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1. Sun Y, Wu J, Wu SH, Thakur A, Bollig A, Huang Y, Liao DJ: Expression profile of microRNAs in c-Myc induced mouse mammary tumors. Breast Cancer Res Treat; 2009 Nov;118(1):185-96
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Expression profile of microRNAs in c-Myc induced mouse mammary tumors.
  • c-Myc is a transcription factor overexpression of which induces mammary cancer in transgenic mice.
  • To explore whether certain microRNAs (mirRNA) mediate c-Myc induced mammary carcinogenesis, we studied mirRNA expression profile in mammary tumors developed from MMTV-c-myc transgenic mice, and found 50 and 59 mirRNAs showing increased and decreased expression, respectively, compared with lactating mammary glands of wild type mice.
  • Moreover, we fortuitously identified a novel non-coding RNA, the level of which was decreased in proliferating mammary glands of MMTV-c-myc mice was further decreased to undetectable level in the mammary tumors.
  • These results suggest that certain mirRNAs and the chromosome 19 derived non-coding RNAs may mediate c-myc induced mammary carcinogenesis.

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  • (PMID = 18777135.001).
  • [ISSN] 1573-7217
  • [Journal-full-title] Breast cancer research and treatment
  • [ISO-abbreviation] Breast Cancer Res. Treat.
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / R01 CA100864; United States / NCI NIH HHS / CA / R01CA100864
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
  • [Publication-country] Netherlands
  • [Chemical-registry-number] 0 / MicroRNAs; 0 / RNA, Neoplasm
  • [Other-IDs] NLM/ NIHMS530230; NLM/ PMC3882315
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2. Ahmed KM, Tsai CY, Lee WH: Derepression of HMGA2 via removal of ZBRK1/BRCA1/CtIP complex enhances mammary tumorigenesis. J Biol Chem; 2010 Feb 12;285(7):4464-71
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  • [Title] Derepression of HMGA2 via removal of ZBRK1/BRCA1/CtIP complex enhances mammary tumorigenesis.
  • Indeed, HMGA2 was overexpressed in many different kinds of tumors.
  • Depletion of any of the proteins in this complex via adenoviral RNA interference in MCF10A mammary epithelial cells activates HMGA2 expression, resulting in increased colony formation in soft agar.
  • Consistently, many BRCA1-deficient mouse breast tumors express higher levels of HMGA2 than BRCA1-proficient tumors.

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  • (PMID = 20007691.001).
  • [ISSN] 1083-351X
  • [Journal-full-title] The Journal of biological chemistry
  • [ISO-abbreviation] J. Biol. Chem.
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / R01 CA094170; United States / NCI NIH HHS / CA / CA94170
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / BRCA1 Protein; 0 / Carrier Proteins; 0 / HMGA2 Protein; 0 / Nuclear Proteins; 0 / RBBP8 protein, human; 0 / RNA, Small Interfering; 0 / Repressor Proteins; 0 / ZNF350 protein, human
  • [Other-IDs] NLM/ PMC2836052
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3. 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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4. 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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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [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


5. 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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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • 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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6. Bertagnolli AC, Cassali GD, Genelhu MC, Costa FA, Oliveira JF, Gonçalves PB: Immunohistochemical expression of p63 and deltaNp63 in mixed tumors of canine mammary glands and its relation with p53 expression. Vet Pathol; 2009 May;46(3):407-15
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  • [Title] Immunohistochemical expression of p63 and deltaNp63 in mixed tumors of canine mammary glands and its relation with p53 expression.
  • The immunohistochemical expression of p63, DeltaNp63, and p53 was studied in mixed tumors of canine mammary glands (13 benign mixed tumors and 19 carcinomas arising from benign mixed tumors) to determine the role of p63 and its isoform DeltaNp63 in the development of mixed tumors, as well as to assess its relation with p53.
  • P63 was expressed in myoepithelial cells of all benign mixed tumors and in 18 of 19 carcinomas in mixed tumors.
  • The p63-negative carcinoma in mixed tumors was invasive, and a loss of p63 was detected in the other malignant tumors showing a discontinuous p63-stained myoepithelial layer.
  • DeltaNp63 was expressed in all benign mixed tumors but only in p63-positive carcinomas in mixed tumors.
  • Despite its positive correlation with p63 expression in carcinomas in mixed tumors (r = 0.8323, P < .00001), DeltaNp63 expression showed a decrease in benign tumors.
  • Positivity for p53 was detected in 2 of 13 and 1 of 19 benign mixed tumors and carcinomas in mixed tumors, respectively.
  • Our data support the notion that the decrease of p63 expression, in particular of its isoform DeltaNp63, seems to be an important factor in the development of carcinomas in mixed tumors.
  • [MeSH-major] Gene Expression Regulation, Neoplastic / physiology. Immunohistochemistry / veterinary. Membrane Proteins / metabolism. Mixed Tumor, Malignant / veterinary. Tumor Suppressor Protein p53 / metabolism
  • [MeSH-minor] Animals. Carcinoma / metabolism. Carcinoma / veterinary. Dog Diseases / genetics. Dog Diseases / metabolism. Dogs. Female. Mammary Neoplasms, Animal / metabolism. Protein Isoforms

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  • (PMID = 19176510.001).
  • [ISSN] 0300-9858
  • [Journal-full-title] Veterinary pathology
  • [ISO-abbreviation] Vet. Pathol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Membrane Proteins; 0 / Protein Isoforms; 0 / Tumor Suppressor Protein p53
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7. Mortara L, Giuliani L, De Lerma Barbaro A, Accolla RS, Noonan DM: Experimental therapeutic approaches to adenocarcinoma: the potential of tumor cells engineered to express MHC class II molecules combined with naked DNA interleukin-12 gene transfer. Surg Oncol; 2007 Dec;16 Suppl 1:S33-6
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  • [Title] Experimental therapeutic approaches to adenocarcinoma: the potential of tumor cells engineered to express MHC class II molecules combined with naked DNA interleukin-12 gene transfer.
  • We have previously shown that TS/A murine mammary adenocarcinoma cells, induced to express high surface expression of MHC class II molecules by stable transfection of CIITA, resulted in high rate (92%) of tumor rejection and tumor immunity to subsequent homologous tumor challenges.
  • The immunological basis of tumor response is based on tumor-specific CD4(+) T helper type 1 (Th1) in the priming phase and tumor-specific CD8(+) T cells as the major effector cells.
  • We have previously shown in the same tumor model that a naked DNA IL-12 gene transfer was effective in preventing tumor angiogenesis in an immunopreventive approach when administrated at least 2 days prior to the tumor inoculation.
  • Here we indicate that the combination of the two approaches in immunotherapy of established tumors is efficacious in delaying tumor growth but not in completely eradicating the tumor.
  • [MeSH-major] Adenocarcinoma / immunology. Mammary Neoplasms, Animal / immunology. Nuclear Proteins / immunology. Trans-Activators / immunology

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  • (PMID = 18035537.001).
  • [ISSN] 0960-7404
  • [Journal-full-title] Surgical oncology
  • [ISO-abbreviation] Surg Oncol
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't; Review
  • [Publication-country] Netherlands
  • [Chemical-registry-number] 0 / MHC class II transactivator protein; 0 / Nuclear Proteins; 0 / Trans-Activators; 187348-17-0 / Interleukin-12
  • [Number-of-references] 21
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8. Orsolić N, Basić I: Antitumor, hematostimulative and radioprotective action of water-soluble derivative of propolis (WSDP). Biomed Pharmacother; 2005 Dec;59(10):561-70
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  • Tumor was a transplantable mammary carcinoma (MCa) of CBA mouse.
  • Metastases in the lung were generated by injecting viable tumor cells intravenously (iv).
  • WSDP (50 or 150 mg/kg) exerted a significant antimetastatic effect (P < 0.001) when given either before or after tumor cell inoculation.
  • In combined treatment WSDP and Epirubicin profoundly inhibited metastasis formation; this synergistic effect is maximal when Epirubicin and WSDP were administrated after tumor cell inoculation.
  • Positive outcome of combined treatment with WSDP and Epirubicin was also found regarding the number of red and white blood cells in peripheral blood while in mice treated with Epirubicin alone the significant drop in all hematological parameters was noticed on day 13 after tumor cell inoculation.
  • [MeSH-major] Antineoplastic Agents / pharmacology. Hematopoiesis / drug effects. Lung Neoplasms / prevention & control. Lung Neoplasms / secondary. Mammary Neoplasms, Experimental / drug therapy. Propolis / pharmacology. Radiation-Protective Agents / pharmacology
  • [MeSH-minor] Administration, Oral. Animals. Antibiotics, Antineoplastic / administration & dosage. Antibiotics, Antineoplastic / adverse effects. Blood Cell Count. Cells, Cultured. Disease Models, Animal. Drug Therapy, Combination. Epirubicin / administration & dosage. Epirubicin / adverse effects. Female. Gamma Rays. Injections, Intraperitoneal. Leukopenia / etiology. Leukopenia / prevention & control. Macrophages, Peritoneal / drug effects. Macrophages, Peritoneal / metabolism. Male. Mice. Mice, Inbred CBA. Neoplasm Transplantation. Solubility. Time Factors

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  • (PMID = 16202559.001).
  • [ISSN] 0753-3322
  • [Journal-full-title] Biomedicine & pharmacotherapy = Biomédecine & pharmacothérapie
  • [ISO-abbreviation] Biomed. Pharmacother.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] France
  • [Chemical-registry-number] 0 / Antibiotics, Antineoplastic; 0 / Antineoplastic Agents; 0 / Radiation-Protective Agents; 3Z8479ZZ5X / Epirubicin; 9009-62-5 / Propolis
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9. 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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10. 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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11. Nakano M, Wu H, Taura Y, Inoue M: Immunohistochemical detection of Mdm2 and p53 in feline mammary gland tumors. J Vet Med Sci; 2006 May;68(5):421-5
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  • [Title] Immunohistochemical detection of Mdm2 and p53 in feline mammary gland tumors.
  • The objective of this study was to evaluate nuclear reactivity of Mdm2 and p53 proteins by immunohistochemical means in feline mammary gland tumors; 12 adenomas which included 6 adenomatous lesions obtained from the tissue adjacent to adenocarcinomas, and 22 adenocarcinomas.
  • These results suggest that nuclear overexpression of Mdm2 is present in the tumors of early stage without p53 overexpression and related to feline mammary gland tumorigenesis.
  • Nuclear overexpression of p53 is more frequent in adenocarcinomas, but not in adenomas.

