats; 0 / Fatty Acids, Omega-3; 0 / Fatty Acids, Omega-6; 0 / Fish Oils; 0 / Plant Oils; 4TI98Z838E / Estradiol; 8001-21-6 / sunflower seed oil
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55. Mertz JA, Simper MS, Lozano MM, Payne SM, Dudley JP: Mouse mammary tumor virus encodes a self-regulatory RNA export protein and is a complex retrovirus. J Virol; 2005 Dec;79(23):14737-47
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  • [Title] Mouse mammary tumor virus encodes a self-regulatory RNA export protein and is a complex retrovirus.
  • Mouse mammary tumor virus (MMTV) has been classified as a simple retrovirus with two accessory genes, dut and sag.
  • [MeSH-major] Mammary Tumor Virus, Mouse / metabolism. Viral Proteins / metabolism

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  • (PMID = 16282474.001).
  • [ISSN] 0022-538X
  • [Journal-full-title] Journal of virology
  • [ISO-abbreviation] J. Virol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / RNA, Viral; 0 / Viral Proteins
  • [Other-IDs] NLM/ PMC1287593
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56. Zhao Y, Li J, Wang J, Xing Y, Geng M: Role of cell surface oligosaccharides of mouse mammary tumor cell lines in cancer metastasis. Indian J Biochem Biophys; 2007 Jun;44(3):145-51
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  • [Title] Role of cell surface oligosaccharides of mouse mammary tumor cell lines in cancer metastasis.
  • In tumor cells, alterations in cellular glycosylation may play a key role in their metastatic behaviour.
  • In the present study, we have assessed the relationship between cell surface oligosaccharides and the metastasis ability of mouse mammary tumor cell lines 67NR and 4TO7.
  • The cell lines used in study have different metastasis abilities in vivo - the 67NR form primary tumors, but no tumor cells are detectable in any distant tissues, while cells of the 4TO7 line are able to spread to lung.
  • The study suggests that the sialic acids are not crucial for the cell migration and invasion in the 4TO7 cells.
  • [MeSH-major] Cell Membrane / metabolism. Mammary Neoplasms, Animal / metabolism. Mammary Neoplasms, Animal / pathology. Oligosaccharides / chemistry. Oligosaccharides / physiology
  • [MeSH-minor] Animals. Cell Adhesion. Cell Line, Tumor. Cell Movement. Cells. Glycosylation. Lectins / chemistry. Mice. Neoplasm Invasiveness. Neoplasm Metastasis. Polysaccharides / chemistry. Sialic Acids / chemistry

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  • (PMID = 17650582.001).
  • [ISSN] 0301-1208
  • [Journal-full-title] Indian journal of biochemistry & biophysics
  • [ISO-abbreviation] Indian J. Biochem. Biophys.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] India
  • [Chemical-registry-number] 0 / Lectins; 0 / Oligosaccharides; 0 / Polysaccharides; 0 / Sialic Acids
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57. Perry G, Iragavarapu-Charyulu V, Harhaj EW, Torroella-Kouri M: Role of the proteasome in the downregulation of transcription factors NFkappaB and C/EBP in macrophages from tumor hosts. Oncol Rep; 2010 Mar;23(3):875-81
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  • [Title] Role of the proteasome in the downregulation of transcription factors NFkappaB and C/EBP in macrophages from tumor hosts.
  • Macrophages from mice bearing advanced mammary tumors are critically impaired in their immune functions, exhibiting reduced expression at the mRNA and protein levels of the crucial transcription factors, nuclear factor kappaB (NFkappaB) and CCAAT enhancer binding protein (C/EBP).
  • We have previously shown that tumor-derived factors such as transforming growth factor beta (TGFbeta) and prostaglandin E2 (PGE2) modulate NFkappaB and C/EBP expression in macrophages.
  • Transcriptional, post-transcriptional, translational and/or post-translational mechanisms may also play a role in altered levels of NFkappaB and C/EBP in macrophages from tumor hosts, contributing to impaired inflammatory response.
  • Since upregulation of ubiquitin/proteasomal pathways has been described under cancer-induced cachexia, we examined the possible role of this proteolytic machinery in the decrease of NFkappaB and C/EBP proteins in macrophages from tumor hosts.
  • Using MG-132 proteasome inhibitor to block the proteasome machinery in macrophages from normal and tumor-bearing animals we found that macrophages from tumor hosts display higher ubiquitination and proteolysis compared to those from normal mice and also that NFkappaB and C/EBP downregulation is reversed in these treated cells.
  • Thus, proteasome degradation may contribute, at least in part, to NFkappaB and C/EBP impairment in macrophages from tumor-bearers.
  • [MeSH-major] CCAAT-Enhancer-Binding Proteins / antagonists & inhibitors. Macrophages / metabolism. NF-kappa B / antagonists & inhibitors. Neoplasms, Experimental / immunology. Proteasome Endopeptidase Complex / physiology

