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1. el-Aziz MA, Hassan HA, Mohamed MH, Meki AR, Abdel-Ghaffar SK, Hussein MR: The biochemical and morphological alterations following administration of melatonin, retinoic acid and Nigella sativa in mammary carcinoma: an animal model. Int J Exp Pathol; 2005 Dec;86(6):383-96
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  • [Title] The biochemical and morphological alterations following administration of melatonin, retinoic acid and Nigella sativa in mammary carcinoma: an animal model.
  • Worldwide, breast cancer is the second leading cause of cancer death among women and the third most common cancer.
  • To date, our understanding of the mechanisms of therapeutic effects of these products in mammary cancer is still marginal.
  • An animal model formed of 80 rats was established.
  • (b) carcinogen group injected with the known carcinogenic substance 7,12-di-methylbenz(a)anthracene (DMBA) that induces mammary carcinoma;.
  • Carcinoma was absent both in the control and in the NS-Pro groups.
  • Mammary carcinoma occurred in DMBA and other Pro and Tr groups.
  • The frequency of mammary carcinoma was high in the carcinogen DMBA group (60%), followed by the Tr (56%) and finally the Pro groups (33%).
  • These tumours included papillary, comedo and cribriform carcinomas.
  • As compared with the control group, the development of carcinoma in the carcinogen DMBA group was associated with increased levels of (a) markers of tumorigenicity (77.0 +/- 3.3 vs. 209.0 +/- 5.6 and P < 0.05 for TSA; 28.7 +/- 1.7 vs. 41.8 +/- 1.2 and P < 0.01 for LSA), (b) markers of endocrine derangement (2.5 +/- 0.1 vs. 3.6 +/- 0.3 and P < 0.05 for prolactin; 39.6 +/- 1.3 vs. 24.8 +/- 2.1 and P < 0.01 for progesterone and 31.0 +/- 0.7 vs. 51.1 +/- 3.4 and P < 0.01 for estradiol) and (c) markers of oxidative stress (2.3 +/- 0.2 vs. 5.2 +/- 0.7 and P < 0.01 for lipid peroxides and 4.4 +/- 0.2 vs. 7.6 +/- 0.8 and P < 0.01 for nitric oxide).
  • When compared with the carcinogen DMBA group, the development of carcinoma in the Pro and Tr groups was associated with decreased levels of (a) markers of tumorigenicity, (b) markers of endocrine derangement and (c) markers of oxidative stress.
  • [MeSH-major] Mammary Neoplasms, Experimental / metabolism. Melatonin / therapeutic use. Nigella sativa. Phytotherapy / methods. Plant Extracts / therapeutic use. Tretinoin / therapeutic use

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  • (PMID = 16309544.001).
  • [ISSN] 0959-9673
  • [Journal-full-title] International journal of experimental pathology
  • [ISO-abbreviation] Int J Exp Pathol
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Biomarkers, Tumor; 0 / Plant Extracts; 31C4KY9ESH / Nitric Oxide; 4G7DS2Q64Y / Progesterone; 4TI98Z838E / Estradiol; 5688UTC01R / Tretinoin; 9002-62-4 / Prolactin; GZP2782OP0 / N-Acetylneuraminic Acid; JL5DK93RCL / Melatonin
  • [Other-IDs] NLM/ PMC2517452
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2. Sassi F, Benazzi C, Castellani G, Sarli G: Molecular-based tumour subtypes of canine mammary carcinomas assessed by immunohistochemistry. BMC Vet Res; 2010;6:5
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  • [Title] Molecular-based tumour subtypes of canine mammary carcinomas assessed by immunohistochemistry.
  • BACKGROUND: Human breast cancer is classified by gene expression profile into subtypes consisting of two hormone (oestrogen and/or progesterone) receptor-positive types (luminal-like A and luminal-like B) and three hormone receptor-negative types [human epidermal growth factor receptor 2-expressing, basal-like, and unclassified ("normal-like")].
  • The present study aimed to apply an immunohistochemical panel (anti-ER, -PR, -ERB-B2, -CK 5/6 and -CK14) in a series of canine malignant mammary tumours to verify the molecular-based classification, its correlation with invasion and grade, and its use as a prognostic aid in veterinary practice.
  • Most luminal-like A and basal-like tumours were grade 1 carcinomas, while the percentage of luminal B tumours was higher in grades 2 and 3 (Pearson Chi-square P = 0.009).
  • No difference in the percentage of molecular subtypes was found between simple and complex/mixed carcinomas (Pearson Chi-square P = 0.47).
  • Even though canine mammary tumours may be a model of human breast cancer, the existence of the same carcinoma molecular subtypes in women awaits confirmation.
  • Canine mammary carcinomas show high molecular heterogeneity, which would benefit from a classification based on molecular differences.
  • [MeSH-major] Biomarkers, Tumor / metabolism. Dog Diseases / diagnosis. Mammary Neoplasms, Animal / diagnosis
  • [MeSH-minor] Animals. Dogs. Female. Immunohistochemistry. Kaplan-Meier Estimate. Mammary Glands, Animal / pathology