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  • (PMID = 16757883.001).
  • [ISSN] 0916-7250
  • [Journal-full-title] The Journal of veterinary medical science
  • [ISO-abbreviation] J. Vet. Med. Sci.
  • [Language] ENG
  • [Publication-type] Journal Article
  • [Publication-country] Japan
  • [Chemical-registry-number] 0 / Biomarkers, Tumor; 0 / Tumor Suppressor Protein p53; EC 6.3.2.19 / Proto-Oncogene Proteins c-mdm2
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12. 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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13. Burrai GP, Mohammed SI, Miller MA, Marras V, Pirino S, Addis MF, Uzzau S, Antuofermo E: Spontaneous feline mammary intraepithelial lesions as a model for human estrogen receptor- and progesterone receptor-negative breast lesions. BMC Cancer; 2010;10:156
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  • [Title] Spontaneous feline mammary intraepithelial lesions as a model for human estrogen receptor- and progesterone receptor-negative breast lesions.
  • Therefore, a comparative study that establishes an animal model of pre-invasive lesions is needed for the development of preventative measures and effective treatment for both mammary IELs and tumors.
  • The purpose of this study was to characterize the histologic and molecular features of feline mammary IELs and compare them with those in women.
  • METHODS: Formalin-fixed, paraffin-embedded specimens (n = 205) from 203 female cats with clinical mammary disease were retrieved from the archives of the Purdue University Animal Disease Diagnostic Laboratory and Veterinary Teaching Hospital (West Lafayette, IN), and the Department of Pathology and Veterinary Clinic, School of Veterinary Medicine (Sassari, Italy).
  • Histologic sections, stained with hematoxylin and eosin (HE), were evaluated for the presence of IELs in tissue adjacent to excised mammary tumors.
  • Immunohistochemistry for estrogen receptor (ER-alpha), progesterone receptor (PR), human epidermal growth factor receptor 2 (HER-2/neu) and Ki-67 was performed in IELs and adjacent tumor tissues.
  • RESULTS: Intraepithelial lesions were found in 57 of 203 (28%) feline mammary specimens and were categorized as UH (27%), ADH (29%), and DCIS (44%).
  • Most IELs with atypia (ADH and DCIS) were associated with mammary cancer (91%), whereas UH was associated with benign lesions in 53% of cases.
  • No ER or PR immunoreactivity was detected in intermediate-grade or high-grade DCIS or their associated malignant tumors.
  • CONCLUSION: The remarkable similarity of feline mammary IELs to those of humans, with the tendency to lose hormone receptor expression in atypical IELs, supports the cat as a possible model to study ER- and PR-negative breast lesions.
  • [MeSH-major] Breast Neoplasms / pathology. Disease Models, Animal. Estrogen Receptor alpha / biosynthesis. Mammary Neoplasms, Experimental / pathology. Receptors, Progesterone / biosynthesis


14. Wu H, Micca PL, Makar MS, Miura M: Total syntheses of three copper (II) tetracarboranylphenylporphyrins containing 40 or 80 boron atoms and their biological properties in EMT-6 tumor-bearing mice. Bioorg Med Chem; 2006 Aug 1;14(15):5083-92
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  • [Title] Total syntheses of three copper (II) tetracarboranylphenylporphyrins containing 40 or 80 boron atoms and their biological properties in EMT-6 tumor-bearing mice.
  • Three carboranyltetraphenylporphyrins containing 40 or 80 boron atoms were synthesized and evaluated for their biodistribution and toxicity in EMT-6 tumor-bearing mice.
  • Two days after the last of a series of i.p. injections in BALB/c mice bearing EMT-6 mammary tumors, a dose of 185 mg/kg 6 (54 mg/kg B) delivered over 3.5 times the concentration of boron to tumor (169 microg/g B) than did 118 mg/kg 8 (36 mg/kg B), which delivered 35 microg/g B, or 87 mg/kg 18 (30 mg/kg B), which delivered 46 microg/g B.
  • The tumor-to-blood and tumor-to-brain boron concentration ratios at that time for all three porphyrins exceeded 80:1.
  • Thus, 6 may rank among the most clinically promising carboranyl porphyrins ever made to deliver 10B to tumors for boron neutron-capture therapy (BNCT) that has also been tested for its toxicity in vivo.
  • [MeSH-major] Antineoplastic Agents / chemical synthesis. Antineoplastic Agents / pharmacokinetics. Boron Compounds / chemical synthesis. Copper / chemistry. Mammary Neoplasms, Experimental / metabolism. Metalloporphyrins / chemical synthesis. Metalloporphyrins / pharmacokinetics
  • [MeSH-minor] Animals. Cell Line, Tumor. Disease Models, Animal. Drug Screening Assays, Antitumor. Mice. Mice, Inbred BALB C. Molecular Structure. Stereoisomerism. Tissue Distribution. Transplantation, Heterologous

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  • (PMID = 16651000.001).
  • [ISSN] 0968-0896
  • [Journal-full-title] Bioorganic & medicinal chemistry
  • [ISO-abbreviation] Bioorg. Med. Chem.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, U.S. Gov't, Non-P.H.S.
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / Boron Compounds; 0 / Metalloporphyrins; 0 / copper (II) meso-5,10,15,20-tetrakis(3-methoxy-4-(o-carboranylmethoxy)phenyl)porphyrin; 789U1901C5 / Copper
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15. Jarrar MH, Baranova A: PPARgamma activation by thiazolidinediones (TZDs) may modulate breast carcinoma outcome: the importance of interplay with TGFbeta signalling. J Cell Mol Med; 2007 Jan-Feb;11(1):71-87
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  • There is evidence that TZDs act as breast carcinoma suppression agents, at least in the in vitro and animal models.

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  • (PMID = 17367502.001).
  • [ISSN] 1582-1838
  • [Journal-full-title] Journal of cellular and molecular medicine
  • [ISO-abbreviation] J. Cell. Mol. Med.
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / R15 CA113331; United States / NCI NIH HHS / CA / R15CA113331-01
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't; Review
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Hypoglycemic Agents; 0 / PPAR gamma; 0 / Thiazolidinediones; 0 / Transforming Growth Factor beta
  • [Number-of-references] 143
  • [Other-IDs] NLM/ PMC4401221
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16. Samant GV, Wali VB, Sylvester PW: Anti-proliferative effects of gamma-tocotrienol on mammary tumour cells are associated with suppression of cell cycle progression. Cell Prolif; 2010 Feb;43(1):77-83
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  • [Title] Anti-proliferative effects of gamma-tocotrienol on mammary tumour cells are associated with suppression of cell cycle progression.
  • OBJECTIVES: Previous studies have shown that gamma-tocotrienol induces potent anti-proliferative effects on +SA mammary tumour cells in culture; here, investigations have been conducted to determine its effects on intracellular signalling proteins involved in regulating cell cycle progression.
  • [MeSH-major] Cell Cycle / drug effects. Chromans / pharmacology. Mammary Neoplasms, Experimental / metabolism. Vitamin E / analogs & derivatives
  • [MeSH-minor] Animals. Cell Line. Cyclin D1 / metabolism. Cyclin-Dependent Kinase 2 / metabolism. Cyclin-Dependent Kinase 4 / metabolism. Cyclin-Dependent Kinase 6 / metabolism. Cyclin-Dependent Kinase Inhibitor p27 / metabolism. Epidermal Growth Factor / pharmacology. Female. G0 Phase. Mammary Glands, Animal / metabolism. Mice. Phosphorylation

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  • (PMID = 19922488.001).
  • [ISSN] 1365-2184
  • [Journal-full-title] Cell proliferation
  • [ISO-abbreviation] Cell Prolif.
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / CA86833
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Chromans; 136601-57-5 / Cyclin D1; 1406-18-4 / Vitamin E; 147604-94-2 / Cyclin-Dependent Kinase Inhibitor p27; 4382-43-8 / plastochromanol 8; 62229-50-9 / Epidermal Growth Factor; EC 2.7.11.22 / CDK2 protein, human; EC 2.7.11.22 / CDK4 protein, human; EC 2.7.11.22 / CDK6 protein, human; EC 2.7.11.22 / Cyclin-Dependent Kinase 2; EC 2.7.11.22 / Cyclin-Dependent Kinase 4; EC 2.7.11.22 / Cyclin-Dependent Kinase 6
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17. Visbal AP, Lewis MT: Hedgehog signaling in the normal and neoplastic mammary gland. Curr Drug Targets; 2010 Sep;11(9):1103-11
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  • [Title] Hedgehog signaling in the normal and neoplastic mammary gland.
  • Genetic evidence in mice as well as molecular biological studies in human cells clearly indicate that activated signaling can lead to mammary hyperplasia and, in some cases, tumor formation.
  • In this review, we have discussed recent data regarding the mechanism(s) by which the hedgehog network may signal in the mammary gland, as well as the data implicating activated signaling as a contributing factor to breast cancer development.
  • Given the growing intensity with which the hedgehog signaling network is being studied in the normal and neoplastic mammary gland, a more complete understanding of this network should allow more effective targeting of its activities in breast cancer treatment or prevention.
  • [MeSH-major] Breast Neoplasms / metabolism. Hedgehog Proteins / metabolism. Mammary Glands, Human / metabolism. Signal Transduction
  • [MeSH-minor] Animals. Female. Humans. Mammary Glands, Animal / growth & development. Mammary Glands, Animal / metabolism. Mammary Glands, Animal / pathology. Mice. Mice, Knockout. Mice, Transgenic

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  • (PMID = 20545610.001).
  • [ISSN] 1873-5592
  • [Journal-full-title] Current drug targets
  • [ISO-abbreviation] Curr Drug Targets
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / P01 CA030195; United States / NCI NIH HHS / CA / R01 CA127857; United States / NCI NIH HHS / CA / R01 CA127857-01A1
  • [Publication-type] Journal Article; Review
  • [Publication-country] Netherlands
  • [Chemical-registry-number] 0 / Hedgehog Proteins
  •  go-up   go-down


18. 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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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [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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19. 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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20. 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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21. 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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22. Ferreira E, Bertagnolli AC, Cavalcanti MF, Schmitt FC, Cassali GD: The relationship between tumour size and expression of prognostic markers in benign and malignant canine mammary tumours. Vet Comp Oncol; 2009 Dec;7(4):230-5
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  • [Title] The relationship between tumour size and expression of prognostic markers in benign and malignant canine mammary tumours.
  • The aim of this study was to assess the value of tumour size as an indicator of the differentiation of mammary neoplasias in female dogs.
  • The tumour, nodes metastates (TNM) system, based on primary lesion size, the extent of its dissemination to regional lymph nodes and the presence or absence of distant metastases, was applied to 120 female dogs diagnosed with mammary neoplasias.
  • This study highlights the importance of tumour size as a prognostic indicator of mammary neoplasias in female dogs.
  • [MeSH-major] Biomarkers, Tumor / metabolism. Dog Diseases / metabolism. Gene Expression Regulation, Neoplastic / physiology. Mammary Neoplasms, Animal / pathology. Neoplasms / veterinary