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  • (PMID = 20127032.001).
  • [ISSN] 1791-2431
  • [Journal-full-title] Oncology reports
  • [ISO-abbreviation] Oncol. Rep.
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / K01CA101926
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural
  • [Publication-country] Greece
  • [Chemical-registry-number] 0 / CCAAT-Enhancer-Binding Proteins; 0 / Lipopolysaccharides; 0 / NF-kappa B; 0 / Transforming Growth Factor beta1; EC 3.4.25.1 / Proteasome Endopeptidase Complex
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58. Mosley JD, Poirier JT, Seachrist DD, Landis MD, Keri RA: Rapamycin inhibits multiple stages of c-Neu/ErbB2 induced tumor progression in a transgenic mouse model of HER2-positive breast cancer. Mol Cancer Ther; 2007 Aug;6(8):2188-97
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  • [Title] Rapamycin inhibits multiple stages of c-Neu/ErbB2 induced tumor progression in a transgenic mouse model of HER2-positive breast cancer.
  • Gene expression analysis of mammary tumors collected from mouse mammary tumor virus-c-Neu transgenic mice revealed that mRNA levels of several mTOR pathway members were either up-regulated (p85/phosphatidylinositol 3-kinase and p70S6 kinase) or down-regulated (eIF-4E-BP1) in a manner expected to enhance signaling through this pathway.
  • Treatment of these mice with the mTOR inhibitor rapamycin caused growth arrest and regression of primary tumors with no evidence of weight loss or generalized toxicity.
  • The treatment effects were due to decreased proliferation, associated with reduced cyclin D1 expression, and increased cell death in primary tumors.
  • Whereas many of the dead epithelial cells had the histopathologic characteristics of ischemic necrosis, rapamycin treatment was not associated with changes in microvascular density or apoptosis.


59. De Palma M, Naldini L: Antagonizing metastasis. Nat Biotechnol; 2010 Apr;28(4):331-2
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  • [MeSH-major] Disease Models, Animal. Mammary Neoplasms, Experimental / genetics. Mammary Neoplasms, Experimental / therapy. MicroRNAs / administration & dosage. MicroRNAs / genetics. Neoplasm Metastasis / genetics. Neoplasm Metastasis / therapy

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  • (PMID = 20379176.001).
  • [ISSN] 1546-1696
  • [Journal-full-title] Nature biotechnology
  • [ISO-abbreviation] Nat. Biotechnol.
  • [Language] eng
  • [Grant] Italy / Telethon / / TGT06S01
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / MIRN10 microRNA, human; 0 / MicroRNAs
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60. Iyengar P, Cody HS 3rd, Brogi E: Pleomorphic adenoma of the breast: case report and review of the literature. Diagn Cytopathol; 2005 Dec;33(6):416-20
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  • Pleomorphic adenoma of the breast (PAB) is a very rare neoplasm.
  • On cytologic material, fibroadenoma and phyllodes tumor should also be considered within the differential diagnosis.
  • Correct identification of this benign mammary neoplasm is important to avoid unnecessarily aggressive treatment.
  • [MeSH-major] Adenoma, Pleomorphic / pathology. Breast Neoplasms / pathology