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  • (PMID = 20109214.001).
  • [ISSN] 1746-6148
  • [Journal-full-title] BMC veterinary research
  • [ISO-abbreviation] BMC Vet. Res.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Biomarkers, Tumor
  • [Other-IDs] NLM/ PMC2837647
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3. Papaconstantinou AD, Snyderwine EG: Proliferation and apoptosis in PhIP-induced rat mammary gland carcinomas with elevated phosphotyrosine-STAT5a. FEBS Lett; 2007 Jan 9;581(1):29-33
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  • [Title] Proliferation and apoptosis in PhIP-induced rat mammary gland carcinomas with elevated phosphotyrosine-STAT5a.
  • In the present study we addressed whether proliferation and apoptosis in 2-amino-1-methyl-6-phenylimidazo[4,5-b]pyridine-induced rat mammary gland carcinomas were different between carcinomas with high and low expression of phosphotyrosine (pY)-STAT5a.
  • We determined that carcinomas with high pY-STAT5a were more proliferative (MIB5 immunostaining) and had a higher expression of cyclin D1 and estrogen receptor alpha.
  • Furthermore, carcinomas with elevated pY-STAT5a demonstrated lower apoptosis as measured by the TUNEL assay and the Bcl-2 to Bax ratio, and showed increased expression of the long and short isoforms of the prolactin receptor.
  • The results of this study are consistent with the notion that activated STAT5a may provide a growth advantage in some types of mammary gland cancers.
  • [MeSH-major] Apoptosis. Carcinogens / toxicity. Cell Proliferation. Imidazoles / toxicity. Mammary Neoplasms, Experimental / metabolism. Phosphotyrosine / metabolism. STAT5 Transcription Factor / metabolism
  • [MeSH-minor] Animals. Cyclin D. Cyclins / metabolism. Estrogen Receptor alpha / metabolism. Female. Mammary Glands, Animal / metabolism. Mammary Glands, Animal / pathology. Rats. Rats, Sprague-Dawley. Tumor Cells, Cultured. bcl-2-Associated X Protein / metabolism

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  • (PMID = 17173897.001).
  • [ISSN] 0014-5793
  • [Journal-full-title] FEBS letters
  • [ISO-abbreviation] FEBS Lett.
  • [Language] eng
  • [Publication-type] Comparative Study; Journal Article
  • [Publication-country] Netherlands
  • [Chemical-registry-number] 0 / Bax protein, rat; 0 / Carcinogens; 0 / Cyclin D; 0 / Cyclins; 0 / Estrogen Receptor alpha; 0 / Imidazoles; 0 / STAT5 Transcription Factor; 0 / Stat5a protein, rat; 0 / bcl-2-Associated X Protein; 21820-51-9 / Phosphotyrosine; 909C6UN66T / 2-amino-1-methyl-6-phenylimidazo(4,5-b)pyridine
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4. Woditschka S, Haag JD, Waller JL, Monson DM, Hitt AA, Brose HL, Hu R, Zheng Y, Watson PA, Kim K, Lindstrom MJ, Mau B, Steele VE, Lubet RA, Gould MN: Neu-induced retroviral rat mammary carcinogenesis: a novel chemoprevention model for both hormonally responsive and nonresponsive mammary carcinomas. Cancer Res; 2006 Jul 1;66(13):6884-91
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  • [Title] Neu-induced retroviral rat mammary carcinogenesis: a novel chemoprevention model for both hormonally responsive and nonresponsive mammary carcinomas.
  • Clinically relevant animal models of mammary carcinogenesis are crucial for the development and evaluation of new breast cancer chemopreventive agents.
  • The neu-induced retroviral rat mammary carcinogenesis model is based on the direct in situ transfer of the activated neu oncogene into the mammary epithelium using a replication-defective retroviral vector.
  • The resulting mammary carcinomas in intact Wistar-Furth rats exhibit a mixed hormonal response in the same proportion as has been observed in women.
  • In intact rats, approximately 50% of mammary carcinomas can be prevented by tamoxifen treatment.
  • In ovariectomized animals, the mammary carcinomas are hormonally nonresponsive and cannot be prevented by tamoxifen.
  • We evaluated the efficacy of retinoic X receptor-selective retinoids (rexinoids) in this novel model of mammary carcinogenesis.
  • The rexinoids LG100268 and bexarotene (LG1069, Targretin) were highly efficacious in the prevention of neu-induced mammary carcinomas.
  • The neu-induced retroviral rat mammary carcinogenesis model represents a valuable addition to existing rodent chemoprevention models.
  • [MeSH-major] Anticarcinogenic Agents / pharmacology. Disease Models, Animal. Genes, erbB-2. Mammary Neoplasms, Experimental / genetics. Mammary Neoplasms, Experimental / prevention & control. Neoplasms, Hormone-Dependent / genetics. Neoplasms, Hormone-Dependent / prevention & control