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  • (PMID = 19891693.001).
  • [ISSN] 1476-5829
  • [Journal-full-title] Veterinary and comparative oncology
  • [ISO-abbreviation] Vet Comp Oncol
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Biomarkers, Tumor
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23. 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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24. Hermes GL, McClintock MK: Isolation and the timing of mammary gland development, gonadarche, and ovarian senescence: implications for mammary tumor burden. Dev Psychobiol; 2008 May;50(4):353-60
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  • [Title] Isolation and the timing of mammary gland development, gonadarche, and ovarian senescence: implications for mammary tumor burden.
  • In this study of Norway rats, we hypothesized that lifelong psychosocial experiences, social isolation or group living, trigger different developmental trajectories in the ovarian system, contributing to predisease pathways for spontaneous mammary tumors.
  • We assessed ovarian function at both points, as well as mammary gland development at puberty and mammary tumor burden in middle age.
  • Social isolation dissociated two components of puberty; it accelerated maturation of ovarian function while it simultaneously delayed mammary tissue development thereby increasing the exposure of developing breast parenchyma to high levels of estrogen.
  • By mid-life, socially isolated rats had greater tumor burden despite having entered estropause prematurely, demonstrating that isolation did not increase tumorigenesis by prolonging ovarian function.
  • [MeSH-major] Cell Aging / physiology. Estrus / physiology. Gonads / pathology. Mammary Glands, Animal / growth & development. Mammary Neoplasms, Animal / pathology. Ovary / pathology. Social Isolation

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  • (PMID = 18393277.001).
  • [ISSN] 1098-2302
  • [Journal-full-title] Developmental psychobiology
  • [ISO-abbreviation] Dev Psychobiol
  • [Language] eng
  • [Grant] United States / NIA NIH HHS / AG / P01 AG18911; United States / NIEHS NIH HHS / ES / P50 ES012382-01; United States / NIMH NIH HHS / MH / R37 MH41788; United States / NICHD NIH HHS / HD / T32 HD007009
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, U.S. Gov't, Non-P.H.S.
  • [Publication-country] United States
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25. Lebret SC, Newgreen DF, Waltham MC, Price JT, Thompson EW, Ackland ML: Myoepithelial molecular markers in human breast carcinoma PMC42-LA cells are induced by extracellular matrix and stromal cells. In Vitro Cell Dev Biol Anim; 2006 Nov-Dec;42(10):298-307
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  • [Title] Myoepithelial molecular markers in human breast carcinoma PMC42-LA cells are induced by extracellular matrix and stromal cells.
  • It is not clear, however, how the components of the microenvironment control the development of these cell lineages.
  • To investigate how lineage development is regulated by 3-D culture and microenvironment components, we used the PMC42-LA human breast carcinoma cell line, which possesses stem cell characteristics.
  • When cultured on a two-dimensional glass substrate, PMC42-LA cells formed a monolayer and expressed predominantly luminal epithelial markers, including cytokeratins 8, 18, and 19; E-cadherin; and sialomucin.
  • The key myoepithelial-specific proteins alpha-smooth muscle actin and cytokeratin 14 were not expressed.
  • When cultured within Engelbreth-Holm- Swarm sarcoma-derived basement membrane matrix (EHS matrix), PMC42-LA cells formed organoids in which the expression of luminal markers was reduced and the expression of other myoepithelial-specific markers (cytokeratin 17 and P-cadherin) was promoted.
  • The presence of primary human mammary gland fibroblasts within the EHS matrix induced expression of the key myoepithelial-specific markers, alpha-smooth muscle actin and cytokeratin 14.
  • Confocal dual-labeling showed that individual cells expressed luminal or myoepithelial proteins, but not both.
  • Conditioned medium from the mammary fibroblasts was equally effective in inducing myoepithelial marker expression.
  • [MeSH-major] Breast Neoplasms / metabolism. Breast Neoplasms / pathology. Cell Lineage. Epithelial Cells / metabolism. Extracellular Matrix / metabolism. Stromal Cells / metabolism
  • [MeSH-minor] Biomarkers / metabolism. Cell Line, Transformed. Cell Line, Tumor. Culture Media, Conditioned. Fibroblasts / cytology. Fibroblasts / metabolism. Humans. Keratin-8 / metabolism. Mammary Glands, Human / cytology. Mammary Glands, Human / pathology. Phenotype. Protein Transport

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  • (PMID = 17316063.001).
  • [ISSN] 1071-2690
  • [Journal-full-title] In vitro cellular & developmental biology. Animal
  • [ISO-abbreviation] In Vitro Cell. Dev. Biol. Anim.
  • [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] Germany
  • [Chemical-registry-number] 0 / Biomarkers; 0 / Culture Media, Conditioned; 0 / Keratin-8
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26. Zsebik B, Symonowicz K, Saleh Y, Ziolkowski P, Bronowicz A, Vereb G: Photodynamic therapy combined with a cysteine proteinase inhibitor synergistically decrease VEGF production and promote tumour necrosis in a rat mammary carcinoma. Cell Prolif; 2007 Feb;40(1):38-49
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  • [Title] Photodynamic therapy combined with a cysteine proteinase inhibitor synergistically decrease VEGF production and promote tumour necrosis in a rat mammary carcinoma.
  • We have investigated the efficacy of PDT and CPI alone and in combination on a solid mammary carcinoma transplanted into Wistar rats.
  • CPI (500 micro g per animal) was injected around the tumour daily during the 8-day treatment.
  • [MeSH-major] Carcinoma / drug therapy. Cysteine Proteinase Inhibitors / pharmacology. Mammary Neoplasms, Experimental / therapy. Photochemotherapy / methods. Vascular Endothelial Growth Factor A / biosynthesis
  • [MeSH-minor] Animals. Cystatins / pharmacology. Dose-Response Relationship, Drug. Female. Necrosis. Neoplasm Transplantation. Rats. Rats, Wistar

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  • (PMID = 17227294.001).
  • [ISSN] 0960-7722
  • [Journal-full-title] Cell proliferation
  • [ISO-abbreviation] Cell Prolif.
  • [Language] eng
  • [Publication-type] Comparative Study; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Cystatins; 0 / Cysteine Proteinase Inhibitors; 0 / Vascular Endothelial Growth Factor A
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27. 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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28. Moiseeva EV, Semushina SG, Chaadaeva AV, Sadovnikova ES, Kessler IuV: [Criteria for the effectiveness of interleukin-2 immunotherapy in a spontaneous murine mammary tumor model]. Vopr Onkol; 2010;56(4):443-9
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  • [Title] [Criteria for the effectiveness of interleukin-2 immunotherapy in a spontaneous murine mammary tumor model].
  • A novel approach is suggested to identify more homogenous subgroups involved in the follow-up of growth of spontaneous mammary tumors in mice (116, history-based analysis).
  • That depends on subclinical period (preneoplastic and non-invasive stages of tumor growth) as well as rate of growth after clinical manifestation.
  • An analysis of tumor growth rate versus survival of experimental and control animals after primary diagnosis and clinical manifestation of tumor showed that following a single peritumoral 2.5 x 10(6) IU IL-2 treatment tumor growth slowed down (n = 29; p < or = 0.05) while survival tended to improve.
  • Originally fast-growing tumors without significant subclinical stage continued to grow but slowly.
  • Females with such tumors survived longer than untreated controls without showing, however, any improvement on that parameter.
  • [MeSH-major] Antineoplastic Agents / pharmacology. Breast Neoplasms / drug therapy. Interleukin-2 / pharmacology
  • [MeSH-minor] Animals. Disease Models, Animal. Female. Mice. Mice, Inbred Strains. Time Factors. Treatment Outcome

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  • (PMID = 20968024.001).
  • [ISSN] 0507-3758
  • [Journal-full-title] Voprosy onkologii
  • [ISO-abbreviation] Vopr Onkol
  • [Language] rus
  • [Publication-type] English Abstract; Journal Article
  • [Publication-country] Russia (Federation)
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / Interleukin-2
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29. 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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30. Clapp C, Thebault S, Martínez de la Escalera G: Role of prolactin and vasoinhibins in the regulation of vascular function in mammary gland. J Mammary Gland Biol Neoplasia; 2008 Mar;13(1):55-67
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  • [Title] Role of prolactin and vasoinhibins in the regulation of vascular function in mammary gland.
  • The formation of new blood vessels has become a major focus of mammary gland research stimulated by the therapeutic opportunities of controlling angiogenesis in breast cancer.
  • Normal growth and involution of the mammary gland are profoundly affected by the expansion and regression of blood vessels, whereas dysregulation of angiogenesis is characteristic of breast cancer growth and metastasis.
  • Prolactin stimulates the growth and differentiation of the mammary gland under normal conditions, but its role in breast cancer is controversial.
  • This review summarizes our current knowledge about the vascular effects of prolactin and the generation and action of vasoinhibins, and discusses their possible contribution to the regulation of blood vessels in the normal and malignant mammary gland.
  • [MeSH-major] Angiogenesis Inhibitors / metabolism. Mammary Glands, Animal / blood supply. Mammary Glands, Animal / metabolism. Mammary Glands, Human / blood supply. Mammary Glands, Human / metabolism. Prolactin / metabolism. Vasodilation
  • [MeSH-minor] Animals. Breast Neoplasms / blood supply. Breast Neoplasms / metabolism. Humans

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  • (PMID = 18204888.001).
  • [ISSN] 1573-7039
  • [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; Review
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Angiogenesis Inhibitors; 9002-62-4 / Prolactin
  • [Number-of-references] 160
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31. Kaur S, Greaves P, Cooke DN, Edwards R, Steward WP, Gescher AJ, Marczylo TH: Breast cancer prevention by green tea catechins and black tea theaflavins in the C3(1) SV40 T,t antigen transgenic mouse model is accompanied by increased apoptosis and a decrease in oxidative DNA adducts. J Agric Food Chem; 2007 May 02;55(9):3378-85
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  • Tea consumption is associated with a reduced risk of mammary cancer as reflected by epidemiological studies and experiments in carcinogen-induced rodent models of mammary carcinogenesis.
  • We tested the hypothesis that green tea catechins (GTC) or theaflavins from black tea (BTT) interfere with mammary carcinogenesis in C3(1) SV40 T,t antigen transgenic multiple mammary adenocarcinoma (TAg) mice and that GTC/BTT affect tumor survival or oxidation status.
  • As compared to control mice, they survived longer and had smaller tumors.
  • On microscopic inspection, the size of the largest tumor per mouse was decreased by 40-42% (p<0.01).
  • GTC (0.01%) and BTT (0.05%) increased levels of cleaved caspase 3 in tumor tissue by 67 and 38%, respectively (p<0.05), intimating increased apoptosis.
  • Tumor levels of the malondialdehyde-DNA adduct M1dG in mice receiving GTC or BTT (0.05%) were reduced by 78 (p<0.001) or 63% (p<0.05), respectively, as compared to controls.
  • [MeSH-major] Apoptosis / drug effects. Biflavonoids / administration & dosage. Catechin / administration & dosage. DNA Adducts / analysis. Mammary Neoplasms, Animal / prevention & control. Tea / chemistry
  • [MeSH-minor] Animals. Antigens, Polyomavirus Transforming / genetics. Caspase 3 / analysis. Cell Line, Tumor. Humans. Mice. Mice, Transgenic