  • MedlinePlus Health Information. consumer health - Breast Cancer.
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  • [Copyright] Copyright 2005 Wiley-Liss, Inc
  • (PMID = 16299746.001).
  • [ISSN] 8755-1039
  • [Journal-full-title] Diagnostic cytopathology
  • [ISO-abbreviation] Diagn. Cytopathol.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] United States
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61. Hsu WL, Lin HY, Chiou SS, Chang CC, Wang SP, Lin KH, Chulakasian S, Wong ML, Chang SC: Mouse mammary tumor virus-like nucleotide sequences in canine and feline mammary tumors. J Clin Microbiol; 2010 Dec;48(12):4354-62
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  • [Title] Mouse mammary tumor virus-like nucleotide sequences in canine and feline mammary tumors.
  • Mouse mammary tumor virus (MMTV) has been speculated to be involved in human breast cancer.
  • The aim of this study was to detect MMTV-like nucleotide sequences in canine and feline mammary tumors by nested PCR.
  • Results showed that the presence of MMTV-like env and LTR sequences in canine malignant mammary tumors was 3.49% (3/86) and 18.60% (16/86), respectively.
  • For feline malignant mammary tumors, the presence of both env and LTR sequences was found to be 22.22% (2/9).
  • Nevertheless, the MMTV-like LTR and env sequences also were detected in normal mammary glands of dogs and cats.
  • Taken together, our study provides evidence for the existence and expression of MMTV-like sequences in neoplastic and normal mammary glands of dogs and cats.
  • [MeSH-major] Cat Diseases / virology. Dog Diseases / virology. Mammary Glands, Animal / virology. Mammary Neoplasms, Animal / virology. Mammary Tumor Virus, Mouse / isolation & purification. RNA, Viral / isolation & purification

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  • (PMID = 20881168.001).
  • [ISSN] 1098-660X
  • [Journal-full-title] Journal of clinical microbiology
  • [ISO-abbreviation] J. Clin. Microbiol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
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  • [Other-IDs] NLM/ PMC3008461
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62. Liu B, Edgerton S, Yang X, Kim A, Ordonez-Ercan D, Mason T, Alvarez K, McKimmey C, Liu N, Thor A: Low-dose dietary phytoestrogen abrogates tamoxifen-associated mammary tumor prevention. Cancer Res; 2005 Feb 1;65(3):879-86
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  • [Title] Low-dose dietary phytoestrogen abrogates tamoxifen-associated mammary tumor prevention.
  • In placebo-treated mice, soy meal diet (but not diets supplemented with low-dose or high-dose isoflavones or a casein diet) resulted in prolongation of tumor latency.
  • In tamoxifen-treated mice fed the soy meal, casein, or high-dose isoflavone enriched diets, the majority (>80%) showed no tumor formation by 60 weeks of age.
  • Of the mice that developed tumors, latency was significantly prolonged.
  • In tamoxifen-treated mice fed the low-dose isoflavone enriched diet, a much higher rate of mammary tumor development (>50%; P < 0.002) and a shorter tumor latency were observed.
  • In vitro studies of human and mouse mammary tumor cell lines confirm that low doses of genistein, co-administered with tamoxifen, promote cell proliferation.
  • In summary, low-dose dietary isoflavones abrogated tamoxifen-associated mammary tumor prevention in vivo.
  • These interactions are supported by in vitro data from human and mouse mammary tumor cell lines.
  • [MeSH-major] Breast Neoplasms / prevention & control. Mammary Neoplasms, Experimental / prevention & control. Phytoestrogens / pharmacology. Tamoxifen / pharmacology
  • [MeSH-minor] Animals. Cell Line, Tumor. Dose-Response Relationship, Drug. Drug Interactions. Female. Humans. Isoflavones / adverse effects. Isoflavones / pharmacology. Mice. Mice, Transgenic


63. Schmitt M, Walker MP, Richards RG, Bocchinfuso WP, Fukuda T, Medina D, Kittrell FS, Korach KS, DiAugustine RP: Expression of heregulin by mouse mammary tumor cells: role in activation of ErbB receptors. Mol Carcinog; 2006 Jul;45(7):490-505
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  • [Title] Expression of heregulin by mouse mammary tumor cells: role in activation of ErbB receptors.
  • The major goal of the present study was to determine whether endogenous HRG causes autocrine/paracrine activation of ErbB-2/ErbB-3 and contributes to the proliferation of mammary epithelial tumor cells.
  • Tyrosine-phosphorylated (activated) ErbB-2 and ErbB-3 receptors were detected in the majority of extracts from tumors that had formed spontaneously or as a result of oncogene expression.
  • HRG-1 transcripts and protein were found in the epithelial cells of most of these mouse mammary tumors.
  • Various mouse mammary cell lines also contained activated ErbB-2/ErbB-3 and HRG transcripts.
  • Addition of an antiserum against HRG to the mammary epithelial tumor cell line TM-6 reduced ErbB-3 Tyr-phosphorylation.
  • The cumulative findings from these experiments show that coexpression of the HRG ligand contributes to activation of ErbB-2/Erb-3 in mouse mammary tumor cells in an autocrine or paracrine fashion.
  • [MeSH-major] Mammary Neoplasms, Experimental / genetics. Neuregulin-1 / genetics. Receptor, ErbB-2 / physiology
  • [MeSH-minor] Amino Acid Sequence. Animals. Cell Line, Tumor. DNA Primers. Female. Gene Expression Regulation, Neoplastic. Humans. Immunohistochemistry. Mice. Peptide Fragments / chemistry. Plasmids. Polymerase Chain Reaction. RNA, Small Interfering / genetics. Recombinant Proteins / metabolism. Transfection