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  • (PMID = 16818667.001).
  • [ISSN] 0008-5472
  • [Journal-full-title] Cancer research
  • [ISO-abbreviation] Cancer Res.
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / CA 101201; United States / NCI NIH HHS / CN / CN 05116; United States / NCI NIH HHS / CN / CN 15124; United States / NCI NIH HHS / CN / CN 85176
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, U.S. Gov't, Non-P.H.S.
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Anticarcinogenic Agents; 0 / LG 100268; 0 / Nicotinic Acids; 0 / Tetrahydronaphthalenes; 094ZI81Y45 / Tamoxifen; A61RXM4375 / bexarotene
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5. Shakya R, Szabolcs M, McCarthy E, Ospina E, Basso K, Nandula S, Murty V, Baer R, Ludwig T: The basal-like mammary carcinomas induced by Brca1 or Bard1 inactivation implicate the BRCA1/BARD1 heterodimer in tumor suppression. Proc Natl Acad Sci U S A; 2008 May 13;105(19):7040-5
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  • [Title] The basal-like mammary carcinomas induced by Brca1 or Bard1 inactivation implicate the BRCA1/BARD1 heterodimer in tumor suppression.
  • Women with germ-line mutations of the BRCA1 tumor suppressor gene are highly susceptible to breast and ovarian cancer.
  • To address this question, we generated mouse strains carrying conditional alleles of either Bard1 or Brca1 and used Cre recombination to inactivate these genes in mammary epithelial cells.
  • Significantly, the conditional Bard1- and Brca1-mutant mice developed breast carcinomas that are indistinguishable from each other (and from those of double conditional Bard1/Brca1-mutant animals) with respect to their frequency, latency, histopathology, and cytogenetic features.
  • Reminiscent of the basal-like breast carcinomas seen in human BRCA1 mutation carriers, these tumors are "triple negative" for estrogen and progesterone receptor expression and HER2/neu amplification.
  • The remarkable similarities between the mammary carcinomas of Bard1-, Brca1-, and Bard1/Brca1-mutant mice indicate that the tumor suppressor activities of both genes are mediated through the BRCA1/BARD1 heterodimer.

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  • (PMID = 18443292.001).
  • [ISSN] 1091-6490
  • [Journal-full-title] Proceedings of the National Academy of Sciences of the United States of America
  • [ISO-abbreviation] Proc. Natl. Acad. Sci. U.S.A.
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / P01 CA097403; United States / NCI NIH HHS / CA / T32 CA009503; United States / NCI NIH HHS / CA / 1P01-CA97403; United States / NCI NIH HHS / CA / T32-CA09503
  • [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 / BRCA1 Protein; 0 / Bard1 protein, mouse; 0 / Tumor Suppressor Protein p53; 0 / Tumor Suppressor Proteins; EC 6.3.2.19 / Ubiquitin-Protein Ligases
  • [Other-IDs] NLM/ PMC2365565
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6. Umesako S, Fujisawa K, Iiga S, Mori N, Takahashi M, Hong DP, Song CW, Haga S, Imai S, Niwa O, Okumoto M: Atm heterozygous deficiency enhances development of mammary carcinomas in p53 heterozygous knockout mice. Breast Cancer Res; 2005;7(1):R164-70
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Atm heterozygous deficiency enhances development of mammary carcinomas in p53 heterozygous knockout mice.
  • Although ataxia-telangiectasia mutated (ATM) heterozygous deficiency has been proposed to increase susceptibility to breast cancer, some studies have not found excess risk.
  • In experimental animals, increased susceptibility to breast cancer is not observed in the Atm heterozygous deficient mice (Atm+/-) carrying a knockout null allele.
  • In order to determine the effect of Atm heterozygous deficiency on mammary tumourigenesis, we generated a series of Atm+/- mice on the p53+/- background with a certain predisposition to spontaneous development of mammary carcinomas, and we examined the development of the tumours after X-irradiation.
  • RESULTS: We tested the effect of haploinsufficiency of the Atm gene on mammary tumourigenesis after X-irradiation in the p53+/- mice of the BALB/cHeA x MSM/Ms background.
  • The singly heterozygous p53+/- mice subjected to X-irradiation developed mammary carcinomas at around 25 weeks of age, and the final incidence of mammary carcinomas at 39 weeks was 31% (19 out of 61).
  • The introduction of the heterozygous Atm knockout alleles into the background of the p53+/- genotype significantly increased the incidence of mammary carcinoma to 58% (32 out of 55) and increased the average number of mammary carcinomas per mouse.
  • However, introduction of Atm alleles did not change the latency of development of mammary carcinoma.
  • CONCLUSION: Our results indicate a strong enhancement in mammary carcinogenesis by Atm heterozygous deficiency in p53+/- mice.
  • Thus, doubly heterozygous mice represent a useful model system with which to analyze the interaction of heterozygous genotypes for p53, Atm and other genes, and their effects on mammary carcinogenesis.
  • [MeSH-major] Carcinoma / genetics. Carcinoma / physiopathology. Cell Cycle Proteins / genetics. DNA-Binding Proteins / genetics. Genes, p53. Mammary Neoplasms, Animal / genetics. Mammary Neoplasms, Animal / physiopathology. Protein-Serine-Threonine Kinases / genetics. Tumor Suppressor Proteins / genetics

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  • (PMID = 15642165.001).
  • [ISSN] 1465-542X
  • [Journal-full-title] Breast cancer research : BCR
  • [ISO-abbreviation] Breast Cancer Res.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Cell Cycle Proteins; 0 / DNA-Binding Proteins; 0 / Tumor Suppressor Proteins; EC 2.7.11.1 / Ataxia Telangiectasia Mutated Proteins; EC 2.7.11.1 / Atm protein, mouse; EC 2.7.11.1 / Protein-Serine-Threonine Kinases
  • [Other-IDs] NLM/ PMC1064114
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7. Luth JA, Hubbard GB, Dick EJ Jr, Frazier SR, Barrier BF: Characterization of spontaneous mammary gland carcinomas in female baboons. J Med Primatol; 2008 Feb;37(1):55-61
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Characterization of spontaneous mammary gland carcinomas in female baboons.
  • Spontaneous mammary gland carcinomas occurred in five baboons during a 13-year period at Southwest Foundation for Biomedical Research.
  • All five animals had typical invasive ductal carcinoma.
  • Applying a grading system used for breast cancer in women, four tumors were graded as poorly differentiated carcinomas and one was graded as moderately differentiated.
  • Co-existent ductal carcinoma in situ (DCIS) was observed in three of the mammary tumors.
  • Distant metastases were observed in only one animal.
  • Although the incidence appears to be low, these five cases of mammary carcinoma in female baboons suggest that when present baboon mammary carcinoma is usually of ductal origin and behaves similar to a human breast carcinoma.
  • [MeSH-major] Carcinoma, Ductal, Breast / veterinary. Mammary Neoplasms, Animal / pathology. Monkey Diseases / pathology. Papio