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  • (PMID = 17407311.001).
  • [ISSN] 0021-8561
  • [Journal-full-title] Journal of agricultural and food chemistry
  • [ISO-abbreviation] J. Agric. Food Chem.
  • [Language] eng
  • [Grant] United Kingdom / Medical Research Council / / G0100874
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antigens, Polyomavirus Transforming; 0 / Biflavonoids; 0 / DNA Adducts; 0 / Tea; 1IA46M0D13 / theaflavin; 8R1V1STN48 / Catechin; EC 3.4.22.- / Caspase 3
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32. 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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  • [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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33. Hynes NE, Watson CJ: Mammary gland growth factors: roles in normal development and in cancer. Cold Spring Harb Perspect Biol; 2010 Aug;2(8):a003186
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  • [Title] Mammary gland growth factors: roles in normal development and in cancer.
  • Normal development of the mammary gland proceeds via interactions between the epithelium and the mesenchyme that start during embryogenesis and continue during pubertal outgrowth and differentiation.
  • Mammary tumor cells often produce a peptide and express the receptor on the same cell leading to autocrine activation of signaling pathways, a mechanism that is characteristic for cancer cells.

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  • (PMID = 20554705.001).
  • [ISSN] 1943-0264
  • [Journal-full-title] Cold Spring Harbor perspectives in biology
  • [ISO-abbreviation] Cold Spring Harb Perspect Biol
  • [Language] ENG
  • [Grant] United Kingdom / Biotechnology and Biological Sciences Research Council / /
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't; Review
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Peptides; 0 / Protein Isoforms; 0 / Receptors, Cytokine; 62229-50-9 / Epidermal Growth Factor
  • [Other-IDs] NLM/ PMC2908768
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34. 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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35. 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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36. Okugawa H, Yamamoto D, Uemura Y, Sakaida N, Tanano A, Tanaka K, Kamiyama Y: Effect of perductal paclitaxel exposure on the development of MNU-induced mammary carcinoma in female S-D rats. Breast Cancer Res Treat; 2005 May;91(1):29-34
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  • [Title] Effect of perductal paclitaxel exposure on the development of MNU-induced mammary carcinoma in female S-D rats.
  • After mammary tumors were identified macroscopically using fiberscope, the rats were treated with perductal (pd) or ip injection of paclitaxel tri-weekly.
  • At 36 weeks after MNU injection, tumor burden (No. of >1cm palpable mammary tumors/rat), total number of mammary carcinoma, apoptosis (AI), and microvessel density (MVD) were measured.
  • RESULTS: The administration of paclitaxel through the duct did not produce any toxic side effect.
  • The tumor burden and total number of mammary carcinoma in the pd paclitaxel-treated group were significantly reduced compared to those seen in the ip paclitaxel-treated group.
  • [MeSH-major] Antineoplastic Agents, Phytogenic / administration & dosage. Antineoplastic Agents, Phytogenic / pharmacology. Mammary Neoplasms, Animal / drug therapy. Paclitaxel / administration & dosage. Paclitaxel / pharmacology
  • [MeSH-minor] Alkylating Agents / administration & dosage. Animals. Female. Infusions, Parenteral. Mammary Glands, Animal. Mammary Neoplasms, Experimental. Methylnitrosourea / administration & dosage. Rats. Rats, Sprague-Dawley

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  • (PMID = 15868429.001).
  • [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 / Alkylating Agents; 0 / Antineoplastic Agents, Phytogenic; 684-93-5 / Methylnitrosourea; P88XT4IS4D / Paclitaxel
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37. 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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38. Simeonov R, Simeonova G: Computerized morphometry of mean nuclear diameter and nuclear roundness in canine mammary gland tumors on cytologic smears. Vet Clin Pathol; 2006 Mar;35(1):88-90
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  • [Title] Computerized morphometry of mean nuclear diameter and nuclear roundness in canine mammary gland tumors on cytologic smears.
  • OBJECTIVES: The aim of this study was to define whether the morphometric parameters of mean nuclear diameter and nuclear roundness could be used to differentiate benign from malignant canine mammary gland tumors on cytologic specimens.
  • METHODS: Mean nuclear diameter and nuclear roundness were determined by computer-assisted morphometry of epithelial cells in Hemacolor-stained cytologic smears from normal canine mammary gland (n = 7) and from canine mammary adenomas (n = 8), tubulopapillary carcinomas (n = 9), and solid carcinomas (n = 6).
  • RESULTS: Significant differences (P <.001) were found in mean nuclear diameter and nuclear roundness among all tumor types and in comparison with normal canine mammary gland epithelial cells (except for nuclear roundness between tubulopapillary carcinomas and solid carcinomas).
  • CONCLUSIONS: The morphometric parameters of mean nuclear diameter and nuclear roundness can be used in the preoperative differentiation of benign from malignant canine mammary gland tumors.

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  • (PMID = 16511796.001).
  • [ISSN] 0275-6382
  • [Journal-full-title] Veterinary clinical pathology
  • [ISO-abbreviation] Vet Clin Pathol
  • [Language] ENG
  • [Publication-type] Journal Article
  • [Publication-country] United States
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39. Cavigelli SA, Yee JR, McClintock MK: Infant temperament predicts life span in female rats that develop spontaneous tumors. Horm Behav; 2006 Sep;50(3):454-62
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  • [Title] Infant temperament predicts life span in female rats that develop spontaneous tumors.
  • At death, these males had various complex pathologies, precluding identification of specific hormonal mechanisms underlying adult disease progression and mortality.
  • To minimize the variance of disease processes at the end of life, we conducted a longitudinal study with female Sprague-Dawley rats prone to high rates of spontaneous mammary and pituitary tumors.
  • For females that developed either mammary or pituitary tumors, those that had been neophobic (least exploratory) as infants died approximately 6 months earlier than their neophilic (most exploratory) sisters.
  • In the case of mammary tumors, both benign and malignant, neophobic females developed palpable tumors earlier than neophilic females, whereas the interval between first palpation and death was the same for all females, indicating psychosocial regulation of early rather than later stages of the disease.
  • During puberty, when mammary tissue is proliferating and differentiating, neophobic females experienced more irregular cycles with prolonged "luteal" phases, suggesting a role for prolactin, prolonged progesterone and fewer estrogen surges during this sensitive period for mammary tumor risk.
  • Thus, we identified prolactin, estrogen, progesterone and possibly corticosterone dynamics as candidates for neuroendocrine mechanisms linking infant temperament with onset of adult neoplastic disease.
  • [MeSH-major] Exploratory Behavior / physiology. Longevity / physiology. Mammary Neoplasms, Animal / physiopathology. Pituitary Neoplasms / physiopathology. Temperament / physiology

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  • (PMID = 16836996.001).
  • [ISSN] 0018-506X
  • [Journal-full-title] Hormones and behavior
  • [ISO-abbreviation] Horm Behav
  • [Language] eng
  • [Grant] United States / NICHD NIH HHS / HD / F32 HD008693; United States / NICHD NIH HHS / HD / F32 HD08693; United States / NIA NIH HHS / AG / P01 AG018911; United States / NIMH NIH HHS / MH / R37 MH41788
  • [Publication-type] Comparative Study; Journal Article; Research Support, N.I.H., Extramural
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Glucocorticoids
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40. Thayer KA, Foster PM: Workgroup report: National Toxicology Program workshop on Hormonally Induced Reproductive Tumors - Relevance of Rodent Bioassays. Environ Health Perspect; 2007 Sep;115(9):1351-6
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  • [Title] Workgroup report: National Toxicology Program workshop on Hormonally Induced Reproductive Tumors - Relevance of Rodent Bioassays.
  • This review includes a recent workshop, "Hormonally Induced Reproductive Tumors-Relevance of Rodent Bioassays," held 22-24 May 2006, that was organized to determine the adequacy and relevance to human disease outcome of rodent models currently used in the 2-year bioassay for four types of hormonally induced reproductive tumors (ovary, mammary gland, prostate, and testis).
  • For some types of tumors such as prostate, no adequate animal models exist, and for others such as ovary, the predominant tumors in humans are of different cellular origins than those induced by chemicals in rodents.

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  • (PMID = 17805427.001).
  • [ISSN] 0091-6765
  • [Journal-full-title] Environmental health perspectives
  • [ISO-abbreviation] Environ. Health Perspect.
  • [Language] ENG
  • [Grant] United States / Intramural NIH HHS / /
  • [Publication-type] Journal Article; Research Support, N.I.H., Intramural
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Carcinogens; 0 / Hormones
  • [Other-IDs] NLM/ PMC1964911
  • [Keywords] NOTNLM ; National Toxicology Program / animal models / breast / endocrine / hormone / mammary gland / ovary / prostate / reproductive tumors / species differences / testis
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41. Klopfleisch R, Schütze M, Gruber AD: RAD51 protein expression is increased in canine mammary carcinomas. Vet Pathol; 2010 Jan;47(1):98-101
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  • [Title] RAD51 protein expression is increased in canine mammary carcinomas.
  • RAD51 mRNA expression levels are significantly increased in laser-microdissected mammary simple carcinomas and their lymph node metastases when compared to adenomas or nonneoplastic mammary gland of the same dog.
  • Here, RAD51 protein expression was analyzed by immunohistochemistry in paraffin-embedded mammary carcinomas and their lymph node metastases of 40 dogs, adenomas of 48 dogs, and nonneoplastic mammary gland of 88 dogs.
  • RAD51 expression in carcinomas was correlated with expression in metastases but not with histologic grade.
  • Nevertheless, the increased RAD51 mRNA expression in metastases could not be confirmed by immunohistochemistry.
  • [MeSH-major] Dog Diseases / physiopathology. Mammary Neoplasms, Animal / physiopathology. Rad51 Recombinase / biosynthesis
  • [MeSH-minor] Adenoma / enzymology. Adenoma / pathology. Adenoma / physiopathology. Animals. Carcinoma / enzymology. Carcinoma / pathology. Carcinoma / physiopathology. Dogs. Female. Gene Expression Regulation, Neoplastic / physiology. Lymphatic Metastasis. Mammary Glands, Animal / enzymology. Mammary Glands, Animal / pathology. Mammary Glands, Animal / physiopathology