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  • (PMID = 16482517.001).
  • [ISSN] 0899-1987
  • [Journal-full-title] Molecular carcinogenesis
  • [ISO-abbreviation] Mol. Carcinog.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / DNA Primers; 0 / Neuregulin-1; 0 / Peptide Fragments; 0 / RNA, Small Interfering; 0 / Recombinant Proteins; EC 2.7.10.1 / Receptor, ErbB-2
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64. Kang Z, Webster Marketon JI, Johnson A, Sternberg EM: Bacillus anthracis lethal toxin represses MMTV promoter activity through transcription factors. J Mol Biol; 2009 Jun 12;389(3):595-605
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  • In this study, we found that LeTx repressed the activation of the mouse mammary tumor virus promoter related to overexpression of the transcription factors hepatocyte nuclear factor 3, octamer-binding protein 1, and c-Jun.
  • In addition, LeTx repressed phorbol-12-myristate-13-acetate-induced mouse mammary tumor virus promoter activity and phorbol 12-myristate 13-acetate induction of endogenous c-Jun protein.
  • [MeSH-minor] Animals. COS Cells. Cercopithecus aethiops. Genes, Reporter. Mammary Tumor Virus, Mouse / genetics. Promoter Regions, Genetic / drug effects. Tetradecanoylphorbol Acetate / analogs & derivatives. Tetradecanoylphorbol Acetate / pharmacology. Transcription Factor AP-1 / antagonists & inhibitors. Transcription Factor AP-1 / metabolism. Transcriptional Activation

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  • (PMID = 19389405.001).
  • [ISSN] 1089-8638
  • [Journal-full-title] Journal of molecular biology
  • [ISO-abbreviation] J. Mol. Biol.
  • [Language] eng
  • [Grant] United States / Intramural NIH HHS / / Z99 CA999999
  • [Publication-type] Journal Article; Research Support, N.I.H., Intramural
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Antigens, Bacterial; 0 / Bacterial Toxins; 0 / Transcription Factor AP-1; 0 / Transcription Factors; 0 / anthrax toxin; 56937-68-9 / phorbolol myristate acetate; NI40JAQ945 / Tetradecanoylphorbol Acetate
  • [Other-IDs] NLM/ NIHMS112164; NLM/ PMC2754296
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65. Kim S, Welm AL, Bishop JM: A dominant mutant allele of the ING4 tumor suppressor found in human cancer cells exacerbates MYC-initiated mouse mammary tumorigenesis. Cancer Res; 2010 Jun 15;70(12):5155-62
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  • [Title] A dominant mutant allele of the ING4 tumor suppressor found in human cancer cells exacerbates MYC-initiated mouse mammary tumorigenesis.
  • ING4 is a candidate tumor suppressor gene that is deleted in 10% to 20% of human breast cancers and is mutated in various human cancer cell lines.
  • To evaluate whether ING4 has a tumor-suppressive role in breast tissue, we overexpressed it in mouse mammary glands using a transplant system.
  • Ectopic expression of ING4 suppressed MYC-induced mammary hyperplasia, but not tumorigenesis.
  • In the same model system, we show that a COOH-terminal truncation mutant of ING4 found in human cancer cells could act alone to induce abnormal gland structures resembling mammary hyperplasia, which did not progress to tumors.
  • However, coexpression of the ING4 mutant with MYC increased the penetrance and metastasis of MYC-initiated mammary tumors, giving rise to tumors with more organized acinar structures.
  • Similarly, in vitro expression of the ING4 mutant in MCF10A mammary epithelial cells reinforced tight junctional structures.