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  • (PMID = 18199073.001).
  • [ISSN] 0047-2565
  • [Journal-full-title] Journal of medical primatology
  • [ISO-abbreviation] J. Med. Primatol.
  • [Language] eng
  • [Publication-type] Comparative Study; Journal Article
  • [Publication-country] Denmark
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8. Pérez-Martínez C, García-Iglesias MJ, Durán-Navarrete AJ, Espinosa-Alvarez J, García-Fernández RA, Lorenzana-Robles N, Fernández-Pérez S, García-Marín JF: Histopathological and immunohistochemical characteristics of two canine lipid-rich mammary carcinomas. J Vet Med A Physiol Pathol Clin Med; 2005 Mar;52(2):61-6
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  • [Title] Histopathological and immunohistochemical characteristics of two canine lipid-rich mammary carcinomas.
  • Clinicopathological and immunohistochemical findings of two uncommon canine lipid-rich mammary carcinomas are described.
  • [MeSH-major] Carcinoma / veterinary. Dog Diseases / pathology. Mammary Neoplasms, Animal / pathology

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  • (PMID = 15737173.001).
  • [ISSN] 0931-184X
  • [Journal-full-title] Journal of veterinary medicine. A, Physiology, pathology, clinical medicine
  • [ISO-abbreviation] J Vet Med A Physiol Pathol Clin Med
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Germany
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9. Seixas F, Pires MA, Lopes CA: Complex carcinomas of the mammary gland in cats: pathological and immunohistochemical features. Vet J; 2008 May;176(2):210-5

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Complex carcinomas of the mammary gland in cats: pathological and immunohistochemical features.
  • Biphasic epithelial myoepithelial (complex) carcinomas of the feline mammary gland are rare.
  • This article describes the pathological and immunohistochemical features and clinical outcome of eight cases of feline mammary carcinomas displaying complex morphology.
  • This tumour type is a low grade malignancy that shows histopathological features distinctive from more common feline mammary carcinomas and from complex mammary carcinomas of dogs.
  • It appears to have a better overall survival than other carcinomas of the mammary gland of cats.
  • [MeSH-major] Carcinoma / veterinary. Cat Diseases / pathology. Mammary Neoplasms, Animal / pathology

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  • (PMID = 17459738.001).
  • [ISSN] 1090-0233
  • [Journal-full-title] Veterinary journal (London, England : 1997)
  • [ISO-abbreviation] Vet. J.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
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10. Klopfleisch R, Schütze M, Gruber AD: RAD51 protein expression is increased in canine mammary carcinomas. Vet Pathol; 2010 Jan;47(1):98-101

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [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.
  • Number of cells with nuclear RAD51 expression was significantly (P < or = .05) increased in carcinomas when compared to adenomas and metastases.
  • RAD51 expression in carcinomas was correlated with expression in metastases but not with histologic grade.
  • In conclusion, the increased number of RAD51-expressing cells in carcinomas might indicate genomic instability in these cells.
  • [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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11. McAloose D, Munson L, Naydan DK: Histologic features of mammary carcinomas in zoo felids treated with melengestrol acetate (MGA) contraceptives. Vet Pathol; 2007 May;44(3):320-6

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Histologic features of mammary carcinomas in zoo felids treated with melengestrol acetate (MGA) contraceptives.
  • Mammary gland carcinomas have been linked to MGA treatment in zoo felids, but the histologic features of these tumors and steroid receptor expression have not been described.
  • Zoo felid mammary tumors were requested from participating zoos from 1986 through 1998, and 31 mammary carcinomas from 28 MGA-treated and 3 untreated felids were received.
  • The carcinomas were evaluated on the basis of histologic pattern, tumor grade, and occurrence of metastasis; then features of the tumors were compared to determine if carcinomas in MGA-treated felids differed from those that occur spontaneously.
  • Estrogen- and progesterone-receptor expression was evaluated in 17 of the 31 carcinomas.
  • Both MGA-treated and untreated zoo felids had similar patterns and grades of mammary gland cancer as well as prevalence of metastasis.
  • These results indicate that mammary carcinomas in zoo felids are high grade with a predominant tubulopapillary pattern and aggressive behavior.
  • Five of 17 carcinomas expressed progesterone receptors, and 1 of 17 expressed estrogen receptors.
  • Although more zoo felids with cancer had been exposed to MGA in this study, mammary carcinomas were similar in appearance and behavior in untreated and MGA-treated zoo felids.
  • The association of MGA with the development of malignant mammary gland tumors should be considered when using this contraceptive in zoo felids.
  • [MeSH-major] Contraceptive Agents / adverse effects. Mammary Neoplasms, Animal / chemically induced. Melengestrol Acetate / adverse effects. Panthera