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  • (PMID = 20080488.001).
  • [ISSN] 1544-2217
  • [Journal-full-title] Veterinary pathology
  • [ISO-abbreviation] Vet. Pathol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] EC 2.7.7.- / Rad51 Recombinase
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42. Kawaguchi H, Miyoshi N, Miyamoto Y, Souda M, Umekita Y, Yasuda N, Yoshida H: Effects of fetal exposure to diethylstilbestrol on mammary tumorigenesis in rats. J Vet Med Sci; 2009 Dec;71(12):1599-608
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  • [Title] Effects of fetal exposure to diethylstilbestrol on mammary tumorigenesis in rats.
  • The aim of this study was to investigate the effect of fetal exposure to diethylstilbestrol (DES) on the induction of mammary tumors induced by 7,12-dimethylbenz[a]anthracene (DMBA) in female rats.
  • Some rats exposed to DES throughout pregnancy and those from day 13 till the end of pregnancy showed endocrine disrupting effects such as absence of CL and active lactation in mammary glands at necropsy, while no abnormal estrus cycle such as persistent estrus was seen during the observation period until 88 days after birth.
  • Fetal exposure to 0.1 ppm DES throughout pregnancy period, 0.1 and 1 ppm DES from day 13 of pregnancy increased the incidence and number of mammary carcinomas (MCs) at the earlier period while exposure to 0.1 ppm DES throughout pregnancy period enhanced the incidence and number of benign proliferative lesions (PLs) at the later period.

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  • (PMID = 20046027.001).
  • [ISSN] 0916-7250
  • [Journal-full-title] The Journal of veterinary medical science
  • [ISO-abbreviation] J. Vet. Med. Sci.
  • [Language] ENG
  • [Publication-type] Journal Article
  • [Publication-country] Japan
  • [Chemical-registry-number] 731DCA35BT / Diethylstilbestrol
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43. Astolfi A, Landuzzi L, Nicoletti G, De Giovanni C, Croci S, Palladini A, Ferrini S, Iezzi M, Musiani P, Cavallo F, Forni G, Nanni P, Lollini PL: Gene expression analysis of immune-mediated arrest of tumorigenesis in a transgenic mouse model of HER-2/neu-positive basal-like mammary carcinoma. Am J Pathol; 2005 Apr;166(4):1205-16
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  • [Title] Gene expression analysis of immune-mediated arrest of tumorigenesis in a transgenic mouse model of HER-2/neu-positive basal-like mammary carcinoma.
  • We previously showed that a vaccine combining interleukin 12 and allogeneic p185(neu)-positive mammary carcinoma cells completely prevented multifocal mammary carcinogenesis in HER-2/neu transgenic mice.
  • To identify the molecular events responsible for effective tumor prevention and to define the tumor gene expression signature, we used microarrays to analyze the expression profile of mammary tissue of untreated transgenic mice and of vaccine-treated, tumor-free mice at different time points.
  • Mammary tissue from vaccinated mice displayed a gene expression profile different from that of untreated, tumor-bearing mice but similar to that of normal/hyperplastic mammary gland.
  • Comparison of treated and untreated mice at 15 weeks of age revealed up-regulation of genes encoding antibodies, chemokines, gamma-interferon-induced genes and inflammatory molecules, and down-regulation of early genes induced by tumor development.
  • The gene expression signature of HER-2/neu-transformed tumor cells showed modulation of genes promoting proliferation, angiogenesis, migration, invasion, and metastasis and inhibiting apoptosis and immune response.
  • Meta-analysis of microarray data on human breast cancer showed that the signature of tumors arising in murine HER-2/neu transgenic model correctly classified human HER-2/neu-expressing tumors and normal breast tissue.
  • Moreover murine and human HER-2/neu-positive tumors share the signature of basal-like breast cancers.
  • This gene expression analysis reveals the immune events associated with prevention of tumor development and shows that HER-2/neu transgenic mice represent a good model of a poor-prognosis group of human breast tumors.
  • [MeSH-major] Cancer Vaccines / therapeutic use. Gene Expression Regulation, Neoplastic / drug effects. Mammary Neoplasms, Experimental / genetics. Mammary Neoplasms, Experimental / prevention & control. Receptor, ErbB-2 / metabolism
  • [MeSH-minor] Animals. Disease Models, Animal. Gene Expression / drug effects. Gene Expression Profiling. Humans. Male. Mice. Mice, Transgenic

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  • (PMID = 15793299.001).
  • [ISSN] 0002-9440
  • [Journal-full-title] The American journal of pathology
  • [ISO-abbreviation] Am. J. Pathol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Cancer Vaccines; EC 2.7.10.1 / Receptor, ErbB-2
  • [Other-IDs] NLM/ PMC1602398
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44. Gumireddy K, Li A, Gimotty PA, Klein-Szanto AJ, Showe LC, Katsaros D, Coukos G, Zhang L, Huang Q: KLF17 is a negative regulator of epithelial-mesenchymal transition and metastasis in breast cancer. Nat Cell Biol; 2009 Nov;11(11):1297-304
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  • We transduced a genome-wide RNA interference (RNAi) library into the non-metastatic 168FARN breast cancer cell line and orthotopically transplanted the cells into mouse mammary fat pads.
  • Conversely, we demonstrate that ectopic expression of KLF17 in a highly metastatic 4T1 breast cancer cell line inhibits the ability of cells to metastasize from the mammary fat pad to the lung.


45. 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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  • [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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46. 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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  • [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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47. Petterino C, Ratto A, Podestà G, Drigo M, Pellegrino C: Immunohistochemical evaluation of STAT3-p-tyr705 expression in feline mammary gland tumours and correlation with histologic grade. Res Vet Sci; 2007 Apr;82(2):218-24
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  • [Title] Immunohistochemical evaluation of STAT3-p-tyr705 expression in feline mammary gland tumours and correlation with histologic grade.
  • The expression of STAT3 phosphorylated on tyrosine 705 (STAT3-p-tyr705) in normal, hyperplastic and neoplastic feline mammary gland tissue was assessed by immunohistochemistry in 45 cats.
  • The samples included 4 normal mammary non-lactating tissues, 9 hyperplastic tissues (5 fibroepithelial hyperplasia and 4 lobular epithelial hyperplasia), 2 benign tumours (1 complex adenoma, and 1 simple adenoma), and 30 carcinomas (18 simple tubular papillary, 6 simple tubular, 2 simple solid, 3 cribriform, and 1 adenosquamous carcinoma).
  • Normal non-lactating mammary tissue showed a low number of positive cells, similar to hyperplastic tissue.
  • [MeSH-major] Carcinoma / veterinary. Cat Diseases / metabolism. Mammary Neoplasms, Animal / metabolism. STAT3 Transcription Factor / biosynthesis

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  • (PMID = 16934302.001).
  • [ISSN] 0034-5288
  • [Journal-full-title] Research in veterinary science
  • [ISO-abbreviation] Res. Vet. Sci.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / STAT3 Transcription Factor; 42HK56048U / Tyrosine
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48. Duffy PH, Lewis SM, Mayhugh MA, Trotter RW, Hass BS, Latendresse JR, Thorn BT, Tobin G, Feuers RJ: Neoplastic pathology in male Sprague-Dawley rats fed AIN-93M diet ad libitum or at restricted intakes. Nutr Res; 2008 Jan;28(1):36-42
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  • At 58 weeks of age, the predominant types of lesions in AL and DR rats were pituitary and skin tumors.
  • At 114 weeks of age, the most common lesions were pituitary, adrenal gland, skin, mammary, brain, and pancreatic tumors and mononuclear cell leukemia.
  • Primary findings demonstrate that DR significantly reduced the total number of tumors per rat and incidence of benign and primary tumors (all organs) but did not reduce the incidence of malignant tumors (all organs).
  • These results may explain why survival rates for AL and DR rats were not significantly different at 114 weeks (43.3 vs 57.5%, respectively).
  • Factors such as diet composition and digestibility, although not independent of body weight, may have contributed to differences in rat mortality and may affect humans in a similar manner.
  • [MeSH-major] Aging / physiology. Caloric Restriction. Caseins / administration & dosage. Dietary Proteins / administration & dosage. Neoplasms / epidemiology. Neoplasms / pathology
  • [MeSH-minor] Age Factors. Animal Feed. Animal Nutritional Physiological Phenomena. Animals. Incidence. Longevity / physiology. Male. Random Allocation. Rats. Rats, Sprague-Dawley. Severity of Illness Index. Survival Analysis

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  • (PMID = 19083386.001).
  • [ISSN] 1879-0739
  • [Journal-full-title] Nutrition research (New York, N.Y.)
  • [ISO-abbreviation] Nutr Res
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Caseins; 0 / Dietary Proteins
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49. Loveless ME, Whisenant JG, Wilson K, Lyshchik A, Sinha TK, Gore JC, Yankeelov TE: Coregistration of ultrasonography and magnetic resonance imaging with a preliminary investigation of the spatial colocalization of vascular endothelial growth factor receptor 2 expression and tumor perfusion in a murine tumor model. Mol Imaging; 2009 Jul-Aug;8(4):187-98
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  • [Title] Coregistration of ultrasonography and magnetic resonance imaging with a preliminary investigation of the spatial colocalization of vascular endothelial growth factor receptor 2 expression and tumor perfusion in a murine tumor model.
  • Tumor volumes from each data set were segmented independently by two investigators and coregistered using an iterative closest point algorithm.
  • In addition to anatomic images, vascular endothelial growth factor receptor 2 (VEGFR2) distribution images from the central tumor slice using VEGFR2-targeted ultrasound contrast agent (UCA) and measurements of perfusion and extravascular-extracellular volume fraction using dynamic contrast-enhanced MRI were acquired from five mice for multiparametric coregistration.
  • In the preliminary study, VEGFR2-targeted UCA data did not demonstrate direct spatial correlation with magnetic resonance measures of vascular properties.
  • In summary, a method for accurately coregistering small animal US and MRI has been presented that allows for comparison of quantitative metrics provided by the two modalities.