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  • (PMID = 20501848.001).
  • [ISSN] 1538-7445
  • [Journal-full-title] Cancer research
  • [ISO-abbreviation] Cancer Res.
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / K01 CA115681; United States / NCI NIH HHS / CA / K01 CA115681-05; United States / NCI NIH HHS / CA / 5K01CA115681; United States / NCI NIH HHS / CA / 5R35CA044338; United States / NCI NIH HHS / CA / CA115681-05
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Cell Cycle Proteins; 0 / Homeodomain Proteins; 0 / ING4 protein, human; 0 / Proto-Oncogene Proteins c-myc; 0 / Tumor Suppressor Proteins
  • [Other-IDs] NLM/ NIHMS200937; NLM/ PMC2891958
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66. Pal G, Basu S, Mitra K, Vo-Dinh T: Time-resolved optical tomography using short-pulse laser for tumor detection. Appl Opt; 2006 Aug 20;45(24):6270-82
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  • [Title] Time-resolved optical tomography using short-pulse laser for tumor detection.
  • Our objective is to perform a comprehensive experimental and numerical analysis of the short-pulse laser interaction with a tissue medium with the goal of tumor-cancer diagnostics.
  • The final step is to perform in vivo imaging of anesthetized rats with tumor-promoting agents injected inside skin tissues and of an anesthetized mouse with mammary tumors to demonstrate the feasibility of the technique for detecting tumors in an animal model.
  • [MeSH-major] Image Interpretation, Computer-Assisted / instrumentation. Image Interpretation, Computer-Assisted / methods. Lasers. Mammary Neoplasms, Experimental / diagnosis. Tomography, Optical Coherence / instrumentation. Tomography, Optical Coherence / methods

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  • (PMID = 16892133.001).
  • [ISSN] 0003-6935
  • [Journal-full-title] Applied optics
  • [ISO-abbreviation] Appl Opt
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / 1 R01 CA88787-01
  • [Publication-type] Evaluation Studies; Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't; Research Support, U.S. Gov't, Non-P.H.S.
  • [Publication-country] United States
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67. Mrusek S, Classen-Linke I, Vloet A, Beier HM, Krusche CA: Estradiol and medroxyprogesterone acetate regulated genes in T47D breast cancer cells. Mol Cell Endocrinol; 2005 May 12;235(1-2):39-50
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  • Many mammary tumors express estrogen receptors (ER) and progesterone receptors (PR), and there is increasing evidence that progestins influence gene expression of breast tumor cells.
  • To analyse the impact of progestins on breast cancer cells, we compared (a) the expression of two cytokines, involved in tumor progression, and searched (b) for differentially regulated genes by a microarray, containing 2400 genes, on T47D breast cancer cells cultured for 6 days with 17beta-estradiol (E2) or E2+medroxyprogesterone acetate (E2+MPA).
  • [MeSH-major] Breast Neoplasms / genetics. Estradiol / pharmacology. Medroxyprogesterone Acetate / pharmacology
  • [MeSH-minor] Cell Line, Tumor. Estrogen Receptor alpha / metabolism. Female. Gene Expression Regulation, Neoplastic. Humans. Microarray Analysis. Platelet-Derived Growth Factor / metabolism. RNA, Messenger / metabolism. Receptors, Progesterone / metabolism. Reverse Transcriptase Polymerase Chain Reaction. Tumor Necrosis Factor-alpha / metabolism

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  • (PMID = 15866426.001).
  • [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 / Estrogen Receptor alpha; 0 / Platelet-Derived Growth Factor; 0 / RNA, Messenger; 0 / Receptors, Progesterone; 0 / Tumor Necrosis Factor-alpha; 4TI98Z838E / Estradiol; C2QI4IOI2G / Medroxyprogesterone Acetate
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68. Whitehead TL, Monzavi-Karbassi B, Jousheghany F, Artaud C, Elbein A, Kieber-Emmons T: 1H-NMR metabolic markers of malignancy correlate with spontaneous metastases in a murine mammary tumor model. Int J Oncol; 2005 Jul;27(1):257-63
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  • [Title] 1H-NMR metabolic markers of malignancy correlate with spontaneous metastases in a murine mammary tumor model.
  • End-products of glycolysis as well as phospholipid precursors and catabolites have been suggested as metabolic indicators of tumor progression.
  • To test the hypothesis that increased levels of such indicators can distinguish metastatic phenotypes, we determined a limited cellular 1H-NMR metabolic profile of subpopulations of murine mammary 4T1 cells that differ in their metastatic potential.
  • Serum obtained from mice inoculated with either sLeX-negative or sLeX-positive tumor cells contained broader methylene resonances (P = 0.0002; P = 0.0003) and narrower methyl resonances (P = 0.0013; P < 0.0001) when compared to serum of naive mice.
  • However, line widths of methylene and methyl resonances were not useful for distinguishing between the two tumor phenotypes.
  • [MeSH-major] Magnetic Resonance Spectroscopy / methods. Mammary Neoplasms, Animal / pathology
  • [MeSH-minor] Animals. Antigens, Neoplasm. Biomarkers. Biomarkers, Tumor. Cell Adhesion. Cell Proliferation. Cell Separation. Flow Cytometry. Glycolysis. Humans. Hydrocarbons. Methane / analogs & derivatives. Methane / chemistry. Mice. Mice, Inbred BALB C. Neoplasm Metastasis. Oligosaccharides / chemistry. Phenotype. Phosphorylcholine / chemistry. Prognosis. Time Factors