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  • (PMID = 17491073.001).
  • [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 / Contraceptive Agents; 0 / Receptors, Estrogen; 0 / Receptors, Progesterone; 4W5HDS3936 / Melengestrol Acetate
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12. De Vico G, Maiolino P, Cataldi M, Mazzullo G, Restucci B: Nuclear morphometry in relation to lymph node status in canine mammary carcinomas. Vet Res Commun; 2007 Nov;31(8):1005-11

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Nuclear morphometry in relation to lymph node status in canine mammary carcinomas.
  • The assessment of nuclear area and nuclear shape by morphometric analysis, has been investigated in 40 canine mammary carcinomas in relation to their metastatic behaviour to regional lymph-nodes.
  • Node-positive tumours included 6 simple adenocarcinomas, 10 ductular carcinomas, 2 anaplastic carcinomas and 2 carcinomas in mixed tumours; node-negative tumours included 18 adenocarcinomas %96, 10 simple adenocarcinomas, 8 complex adenocarcinomas %96, and 2 carcinomas in mixed tumours.
  • Node-positive tumours showed MNA and mean SDA values significantly higher (p<0.001) than node-negative carcinomas.
  • Data of this study, seems to confirm the importance of an histogenetically based classification in canine mammary tumours, also suggesting that morphometry may increase our prognostic performances allowing a reproducible method for detecting individual tumours with higher metastatic potential.
  • [MeSH-major] Dog Diseases / pathology. Lymph Nodes / pathology. Mammary Neoplasms, Animal / pathology

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  • (PMID = 17279466.001).
  • [ISSN] 0165-7380
  • [Journal-full-title] Veterinary research communications
  • [ISO-abbreviation] Vet. Res. Commun.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Netherlands
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13. Houle CD, Ton TV, Clayton N, Huff J, Hong HH, Sills RC: Frequent p53 and H-ras mutations in benzene- and ethylene oxide-induced mammary gland carcinomas from B6C3F1 mice. Toxicol Pathol; 2006;34(6):752-62
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  • [Title] Frequent p53 and H-ras mutations in benzene- and ethylene oxide-induced mammary gland carcinomas from B6C3F1 mice.
  • In 2-year mouse studies, both chemicals induced mammary carcinomas.
  • We examined spontaneous, benzene-, and ethylene oxide-induced mouse mammary carcinomas for p53 protein expression, using immunohistochemistry, and p53 (exons 5-8) and H-ras (codon 61) mutations using cycle sequencing techniques. p53 protein expression was detected in 42% (8/19) of spontaneous, 43% (6/14) of benzene-, and 67% (8/12) of ethylene oxide-induced carcinomas.
  • However, semiquantitative evaluation of p53 protein expression revealed that benzene- and ethylene oxide-induced carcinomas exhibited expression levels five- to six-fold higher than spontaneous carcinomas. p53 mutations were found in 58% (7/12) of spontaneous, 57% (8/14) of benzene-, and 67% (8/12) of ethylene oxide-induced carcinomas.
  • H-ras mutations were identified in 26% (5/19) of spontaneous, 50% (7/14) of benzene-, and 33% (4/12) of ethylene oxide-induced carcinomas.
  • When H-ras mutations were present, concurrent p53 mutations were identified in 40% (2/5) of spontaneous, 71% (5/7) of benzene-, and 75% (3/4) of ethylene oxide-induced carcinomas.
  • Our results demonstrate that p53 and H-ras mutations are relatively common in control and chemically induced mouse mammary carcinomas although both chemicals can alter the mutational spectra and more commonly induce concurrent mutations.
  • [MeSH-major] Gene Expression Regulation, Neoplastic. Genes, ras. Mammary Neoplasms, Animal / pathology. Mammary Neoplasms, Experimental / pathology. Mutation. Rodent Diseases / pathology. Tumor Suppressor Protein p53 / genetics

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  • (PMID = 17162533.001).
  • [ISSN] 0192-6233
  • [Journal-full-title] Toxicologic pathology
  • [ISO-abbreviation] Toxicol Pathol
  • [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 / Codon; 0 / Tumor Suppressor Protein p53; J64922108F / Benzene; JJH7GNN18P / Ethylene Oxide
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14. Lavalle GE, Bertagnolli AC, Tavares WL, Cassali GD: Cox-2 expression in canine mammary carcinomas: correlation with angiogenesis and overall survival. Vet Pathol; 2009 Nov;46(6):1275-80

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Cox-2 expression in canine mammary carcinomas: correlation with angiogenesis and overall survival.
  • Mammary tumors are among the most common neoplastic processes in female dogs.
  • Angiogenesis is essential for the growth and metastasis of major solid tumors and has been correlated with prognosis in human and canine breast cancer.
  • The aim of this study was to evaluate Cox-2 expression and microvessel density in canine mammary carcinomas and to correlate them with overall survival of the animal.
  • Cox-2 and angiogenesis were assessed by immunohistochemistry in 46 mammary carcinomas (19 ductal and 27 metaplastic) and in healthy mammary glands.
  • Longer overall survival was observed in metaplastic carcinomas (P = .028), in tumors with low microvessel density (P = .0002) and with low Cox-2 score (P = .01).
  • Our results demonstrate that increased microvessel density and increased Cox-2 expression were linearly related in the canine mammary tumors studied and were also related to worse prognosis and shorter overall survival.
  • This suggests that Cox-2 inhibitors could be an alternative for the treatment and control of advanced neoplastic mammary disease in female dogs.
  • [MeSH-major] Carcinoma / enzymology. Cyclooxygenase 2 / metabolism. Dog Diseases / enzymology. Gene Expression Regulation, Enzymologic / physiology. Gene Expression Regulation, Neoplastic / physiology. Mammary Neoplasms, Animal / enzymology. Neovascularization, Pathologic / veterinary