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  • (PMID = 19728973.001).
  • [ISSN] 1535-3508
  • [Journal-full-title] Molecular imaging
  • [ISO-abbreviation] Mol Imaging
  • [Language] ENG
  • [Grant] United States / NIBIB NIH HHS / EB / T32 EB003817-05; United States / NCI NIH HHS / CA / CA068485-139010; United States / NCI NIH HHS / CA / CA126588; United States / NCI NIH HHS / CA / U24 CA126588-03; United States / NCI NIH HHS / CA / U24 CA 126588; United States / NCI NIH HHS / CA / U24 CA126588; United States / NIBIB NIH HHS / EB / K25 EB005936-04; United States / NCI NIH HHS / CA / P30 CA068485-139010; United States / NCI NIH HHS / CA / P30 CA068485; United States / NIBIB NIH HHS / EB / T32 EB003817; United States / NIBIB NIH HHS / EB / K25 EB005936; United States / NIBIB NIH HHS / EB / 1K25 EB005936-01; United States / NIBIB NIH HHS / EB / EB005936-04
  • [Publication-type] Evaluation Studies; Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] EC 2.7.10.1 / Vascular Endothelial Growth Factor Receptor-2
  • [Other-IDs] NLM/ NIHMS136174; NLM/ PMC2739085
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50. John R, Rezaeipoor R, Adie SG, Chaney EJ, Oldenburg AL, Marjanovic M, Haldar JP, Sutton BP, Boppart SA: In vivo magnetomotive optical molecular imaging using targeted magnetic nanoprobes. Proc Natl Acad Sci U S A; 2010 May 4;107(18):8085-90
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  • In this study, we demonstrate in vivo imaging of dynamic functionalized iron oxide MNPs using MM-OCT in a preclinical mammary tumor model.
  • Using targeted MNPs, in vivo MM-OCT images exhibit strong magnetomotive signals in mammary tumor, and no significant signals were measured from tumors of rats injected with nontargeted MNPs or saline.
  • The results of in vivo MM-OCT are validated by MRI, ex vivo MM-OCT, Prussian blue staining of histological sections, and immunohistochemical analysis of excised tumors and internal organs.

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  • (PMID = 20404194.001).
  • [ISSN] 1091-6490
  • [Journal-full-title] Proceedings of the National Academy of Sciences of the United States of America
  • [ISO-abbreviation] Proc. Natl. Acad. Sci. U.S.A.
  • [Language] ENG
  • [Grant] United States / NIBIB NIH HHS / EB / R01 EB005221; United States / NCI NIH HHS / CA / CA147096; United States / NCI NIH HHS / CA / RC1 CA147096; United States / NIBIB NIH HHS / EB / R21 EB005321; United States / NIBIB NIH HHS / EB / R01EB005221; United States / NIBIB NIH HHS / EB / R01 EB009073
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Contrast Media; EC 2.7.10.1 / Receptor, ErbB-2
  • [Other-IDs] NLM/ PMC2889582
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51. Bankhead A 3rd, Magnuson NS, Heckendorn RB: Gene knockout experiments to quantify a G2/M genetic network simulation for mammary cancer susceptibility. In Silico Biol; 2006;6(3):181-92
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  • [Title] Gene knockout experiments to quantify a G2/M genetic network simulation for mammary cancer susceptibility.
  • A G2/M genetic network simulation is trained with tumor incidence data from knockout experiments.
  • We use a novel approach of fixing the network topology that allows knockout TSG (tumor suppressor gene) data from multiple studies to overlap and indirectly inform one another.
  • The trained simulation is validated by reproducing qualitative mammary cancer susceptibilities of ATM, BRCA1, and p53 TSGs.
  • The work described is valuable because it allows TSG mammary cancer susceptibility to be quantified using genetic network topology and in vivo knockout data.
  • [MeSH-major] Breast Neoplasms / genetics. Gene Deletion. Genetic Predisposition to Disease
  • [MeSH-minor] Animals. Cell Cycle. Cell Division. Computer Simulation. Female. G2 Phase. Humans. Mice. Mice, Knockout. Models, Animal. Models, Genetic


52. Gu Y, Chen WR, Xia M, Jeong SW, Liu H: Effect of photothermal therapy on breast tumor vascular contents: noninvasive monitoring by near-infrared spectroscopy. Photochem Photobiol; 2005 Jul-Aug;81(4):1002-9
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  • [Title] Effect of photothermal therapy on breast tumor vascular contents: noninvasive monitoring by near-infrared spectroscopy.
  • The goal of this study was to investigate the effect of photothermal laser irradiation on rat breast tumor (DMBA-4) vascular contents.
  • The dynamic changes of oxygenated hemoglobin and total hemoglobin concentrations, delta[HbO2] and delta[Hb]total, in rat tumors during photothermal irradiation were noninvasively monitored by a near-infrared spectroscopy system.
  • A multichannel thermal detection system was also used simultaneously to record temperatures at different locations within the tumors.
  • (1) photoirradiation did have the ability to induce hyperthermic effects inside the rat breast tumors in a single exponential trend;.
  • (2) the significant changes (P < 0.005) of delta[HbO2] and delta[Hb]total in response to a low dosage of laser irradiation (0.32 W/cm2) have a single exponential increasing trend, similar to that seen in the tumor interior temperature; and (3) the increase in magnitude of delta[HbO2] is nearly two times greater than that of delta[Hb]total, suggesting that photoirradiation may enhance tumor vascular oxygenation.
  • The last observation may be important to reveal the hidden mechanism of photoirradiation on tumors, leading to improvement of tumor treatment efficiency.
  • [MeSH-major] Hyperthermia, Induced. Mammary Neoplasms, Animal / therapy

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  • (PMID = 15807632.001).
  • [ISSN] 0031-8655
  • [Journal-full-title] Photochemistry and photobiology
  • [ISO-abbreviation] Photochem. Photobiol.
  • [Language] eng
  • [Grant] United States / NCRR NIH HHS / RR / P20 RR016478
  • [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] United States
  • [Chemical-registry-number] 0 / Hemoglobins; 0 / Oxyhemoglobins
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53. Koch JG, Gu X, Han Y, El-Naggar AK, Olson MV, Medina D, Jerry DJ, Blackburn AC, Peltz G, Amos CI, Lozano G: Mammary tumor modifiers in BALB/cJ mice heterozygous for p53. Mamm Genome; 2007 May;18(5):300-9
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  • [Title] Mammary tumor modifiers in BALB/cJ mice heterozygous for p53.
  • BALB/c mice are predisposed to developing spontaneous mammary tumors, which are further increased in a p53 heterozygous state.
  • C57BL/6J mice are resistant to induced mammary tumors and develop less than 1% mammary tumors in both wild-type and p53+/- states.
  • To map modifiers of mammary tumorigenesis, we have established F1 and F2 crosses and backcrosses to BALB/cJ (N2-BALB/cJ) and C57BL/6J (N2-C57BL/6J) strains.
  • All cohorts developed mammary carcinomas in p53+/- females, suggesting that multiple loci dominantly and recessively contributed to mammary tumorigenesis.
  • We mapped two modifiers of mammary tumorigenesis in the BALB/cJ strain.
  • Mtsm1 (mammary tumor susceptibility modifier), a dominant-acting modifier, is located on chromosome 7.
  • Mtsm1 is suggestive for linkage to mammary tumorigenesis (p = 0.001).
  • Mtsm2 is located on chromosome X and is significantly linked to mammary tumorigenesis (p = 1.03 x 10(-7)).
  • [MeSH-major] Genes, p53. Heterozygote. Mammary Neoplasms, Animal / genetics
  • [MeSH-minor] Animals. Crosses, Genetic. Female. Genetic Predisposition to Disease. Male. Mice. Mice, Inbred BALB C. Mice, Inbred C57BL. Rats. Specific Pathogen-Free Organisms

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  • (PMID = 17557176.001).
  • [ISSN] 0938-8990
  • [Journal-full-title] Mammalian genome : official journal of the International Mammalian Genome Society
  • [ISO-abbreviation] Mamm. Genome
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / CA009299; United States / NCI NIH HHS / CA / CA16672; United States / NCI NIH HHS / CA / P01 CA34936; United States / NCI NIH HHS / CA / U01 CA-04-002
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
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54. Barry M, Cahill RA, Roche-Nagle G, Neilan TG, Treumann A, Harmey JH, Bouchier-Hayes DJ: Neoplasms escape selective COX-2 inhibition in an animal model of breast cancer. Ir J Med Sci; 2009 Jun;178(2):201-8
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  • [Title] Neoplasms escape selective COX-2 inhibition in an animal model of breast cancer.
  • METHODS: 4T1 cells were injected into the mammary fat pad of BALB/c mice (n = 8).
  • An identical trend was also observed whether COX-2 knockout mice received SC-236 or not, suggesting that this effect is due to increased tumour-derived COX-2 production rather than recovery of host COX-2 functional capacity.
  • CONCLUSION: The anti-neoplastic effects of selective COX-2 inhibition may not be sustained as tumours demonstrate an escape capacity.
  • [MeSH-major] Breast Neoplasms / enzymology. Cyclooxygenase 2 / metabolism. Cyclooxygenase 2 Inhibitors / therapeutic use. Lipoxygenase / metabolism
  • [MeSH-minor] Animals. Disease Progression. Female. Mice. Mice, Inbred BALB C. Models, Animal. Random Allocation

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  • [CommentIn] Ir J Med Sci. 2009 Dec;178(4):517 [19711016.001]
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  • (PMID = 19340516.001).
  • [ISSN] 1863-4362
  • [Journal-full-title] Irish journal of medical science
  • [ISO-abbreviation] Ir J Med Sci
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Ireland
  • [Chemical-registry-number] 0 / Cyclooxygenase 2 Inhibitors; EC 1.13.11.12 / Lipoxygenase; EC 1.14.99.1 / Cyclooxygenase 2
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55. Nagae M, Hiraga T, Yoneda T: Acidic microenvironment created by osteoclasts causes bone pain associated with tumor colonization. J Bone Miner Metab; 2007;25(2):99-104
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  • [Title] Acidic microenvironment created by osteoclasts causes bone pain associated with tumor colonization.
  • To test this notion, we studied an animal model in which inoculation of MRMT-1 rat breast cancer cells into the tibiae in female rats induced hyperalgesia.
  • Behavioral analyses showed that rats exhibited hyperalgesia in the tumor-inoculated legs.
  • The expression of ASIC1a and ASIC1b was increased in the ipsilateral DRGs, whereas the ASIC3 and TRPV1 expression was not changed.
  • [MeSH-major] Bone Diseases / pathology. Bone Neoplasms / pathology. Bone Resorption. Mammary Neoplasms, Animal / pathology. Osteoclasts / physiology. Pain / etiology
  • [MeSH-minor] Animals. Cell Line, Tumor. Female. Genes, fos. Rats. Reverse Transcriptase Polymerase Chain Reaction