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  • (PMID = 15942667.001).
  • [ISSN] 1019-6439
  • [Journal-full-title] International journal of oncology
  • [ISO-abbreviation] Int. J. Oncol.
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / CA089480
  • [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.; Research Support, U.S. Gov't, P.H.S.
  • [Publication-country] Greece
  • [Chemical-registry-number] 0 / 5-acetylneuraminyl-(2-3)-galactosyl-(1-4)-(fucopyranosyl-(1-3))-N-acetylglucosamine; 0 / Antigens, Neoplasm; 0 / Biomarkers; 0 / Biomarkers, Tumor; 0 / Hydrocarbons; 0 / Oligosaccharides; 107-73-3 / Phosphorylcholine; 2465-56-7 / carbene; OP0UW79H66 / Methane
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69. Kupumbati TS, Cattoretti G, Marzan C, Farias EF, Taneja R, Mira-y-Lopez R: Dominant negative retinoic acid receptor initiates tumor formation in mice. Mol Cancer; 2006 Mar 24;5:12
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  • [Title] Dominant negative retinoic acid receptor initiates tumor formation in mice.
  • RESULTS: To address this question, we generated transgenic mice in which expression of a ligand binding defective dominant negative RARalpha (RARalphaG303E) was under the control of the mouse mammary tumor virus (MMTV) promoter.
  • The transgene was expressed in the lymphoid compartment and in the mammary epithelium.
  • We postulated that mammary tumors might arise after a long latency period as seen in other transgenic models of breast cancer.
  • At 17 months post-transplantation, a metastatic mammary adenocarcinoma developed in one of four transplanted glands whereas no tumors developed in sixteen of sixteen endogenous glands with wild type epithelium.
  • CONCLUSION: These findings suggest that physiological RAR activity may normally suppress B lymphocyte and mammary epithelial cell growth and that global RAR inactivation is sufficient to initiate a stochastic process of tumor development requiring multiple transforming events.
  • Our work makes available to the research community a new animal resource that should prove useful as an experimental model of aggressive sporadic lymphoma in immunologically uncompromised hosts.

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  • (PMID = 16563162.001).
  • [ISSN] 1476-4598
  • [Journal-full-title] Molecular cancer
  • [ISO-abbreviation] Mol. Cancer
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / R01 CA054273; United States / NCI NIH HHS / CA / R24 CA088302; United States / NCI NIH HHS / CA / CA54273; United States / NCI NIH HHS / CA / CA88302
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Receptors, Retinoic Acid; 0 / retinoic acid receptor alpha; TE7660XO1C / Glycine
  • [Other-IDs] NLM/ PMC1444935
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70. Day CP, Rau KM, Qiu L, Liu CW, Kuo HP, Xie X, Lopez-Berestein G, Hortobagyi GN, Hung MC: Mutant Bik expression mediated by the enhanced minimal topoisomerase IIalpha promoter selectively suppressed breast tumors in an animal model. Cancer Gene Ther; 2006 Jul;13(7):706-19
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  • [Title] Mutant Bik expression mediated by the enhanced minimal topoisomerase IIalpha promoter selectively suppressed breast tumors in an animal model.
  • To ensure the success of systemic gene therapy, it is critical to enhance the tumor specificity and activity of the promoter.
  • A CT90-driven construct expressing BikDD, a potent proapoptotic gene, was shown to selectively kill breast cancer cells in vitro, and to suppress mammary tumor development in an animal model of intravenously administrated, liposome-delivered gene therapy.
  • Expression of BikDD was readily detectable in the tumors but not in the normal organs (such as heart) of CT90-BikDD-treated animals.
  • [MeSH-major] Antigens, Neoplasm / genetics. Apoptosis Regulatory Proteins / genetics. Breast Neoplasms / therapy. DNA Topoisomerases, Type II / genetics. DNA-Binding Proteins / genetics. Genetic Therapy. Membrane Proteins / genetics. Mutation. Response Elements / genetics
  • [MeSH-minor] Animals. Cell Line, Tumor. Cytomegalovirus / genetics. Enhancer Elements, Genetic / genetics. Female. Gene Expression. Genetic Vectors. Humans. Liposomes. Mice. Mice, Nude. Neoplasms, Experimental