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  • (PMID = 19605908.001).
  • [ISSN] 1544-2217
  • [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] EC 1.14.99.1 / Cyclooxygenase 2
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15. Madrazo J, García-Fernández RA, García-Iglesias MJ, Durán AJ, Espinosa J, Pérez-Martínez C: The role of CD44 adhesion factor in canine mammary carcinomas. Vet J; 2009 Jun;180(3):371-6
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  • [Title] The role of CD44 adhesion factor in canine mammary carcinomas.
  • CD44 is an adhesion molecule implicated in the progression of human breast cancer.
  • The purpose of this study was to describe CD44 antigen expression in canine mammary carcinomas and to evaluate its prognostic significance in relation to other clinico-pathological variables.
  • Complex (grade I) and anaplastic (grade III) carcinomas exhibited more intense expression of this antigen than did some tubulopapillary and most solid carcinomas (grade II).
  • Although reduced CD44 expression was associated with infiltrative growth and vascular invasion in solid carcinomas, intense expression was also observed in anaplastic tumours.
  • Although overall these findings suggest a role for this adhesion factor in canine mammary tumour development and progression, the complexity and apparently paradoxical nature of some of the findings currently limit the use of this immunohistochemical marker as a prognostic indicator.
  • [MeSH-major] Antigens, CD44 / metabolism. Carcinoma / veterinary. Dog Diseases / metabolism. Mammary Neoplasms, Animal / metabolism

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  • (PMID = 18299241.001).
  • [ISSN] 1090-0233
  • [Journal-full-title] Veterinary journal (London, England : 1997)
  • [ISO-abbreviation] Vet. J.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Antigens, CD44
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16. Gama A, Alves A, Schmitt F: Identification of molecular phenotypes in canine mammary carcinomas with clinical implications: application of the human classification. Virchows Arch; 2008 Aug;453(2):123-32
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  • [Title] Identification of molecular phenotypes in canine mammary carcinomas with clinical implications: application of the human classification.
  • Similarly to humans, canine mammary cancer represents a heterogeneous group in terms of morphology and biological behaviour.
  • In the present study, we evaluated a series of canine mammary carcinomas based on a new human classification, initially based on gene expression profiling analysis.
  • Similarly to human breast cancer, by using an immunohistochemistry surrogate panel based on five molecular markers [estrogen receptor, human epidermal growth factor receptor 2 (HER2), cytokeratin 5, p63 and P-cadherin], we were able to classify canine mammary carcinomas into four different subtypes: luminal A [estrogen receptor (ER)+/HER2-; 44.8%], luminal B (ER+/HER2+; 13.5%), basal (ER-/HER2- and a basal marker positive; 29.2%) and HER2 overexpressing tumours (ER-/HER2+; 8.3%).
  • In addition, as in humans, basal subtype was significantly associated with shorter disease-free and overall survival rates, and we propose canine mammary carcinomas as a suitable natural model for the study of this particular subset of human carcinomas.
  • [MeSH-major] Dog Diseases / pathology. Mammary Neoplasms, Animal / metabolism. Mammary Neoplasms, Animal / pathology

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  • (PMID = 18677512.001).
  • [ISSN] 0945-6317
  • [Journal-full-title] Virchows Archiv : an international journal of pathology
  • [ISO-abbreviation] Virchows Arch.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Germany
  • [Chemical-registry-number] 0 / Cadherins; 0 / Keratin-5; 0 / Phosphoproteins; 0 / Receptors, Estrogen; 0 / Trans-Activators; EC 2.7.10.1 / Receptor, ErbB-2
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17. Sayasith K, Sirois J, Doré M: Molecular characterization of feline COX-2 and expression in feline mammary carcinomas. Vet Pathol; 2009 May;46(3):423-9
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Molecular characterization of feline COX-2 and expression in feline mammary carcinomas.
  • COX-2 primary structure has been characterized in many species and its expression demonstrated in a variety of cancers in humans and dogs, including mammary cancer.
  • Also, information on COX-2 expression in feline mammary cancer is limited and conflicting.
  • The objectives of this study were therefore to characterize the molecular structure of feline COX-2 and to evaluate by immunohistochemistry its expression in mammary carcinomas.
  • Immunohistochemical analysis of 40 mammary carcinomas showed that the majority of tumors studied (35/40; 87%) expressed COX-2 at a level varying from low (20/40; 50%) to intermediate (13/40; 32%) and high (2/40; 5%).
  • These results provide the first molecular characterization of feline COX-2 and demonstrate that COX-2 is expressed in the majority of feline mammary carcinomas.
  • [MeSH-major] Cat Diseases / metabolism. Cyclooxygenase 2 / metabolism. Gene Expression Regulation, Enzymologic / physiology. Gene Expression Regulation, Neoplastic / physiology. Mammary Neoplasms, Animal / metabolism