56. Fleming JM, Miller TC, Meyer MJ, Ginsburg E, Vonderhaar BK: Local regulation of human breast xenograft models. J Cell Physiol; 2010 Sep;224(3):795-806
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  • Patient-derived breast cancer cells were injected into mouse abdominal or thoracic mammary glands +/- estrogen and/or etoposide pretreatment.
  • Abdominal xenografts had increased tumor incidence and volume, and decreased latency (P < 0.001) compared to thoracic tumors.
  • No statistically significant difference in tumor volume was found in abdominal xenografts treated +/- estrogen or etoposide; however, etoposide suppressed tumor volume in thoracic xenografts (P < 0.02).
  • The combination of estrogen and etoposide significantly decreased tumor incidence in both sites.
  • Orthotopic injection increased tumor volume; growth varied with estrogen supplementation.
  • Lastly, vascularization of orthotopic tumors was significantly enhanced compared to subcutaneous tumors.
  • [MeSH-major] Breast Neoplasms. Disease Models, Animal. Transplantation, Heterologous
  • [MeSH-minor] Animals. Antineoplastic Agents, Phytogenic / metabolism. Cell Line, Tumor. DNA Methylation. Estrogens / metabolism. Etoposide / metabolism. Female. Humans. Mice. Mice, Nude. Neoplasm Transplantation. Promoter Regions, Genetic. Receptors, Estrogen / genetics. Receptors, Estrogen / metabolism. Receptors, Progesterone / genetics. Receptors, Progesterone / metabolism

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  • (PMID = 20578247.001).
  • [ISSN] 1097-4652
  • [Journal-full-title] Journal of cellular physiology
  • [ISO-abbreviation] J. Cell. Physiol.
  • [Language] eng
  • [Grant] United States / Intramural NIH HHS / / ZIA BC010768-03
  • [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 / Antineoplastic Agents, Phytogenic; 0 / Estrogens; 0 / Receptors, Estrogen; 0 / Receptors, Progesterone; 6PLQ3CP4P3 / Etoposide
  • [Other-IDs] NLM/ NIHMS206802; NLM/ PMC2897719
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57. Lee SL, Huang PY, Roller P, Cho EG, Park D, Dickson RB: Matriptase/epithin participates in mammary epithelial cell growth and morphogenesis through HGF activation. Mech Dev; 2010 Jan-Feb;127(1-2):82-95
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  • [Title] Matriptase/epithin participates in mammary epithelial cell growth and morphogenesis through HGF activation.
  • We show in this study that epithin/matriptase (Epi/MTP) plays a significant role in mammary epithelial cell growth and morphogenesis.
  • Epi/MTP is expressed at low level in the mouse mammary epithelium of young animals and it accumulates at the terminal end-bud of the growing ducts.
  • The level of Epi/MTP is elevated in the mammary glands at stages when epithelial proliferation and modeling occur.
  • It is primarily present in the luminal epithelial cells of mouse mammary ducts and lobules.
  • Using an ex vivo three-dimensional culture system for mammary epithelial functional assays, we show that mammary epithelial growth and morphogenesis in the presence of the latent form hepatocyte growth factor (pro-HGF) are blocked either by an inhibitor of the Epi/MTP protease activity or by siRNA knockdown of the Epi/MTP expression.
  • These studies demonstrate that Epi/MTP participates in mammary epithelial growth and modeling through activation of pro-HGF.
  • Our findings reveal an important pathway in normal mammary epithelial morphogenesis which may participate in breast cancer progression.
  • [MeSH-minor] Animals. Cell Culture Techniques / methods. Cell Proliferation. Dose-Response Relationship, Drug. Mammary Glands, Animal / metabolism. Mammary Neoplasms, Animal / metabolism. Mice. Microscopy, Confocal / methods. Peptides, Cyclic / metabolism. RNA Interference. RNA, Small Interfering / metabolism. Time Factors

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  • [Copyright] Copyright 2009 Elsevier Ireland Ltd. All rights reserved.
  • (PMID = 19853659.001).
  • [ISSN] 1872-6356
  • [Journal-full-title] Mechanisms of development
  • [ISO-abbreviation] Mech. Dev.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Ireland
  • [Chemical-registry-number] 0 / Peptides, Cyclic; 0 / RNA, Small Interfering; 0 / SFTI-1 peptide, sunflower; 67256-21-7 / Hepatocyte Growth Factor; EC 3.4.21.- / Serine Endopeptidases; EC 3.4.21.- / matriptase
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58. Parrish A, Halama E, Tilli MT, Freedman M, Furth PA: Reflectance confocal microscopy for characterization of mammary ductal structures and development of neoplasia in genetically engineered mouse models of breast cancer. J Biomed Opt; 2005 Sep-Oct;10(5):051602
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  • [Title] Reflectance confocal microscopy for characterization of mammary ductal structures and development of neoplasia in genetically engineered mouse models of breast cancer.
  • The earliest steps of breast cancer begin with aberrations in mammary ductal structure.
  • Cellular confocal microscopy (VivaCell-TiBa, Rochester, New York) is used to image mammary ductal structures and surrounding vasculature in situ in intact wild-type and genetically engineered mice that develop ER alpha-initiated ductal carcinoma in situ (DCIS) and ER alpha-driven invasive mammary cancer.
  • In wild-type mice, normal mammary ductal structures that appear from puberty through lactation are visualized and serially sectioned optically, and a developmental atlas is created.
  • In the genetically engineered mice, aberrant mammary ductal structures and cancers are imaged and compared to corresponding normal structures.
  • Comparative studies demonstrate that reflectance confocal imaging provides more cellular detail than carmine-alum-stained mammary gland whole mounts and equivalent detail with hematoxylin and eosin stained tissue sections.
  • In summary, reflectance confocal microscopy is a tool that can be used to rapidly and accurately analyze mammary gland structure.
  • [MeSH-major] Breast Neoplasms / pathology. Carcinoma, Ductal, Breast / pathology. Disease Models, Animal. Mammary Neoplasms, Experimental / pathology. Microscopy, Confocal / methods
  • [MeSH-minor] Adenocarcinoma. Aging / pathology. Animals. Disease Progression. Female. Mice. Mice, Inbred C57BL. Mice, Transgenic. Reproducibility of Results. Sensitivity and Specificity

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  • (PMID = 16292950.001).
  • [ISSN] 1083-3668
  • [Journal-full-title] Journal of biomedical optics
  • [ISO-abbreviation] J Biomed Opt
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / 2T32CA09686-08; United States / NCI NIH HHS / CA / R01 CA089041-10; United States / NCI NIH HHS / CA / R01 CA112176-05; United States / NCI NIH HHS / CA / T32 CA009686; United States / NCI NIH HHS / CA / R01 CA089041; United States / NCI NIH HHS / CA / R01 CA112176
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't; Research Support, U.S. Gov't, Non-P.H.S.
  • [Publication-country] United States
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59. Li H, Dutuor A, Fu X, Zhang X: Induction of strong antitumor immunity by an HSV-2-based oncolytic virus in a murine mammary tumor model. J Gene Med; 2007 Mar;9(3):161-9
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  • [Title] Induction of strong antitumor immunity by an HSV-2-based oncolytic virus in a murine mammary tumor model.
  • Oncolytic viruses have shown considerable promise for the treatment of solid tumors.
  • In previous studies, we demonstrated that a novel oncolytic virus (FusOn-H2), constructed by replacing the serine/threonine protein kinase (PK) domain of the ICP10 gene of type 2 herpes simplex virus (HSV-2) with the gene encoding the green fluorescent protein, can selectively replicate in and thus lyse tumor cells.
  • 4T1 tumor cells are weakly immunogenic and the mammary tumors derived from them aggressively metastasize to different parts of body, thus providing an attractive model for evaluating anticancer agents.
  • We thus tested the antitumor effect of FusOn-H2 in this tumor model, in comparisons with several other oncolytic HSVs derived from HSV-1, including a nonfusogenic HSV-1 (Baco-1) and a doubly fusogenic virus (Synco-2D).
  • Moreover, FusOn-H2 induced strong T cell responses against primary and metastatic mammary tumors in vivo, and splenocytes adoptively transferred from FusOn-H2-treated mice effectively prevented metastasis in naïve mice bearing implanted mammary tumors.
  • [MeSH-major] Herpesvirus 2, Human / genetics. Lung Neoplasms / therapy. Mammary Neoplasms, Animal / therapy. Oncolytic Virotherapy / methods. Oncolytic Viruses / genetics
  • [MeSH-minor] Adoptive Transfer. Animals. Cell Line, Tumor. Disease Models, Animal. Female. Green Fluorescent Proteins / analysis. Green Fluorescent Proteins / genetics. Mice. Mice, Inbred BALB C. Spleen / immunology. T-Lymphocytes / immunology. Xenograft Model Antitumor Assays

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  • [Copyright] Copyright 2007 John Wiley & Sons, Ltd.
  • (PMID = 17266169.001).
  • [ISSN] 1099-498X
  • [Journal-full-title] The journal of gene medicine
  • [ISO-abbreviation] J Gene Med
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / CA106671
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 147336-22-9 / Green Fluorescent Proteins
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60. 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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61. Chan BT, Lee AV: Insulin receptor substrates (IRSs) and breast tumorigenesis. J Mammary Gland Biol Neoplasia; 2008 Dec;13(4):415-22
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  • IRS levels are developmentally and hormonally regulated in the normal mammary gland and both are essential for normal mammary gland bud formation and lactation.
  • In this review we will discuss the roles of IRSs in mammary gland development and breast cancer.