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  • (PMID = 16514421.001).
  • [ISSN] 0929-1903
  • [Journal-full-title] Cancer gene therapy
  • [ISO-abbreviation] Cancer Gene Ther.
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / CA16672
  • [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 / Antigens, Neoplasm; 0 / Apoptosis Regulatory Proteins; 0 / BIK protein, human; 0 / DNA-Binding Proteins; 0 / Liposomes; 0 / Membrane Proteins; EC 5.99.1.3 / DNA Topoisomerases, Type II; EC 5.99.1.3 / DNA topoisomerase II alpha
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71. Jaskelioff M, Song W, Xia J, Liu C, Kramer J, Koido S, Gendler SJ, Calderwood SK, Gong J: Telomerase deficiency and telomere dysfunction inhibit mammary tumors induced by polyomavirus middle T oncogene. Oncogene; 2009 Dec 3;28(48):4225-36
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  • [Title] Telomerase deficiency and telomere dysfunction inhibit mammary tumors induced by polyomavirus middle T oncogene.
  • Mice transgenic for MUC1 (mucin 1) and polyomavirus middle T (PyMT) develop mammary carcinomas within 15 weeks with 100% penetrance.
  • PyMT-induced mammary tumorigenesis is closely correlated with robust telomerase expression and activity.
  • To assess the role of telomerase activation and telomere maintenance in mammary carcinoma tumorigenesis, we generated mice expressing MUC1 and PyMT (MMT mice) but deficient in the telomerase RNA component, mTerc, on the C57BL/6 background.
  • Successive generational intercrosses of mTerc(-/-)MMT mice produced cohorts with progressively shorter telomeres that were audited for mammary tumor formation.
  • Relative to MMT (N=14) and G0 mTerc(+/-) female controls (G0=14), mTerc(-/-)MMT females (G1=11, G2=15, G3=15 and G4=5) showed decreased tumor volumes and increased tumor latency-MMT=95.6 days; G0 mTerc(+/-)MMT=98.6 days versus G1, G2, G3 and G4 mTerc(-/-)MMT mice with latencies of 122.6, 138.9, 140.7 and 220.9 days, respectively (controls versus G1-G4, P<0.005).
  • The impairment of tumorigenesis was associated with decreased proliferation of mammary epithelial and tumor cells and increased apoptosis of tumor cells.
  • Together, these results indicate that, in the setting of viral oncoprotein mammary tumorigenesis, telomerase-dependent telomere maintenance facilitates the formation and metastatic progression of mammary tumors.
  • [MeSH-major] Mammary Neoplasms, Experimental / genetics. Oncogenes / genetics. Telomerase / deficiency. Telomere / pathology
  • [MeSH-minor] Animals. Cell Cycle / genetics. Cell Transformation, Neoplastic / pathology. Disease Models, Animal. Female. Humans. Mammary Neoplasms, Animal. Mice. Mice, Inbred C57BL. Mice, Transgenic / metabolism. Mucin-1 / genetics. RNA