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  • (PMID = 19176489.001).
  • [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] EC 1.14.99.1 / Cyclooxygenase 2
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18. Injac R, Perse M, Obermajer N, Djordjevic-Milic V, Prijatelj M, Djordjevic A, Cerar A, Strukelj B: Potential hepatoprotective effects of fullerenol C60(OH)24 in doxorubicin-induced hepatotoxicity in rats with mammary carcinomas. Biomaterials; 2008 Aug-Sep;29(24-25):3451-60
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  • [Title] Potential hepatoprotective effects of fullerenol C60(OH)24 in doxorubicin-induced hepatotoxicity in rats with mammary carcinomas.
  • The aim of this study was to investigate the potential protective role of fullerenol C60(OH)24 on doxorubicin-induced liver toxicity using in vivo (female Sprague-Dawley rats) and in vitro (human hepatocellular carcinoma - HepG2; colorectal adenocarcinoma cell lines - Caco-2) approaches.
  • The first (healthy control) and second (control with chemically induced mammary carcinomas) group received saline only.
  • The third, fourth and fifth group (all with breast cancer) were injected (i.p.) with a single dose of doxorubicin (8mg/kg), doxorubicin/fullerenol (100mg/kg of fullerenol 30min before administration of 8mg/kg doxorubicin) and fullerenol (100mg/kg), respectively.
  • [MeSH-major] Doxorubicin / toxicity. Fullerenes / pharmacology. Liver / drug effects. Mammary Neoplasms, Animal / drug therapy

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  • (PMID = 18501960.001).
  • [ISSN] 0142-9612
  • [Journal-full-title] Biomaterials
  • [ISO-abbreviation] Biomaterials
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Antioxidants; 0 / Fullerenes; 0 / Thiobarbituric Acid Reactive Substances; 182024-42-6 / fullerenol; 4Y8F71G49Q / Malondialdehyde; 80168379AG / Doxorubicin; EC 1.1.1.- / 2-hydroxybutyrate dehydrogenase; EC 1.1.1.27 / L-Lactate Dehydrogenase; EC 1.1.1.30 / Hydroxybutyrate Dehydrogenase; EC 1.11.1.6 / Catalase; EC 1.11.1.9 / Glutathione Peroxidase; EC 1.15.1.1 / Superoxide Dismutase; EC 1.8.1.7 / Glutathione Reductase; EC 2.6.1.1 / Aspartate Aminotransferases; EC 2.6.1.2 / Alanine Transaminase; GAN16C9B8O / Glutathione
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19. Millanta F, Calandrella M, Citi S, Della Santa D, Poli A: Overexpression of HER-2 in feline invasive mammary carcinomas: an immunohistochemical survey and evaluation of its prognostic potential. Vet Pathol; 2005 Jan;42(1):30-4
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  • [Title] Overexpression of HER-2 in feline invasive mammary carcinomas: an immunohistochemical survey and evaluation of its prognostic potential.
  • The role of c-erbB-2 protooncogene status in feline invasive mammary carcinomas (FMCs) was assessed through the HER-2 receptor immunohistochemical expression.
  • HER-2 overexpression was detected in 28 of the 47 carcinomas (59.6%).
  • Furthermore, the HER-2 overexpression appeared with a higher percentage in FMCs than what is reported in canine or human mammary carcinomas.
  • [MeSH-major] Carcinoma / veterinary. Cat Diseases / metabolism. Mammary Neoplasms, Animal / metabolism. Receptor, ErbB-2 / biosynthesis

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  • (PMID = 15657269.001).
  • [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] EC 2.7.10.1 / Receptor, ErbB-2
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20. Millanta F, Citi S, Della Santa D, Porciani M, Poli A: COX-2 expression in canine and feline invasive mammary carcinomas: correlation with clinicopathological features and prognostic molecular markers. Breast Cancer Res Treat; 2006 Jul;98(1):115-20
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  • [Title] COX-2 expression in canine and feline invasive mammary carcinomas: correlation with clinicopathological features and prognostic molecular markers.
  • Its expression occurs in a wide range of preneoplastic and neoplastic conditions in humans, including colon and breast carcinomas.
  • We evaluated the role of COX-2 as a mediator of angiogenesis in feline and canine invasive carcinomas (IMCs) and its role as a prognostic indicator.
  • COX-2 expression was assessed in neoplastic samples and healthy mammary glands by immunohistochemistry, and related to the following clinicopathological parameters: age, tumor size, histologic type, tumor grading, vessel invasion, estrogen (ER) and progesterone receptor (PR) status, Ki-67, HER-2 overexpression, microvessel density (MVD), VEGF expression and overall survival (OS).
  • In both species, COX-2 immunoreactivity was not observed in healthy tissues, whereas 96% of feline and 100% of canine invasive carcinomas scored positive.
  • COX-2 is expressed in mammary tissues during tumorigenesis and its expression is associated with a poorer prognosis in bitches and queens.
  • In the canine species, moreover, COX-2 may be important for mediating HER-2 induced mammary tumors.
  • [MeSH-major] Biomarkers, Tumor. Cyclooxygenase 2 / biosynthesis. Gene Expression Regulation, Neoplastic. Mammary Neoplasms, Animal / enzymology