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  • (PMID = 19030971.001).
  • [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 / CA / CA094118-05; United States / NCI NIH HHS / CA / R01 CA094118; United States / NCI NIH HHS / CA / R01 CA094118-05; United States / NCI NIH HHS / CA / R01CA94118
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't; Review
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Insulin Receptor Substrate Proteins; 0 / Oncogene Proteins
  • [Number-of-references] 83
  • [Other-IDs] NLM/ NIHMS173185; NLM/ PMC2819329
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62. Millanta F, Calandrella M, Vannozzi I, Poli A: Steroid hormone receptors in normal, dysplastic and neoplastic feline mammary tissues and their prognostic significance. Vet Rec; 2006 Jun 17;158(24):821-4
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Steroid hormone receptors in normal, dysplastic and neoplastic feline mammary tissues and their prognostic significance.
  • The expression of oestrogen-alpha and progesterone receptors was determined in 13 normal, 21 dysplastic and 53 neoplastic feline mammary tissues.
  • Expression of the receptors was correlated with cell proliferation, as assessed by the MIB-1 immunolabelling index, and with the clinical course of the disease.
  • The oestrogen and progesterone receptor status of the invasive carcinomas did not correlate either with the histological parameters or with the overall survival of the cats, although the oestrogen receptor-negative tumours had a poor prognosis.
  • Oestrogen receptor-positive neoplasms had a significantly lower MIB-1 immunolabelling index than oestrogen receptor-negative neoplasms.
  • [MeSH-major] Carcinoma / veterinary. Cat Diseases / metabolism. Mammary Glands, Animal / metabolism. Mammary Neoplasms, Animal / metabolism. Receptors, Estrogen / analysis. Receptors, Progesterone / analysis

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  • (PMID = 16782855.001).
  • [ISSN] 0042-4900
  • [Journal-full-title] The Veterinary record
  • [ISO-abbreviation] Vet. Rec.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Receptors, Estrogen; 0 / Receptors, Progesterone
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63. Wang RH: The new portrait of mammary gland stem cells. Int J Biol Sci; 2006;2(4):186-7
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] The new portrait of mammary gland stem cells.
  • [MeSH-major] Breast / cytology. Breast / pathology. Cell Cycle / physiology. Mammary Glands, Animal / cytology. Mammary Glands, Animal / pathology. Stem Cells / cytology. Stem Cells / pathology
  • [MeSH-minor] Animals. Antigens, CD / analysis. Antigens, CD31 / analysis. Antigens, CD45 / analysis. Breast Neoplasms / pathology. Breast Neoplasms / prevention & control. Female. Humans

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  • [Cites] J Pathol. 2006 Jan;208(1):7-16 [16294373.001]
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  • (PMID = 16810333.001).
  • [ISSN] 1449-2288
  • [Journal-full-title] International journal of biological sciences
  • [ISO-abbreviation] Int. J. Biol. Sci.
  • [Language] eng
  • [Publication-type] Letter
  • [Publication-country] Australia
  • [Chemical-registry-number] 0 / Antigens, CD; 0 / Antigens, CD31; EC 3.1.3.48 / Antigens, CD45
  • [Other-IDs] NLM/ PMC1483121
  • [General-notes] NLM/ Original DateCompleted: 20070613
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64. Weinberg RA: Leaving home early: reexamination of the canonical models of tumor progression. Cancer Cell; 2008 Oct 7;14(4):283-4
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Leaving home early: reexamination of the canonical models of tumor progression.
  • [MeSH-major] Epithelial Cells / pathology. Lung Neoplasms / secondary. Mammary Glands, Animal / pathology. Mammary Neoplasms, Experimental / pathology. Neoplastic Cells, Circulating / pathology. Proto-Oncogene Proteins c-myc / metabolism. Proto-Oncogene Proteins p21(ras) / metabolism
  • [MeSH-minor] Animals. Cell Proliferation. Cell Survival. Cell Transformation, Neoplastic / metabolism. Cell Transformation, Neoplastic / pathology. Female. Gene Expression Regulation, Neoplastic. Mice. Neoplasm Metastasis. Neoplasm Seeding

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  • (PMID = 18835030.001).
  • [ISSN] 1878-3686
  • [Journal-full-title] Cancer cell
  • [ISO-abbreviation] Cancer Cell
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Proto-Oncogene Proteins c-myc; EC 3.6.5.2 / Proto-Oncogene Proteins p21(ras)
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65. Weidensteiner C, Rausch M, McSheehy PM, Allegrini PR: Quantitative dynamic contrast-enhanced MRI in tumor-bearing rats and mice with inversion recovery TrueFISP and two contrast agents at 4.7 T. J Magn Reson Imaging; 2006 Sep;24(3):646-56
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  • [Title] Quantitative dynamic contrast-enhanced MRI in tumor-bearing rats and mice with inversion recovery TrueFISP and two contrast agents at 4.7 T.
  • PURPOSE: To characterize tumor vascularization by dynamic-contrast enhanced (DCE) MRI using low and medium molecular weight paramagnetic contrast agents (CA) and inversion recovery (IR) true fast imaging with steady state precession (TrueFISP) in tumor-bearing rats and mice.
  • In rat breast tumors, vascular permeability (transfer constant K(trans)), fractional plasma volume v(p), and fractional leakage space v(e) were quantified and parametric maps were generated.
  • The larger molecular weight CA P792 appears to be better for measuring tumor vascular parameters.
  • [MeSH-minor] Animals. Gadolinium DTPA / pharmacology. Heterocyclic Compounds / pharmacology. Kinetics. Mammary Neoplasms, Animal / blood supply. Mammary Neoplasms, Animal / diagnosis. Mice. Mice, Inbred C3H. Mice, Nude. Models, Statistical. Organometallic Compounds / pharmacology. Phantoms, Imaging. Rats. Time Factors

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  • (PMID = 16878308.001).
  • [ISSN] 1053-1807
  • [Journal-full-title] Journal of magnetic resonance imaging : JMRI
  • [ISO-abbreviation] J Magn Reson Imaging
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Contrast Media; 0 / Heterocyclic Compounds; 0 / Organometallic Compounds; 92923-44-9 / gadolinium 1,4,7,10-tetraazacyclododecane-N,N',N'',N'''-tetraacetate; K2I13DR72L / Gadolinium DTPA
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66. de Assis S, Warri A, Cruz MI, Hilakivi-Clarke L: Changes in mammary gland morphology and breast cancer risk in rats. J Vis Exp; 2010 Oct 16;(44)
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  • [Title] Changes in mammary gland morphology and breast cancer risk in rats.
  • Studies in rodent models of breast cancer show that exposures to dietary/hormonal factors during the in utero and pubertal periods, when the mammary gland undergoes extensive modeling and re-modeling, alter susceptibility to carcinogen-induced mammary tumors.
  • It is thought that these prenatal and postnatal dietary modifications induce persistent morphological changes in the mammary gland that in turn modify breast cancer risk later in life.
  • In this article we describe how changes in mammary gland morphology can predict mammary cancer risk in rats.
  • Our protocol specifically describes how to dissect and remove the rat abdominal mammary gland and how to prepare mammary gland whole mounts.
  • It also describes how to analyze mammary gland morphology according to three end-points (number of terminal end buds, epithelial elongation and differentiation) and to use the data to predict risk of developing mammary cancer.

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  • [ISSN] 1940-087X
  • [Journal-full-title] Journal of visualized experiments : JoVE
  • [ISO-abbreviation] J Vis Exp
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / R03 CA150040; United States / NCI NIH HHS / CA / U54 CA100970; United States / NCI NIH HHS / CA / 1 R03 CA150040-01; United States / NCI NIH HHS / CA / U54 CA00100970
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  • [Other-IDs] NLM/ PMC3185639
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67. Noori S, Taghikhani M, Hassan ZM, Allameh A, Mostafaei A: Tehranolide could shift the immune response towards Th1 and modulate the intra-tumor infiltrated T regulatory cells. Iran J Immunol; 2009 Dec;6(4):216-24
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  • [Title] Tehranolide could shift the immune response towards Th1 and modulate the intra-tumor infiltrated T regulatory cells.
  • METHODS: Tehranolide was purified from Artemisia diffusa, and its effect on the tumor volume was investigated.
  • The splenocyte proliferation, shifting of cytokine profile, and the presence of naturally-occurring CD4+CD25+Foxp3+ Treg cells were assessed to describe the anti-tumor immune response.
  • RESULTS: Analysis of immune response showed that, intra-tumoral injection of Tehranolide decreased the rate of tumor growth compared to control group.
  • The results indicated a decrease in tumor CD4+CD25+Foxp3+ T lymphocytes in the Tehranolide-treated group compared to the control group.
  • CONCLUSION: Treatment of tumors with Tehranolide attenuated CD4+CD25+Foxp3+ Treg cell-mediated immune suppression and elicited a persistent anti-tumor immunity against cancer.
  • [MeSH-major] Artemisia / chemistry. Mammary Neoplasms, Animal / prevention & control. Plant Extracts / pharmacology. Sesquiterpenes / pharmacology. T-Lymphocytes, Regulatory / drug effects. Th1 Cells / drug effects
  • [MeSH-minor] Animals. Cell Proliferation / drug effects. Enzyme-Linked Immunosorbent Assay. Female. Interferon-gamma / metabolism. Interleukin-4 / metabolism. Mice. Mice, Inbred BALB C. Molecular Structure. Phytotherapy. Spleen / drug effects. Spleen / metabolism. Spleen / pathology. Treatment Outcome. Tumor Burden / drug effects

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  • (PMID = 20054110.001).
  • [ISSN] 1735-1383
  • [Journal-full-title] Iranian journal of immunology : IJI
  • [ISO-abbreviation] Iran J Immunol
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Iran
  • [Chemical-registry-number] 0 / Plant Extracts; 0 / Sesquiterpenes; 0 / tehranolide; 207137-56-2 / Interleukin-4; 82115-62-6 / Interferon-gamma
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68. 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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69. Matsuda Y, Schlange T, Oakeley EJ, Boulay A, Hynes NE: WNT signaling enhances breast cancer cell motility and blockade of the WNT pathway by sFRP1 suppresses MDA-MB-231 xenograft growth. Breast Cancer Res; 2009;11(3):R32
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  • WNT ligands and Frizzled receptors are coexpressed in primary breast tumors and cancer cell lines.
  • Moreover, many breast tumors show hypermethylation of the secreted Frizzled-related protein 1 (sFRP1) promoter region, causing low expression of this WNT antagonist.
  • Here we examine the role of WNT signaling in breast tumor cell migration and on xenograft outgrowth.
  • Microarray analyses were carried out to identify targets with roles in MDA-MB-231/sFRP1 tumor growth inhibition.
  • Moreover, the ability of MDA-MB-231/sFRP1-expressing cells to grow as xenografts in mammary glands and to form lung metastases is dramatically impaired.
  • Microarray analyses led to the identification of two genes, CCND1 and CDKN1A, whose expression level is selectively altered in vivo in sFRP1-expressing tumors.
  • The encoded proteins cyclin D1 and p21Cip1 were downregulated and upregulated, respectively, in sFRP1-expressing tumors, suggesting that they are downstream mediators of WNT signaling.
  • WNT stimulates tumor cell motility; conversely sFRP1-mediated WNT pathway blockade reduces motility.
  • Moreover, ectopic sFRP1 expression in MDA-MB-231 cells has a strong negative impact on tumor outgrowth and blocked lung metastases.
  • [MeSH-major] Breast Neoplasms / metabolism. Intercellular Signaling Peptides and Proteins / metabolism. Mammary Neoplasms, Animal / metabolism. Membrane Proteins / metabolism. Wnt Proteins / metabolism
  • [MeSH-minor] Animals. Cell Line, Tumor. Cell Movement. Cell Survival. Female. Humans. Mice. Mice, Inbred BALB C. Neoplasm Transplantation. Signal Transduction


70. 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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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • 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