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  • (PMID = 19734944.001).
  • [ISSN] 1476-5594
  • [Journal-full-title] Oncogene
  • [ISO-abbreviation] Oncogene
  • [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 / Mucin-1; 0 / telomerase RNA; 63231-63-0 / RNA; EC 2.7.7.49 / Telomerase
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72. Adamovic T, Roshani L, Chen L, Schaffer BS, Helou K, Levan G, Olsson B, Shull JD: Nonrandom pattern of chromosome aberrations in 17beta-estradiol-induced rat mammary tumors: indications of distinct pathways for tumor development. Genes Chromosomes Cancer; 2007 May;46(5):459-69
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  • [Title] Nonrandom pattern of chromosome aberrations in 17beta-estradiol-induced rat mammary tumors: indications of distinct pathways for tumor development.
  • Estrogens play an important role in breast cancer etiology and the ACI rat provides a novel animal model for defining the mechanisms through which estrogens contribute to mammary cancer development.
  • In crossing experiments between the susceptible ACI strain and two resistant strains, COP (Copenhagen) and BN (Brown Norway), several quantitative trait loci (QTL) that affect development of 17beta-estradiol (E2)-induced mammary tumors have been defined.
  • Using comparative genomic hybridization (CGH), we have analyzed cytogenetic aberrations in E2-induced mammary cancers and have found clear patterns of nonrandom chromosomal involvement.
  • Approximately two thirds of the tumors exhibited copy number changes.
  • A third recurrent aberration involving proximal gain and distal loss in RNO6 probably defined a distinct subgroup of tumors, since it never occurred in combination with RNO5 loss.
  • Interestingly, QTL with powerful effects on mammary cancer development have been mapped to RNO5 and RNO6.
  • These findings suggest that there were at least two genetic pathways to tumor formation in this rat model of E2-induced mammary cancer.
  • By performing CGH on mammary tumors from ACI rats, F1 rats from crosses between the ACI and COP or BN strains and ACI.BN-Emca8 congenic rats, which carry the BN allele of the Emca8 QTL on RNO5 on the ACI genetic background, we were able to determine that the constitution of the germ line influences the pattern of chromosomal aberrations.

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  • [Copyright] (c) 2007 Wiley-Liss, Inc.
  • (PMID = 17285573.001).
  • [ISSN] 1045-2257
  • [Journal-full-title] Genes, chromosomes & cancer
  • [ISO-abbreviation] Genes Chromosomes Cancer
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / R01 CA077876; United States / NCI NIH HHS / CA / R01-CA77867
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 4TI98Z838E / Estradiol
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73. Barr FD, Krohmer LJ, Hamilton JW, Sheldon LA: Disruption of histone modification and CARM1 recruitment by arsenic represses transcription at glucocorticoid receptor-regulated promoters. PLoS One; 2009 Aug 26;4(8):e6766
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  • Significantly, exposure to iAs inhibits steroid hormone-mediated gene activation. iAs exposure is associated with disease, but is also used therapeutically to treat specific cancers complicating an understanding of iAs action.
  • PTMs on histones H3 and H4 at the glucocorticoid receptor (GR)-activated mouse mammary tumor virus (MMTV) promoter were identified by chromatin immunoprecipitation analysis following exposure to steroid hormone+/-iAs.
  • Both are essential for robust transcription at steroid hormone regulated genes and both are associated with disease when inappropriately expressed.

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  • (PMID = 19707557.001).
  • [ISSN] 1932-6203
  • [Journal-full-title] PloS one
  • [ISO-abbreviation] PLoS ONE
  • [Language] ENG
  • [Grant] United States / NIEHS NIH HHS / ES / P42 ES007373; United States / NIEHS NIH HHS / ES / R01 ES013168; United States / NIEHS NIH HHS / ES / ES007373; United States / NIEHS NIH HHS / ES / ES013168
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Histones; 0 / Receptors, Glucocorticoid; EC 2.1.1.- / Protein-Arginine N-Methyltransferases; EC 2.1.1.- / coactivator-associated arginine methyltransferase 1; EC 2.3.1.28 / Chloramphenicol O-Acetyltransferase; N712M78A8G / Arsenic
  • [Other-IDs] NLM/ PMC2727952
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74. Wang BZ, Liu W, Kang SM, Alam M, Huang C, Ye L, Sun Y, Li Y, Kothe DL, Pushko P, Dokland T, Haynes BF, Smith G, Hahn BH, Compans RW: Incorporation of high levels of chimeric human immunodeficiency virus envelope glycoproteins into virus-like particles. J Virol; 2007 Oct;81(20):10869-78
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  • Substitution of the HIV TM-CT with sequences derived from the mouse mammary tumor virus (MMTV) envelope glycoprotein, influenza virus hemagglutinin, or baculovirus (BV) gp64, but not from Lassa fever virus glycoprotein, was found to enhance Env incorporation into VLPs.

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