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  • [CommentIn] Breast Cancer Res Treat. 2007 Jan;101(2):247 [16838111.001]
  • (PMID = 16538539.001).
  • [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 / Biomarkers, Tumor; EC 1.14.99.1 / Cyclooxygenase 2
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21. Klopfleisch R, Klose P, Weise C, Bondzio A, Multhaup G, Einspanier R, Gruber AD: Proteome of metastatic canine mammary carcinomas: similarities to and differences from human breast cancer. J Proteome Res; 2010 Dec 3;9(12):6380-91
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  • [Title] Proteome of metastatic canine mammary carcinomas: similarities to and differences from human breast cancer.
  • Mammary tumors are a major health threat to women and female dogs.
  • Nevertheless, the molecular mechanisms of tumor metastasis are far from being understood, and it is still unknown why some human and canine carcinomas metastasize and others do not.
  • Using 2D-DIGE and MALDI-TOF-MS we identified 21 proteins with significant changes (fold change >1.5; p < 0.05) in protein expression between metastasizing (n = 6) and nonmetastasizing (n = 6) canine mammary carcinomas.
  • Up-regulated proteins in metastatic carcinomas included proliferating cell nuclear antigen, ferritin light chain, bomapin, tropomyosin 3, thioredoxin-containing domain C5, adenosin, ornithine aminotransferase, coronin 1A, RAN-binding protein 1,3-phosphoglycerate dehydrogenase, and eukaryotic translation elongation factor 1.
  • Down-regulated proteins in metastatic carcinomas included calretinin, myosin, light chain 2, peroxiredoxin 6, maspin, ibrinogen beta chain, vinculin, isocitrate dehydrogenase 1, tropomyosin 1, annexin A5, and Rho GTPase activating protein 1.
  • Interestingly, 19 of these 21 proteins have been described with a malignancy-associated expression in human breast cancer and other human cancer types before.
  • Further investigations are now necessary to test whether these markers are of prognostic value for canine mammary carcinomas and whether their expression is directly involved in canine mammary carcinogenesis or represent solely a secondary reactive phenotype.
  • [MeSH-major] Breast Neoplasms / metabolism. Mammary Neoplasms, Animal / metabolism. Proteome / analysis. Proteomics / methods

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  • (PMID = 20932060.001).
  • [ISSN] 1535-3907
  • [Journal-full-title] Journal of proteome research
  • [ISO-abbreviation] J. Proteome Res.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Biomarkers, Tumor; 0 / CALB2 protein, human; 0 / Calbindin 2; 0 / Proliferating Cell Nuclear Antigen; 0 / Proteome; 0 / S100 Calcium Binding Protein G
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22. Woditschka S, Haag JD, Mau B, Lubet RA, Gould MN: Chemopreventive effects of celecoxib are limited to hormonally responsive mammary carcinomas in the neu-induced retroviral rat model. Breast Cancer Res; 2008;10(1):R18
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  • [Title] Chemopreventive effects of celecoxib are limited to hormonally responsive mammary carcinomas in the neu-induced retroviral rat model.
  • INTRODUCTION: While current breast cancer chemoprevention strategies using selective estrogen response modulators and aromatase inhibitors are quite successful, their effects are limited to hormonally responsive breast cancer.
  • Hormonally nonresponsive breast cancer (including estrogen receptor-negative cancer) is associated with poor prognosis for patients, and few chemoprevention agents exist for this type of cancer.
  • The cyclooxygenase-2 inhibitor celecoxib (Celebrex) is a nonsteroidal anti-inflammatory drug and as such is a potential candidate for the prevention of hormonally nonresponsive breast cancer.
  • METHODS: The chemopreventive effects of celecoxib were evaluated in the neu-induced retroviral rat mammary carcinogenesis model, to assess the efficacy of celecoxib on hormonally responsive and hormonally nonresponsive mammary carcinomas.
  • RESULTS: Dietary celecoxib at 1,200 mg/kg diet was highly efficacious in the prevention of hormonally responsive mammary carcinomas in intact rats, decreasing tumor multiplicity by 56% (P < 0.0001) and by 74% (P = 0.0002) in two independent experiments.
  • No significant effect was found, however, on hormonally nonresponsive mammary carcinomas of ovariectomized rats.
  • CONCLUSION: The chemopreventive effects of celecoxib appear to be limited to modulations in multiplicity of hormonally responsive mammary carcinomas.
  • The fact that no synergistic or additive effects were observed in combination diet-treated rats raises the question of whether celecoxib is suitable for the prevention of hormonally nonresponsive breast cancer or for use in combination therapy with selective estrogen response modulators or aromatase inhibitors.

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  • (PMID = 18279516.001).
  • [ISSN] 1465-542X
  • [Journal-full-title] Breast cancer research : BCR
  • [ISO-abbreviation] Breast Cancer Res.
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / R01 CA101201; United States / NCI NIH HHS / CA / CA101201
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, U.S. Gov't, Non-P.H.S.
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Anticarcinogenic Agents; 0 / Cyclooxygenase 2 Inhibitors; 0 / Pyrazoles; 0 / Sulfonamides; 094ZI81Y45 / Tamoxifen; JCX84Q7J1L / Celecoxib
  • [Other-IDs] NLM/ PMC2374974
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23. Lamb R, Harrison H, Clarke RB: Mammary development, carcinomas and progesterone: role of Wnt signalling. Ernst Schering Found Symp Proc; 2007;(1):1-23
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  • [Title] Mammary development, carcinomas and progesterone: role of Wnt signalling.
  • The mammary gland begins development during embryogenesis but after exposure to hormonal changes during puberty and pregnancy undergoes extensive further development.
  • The ovarian steroid progesterone, acting via the secreted factor Wnt4, is known to be essential for side branching of the mammary gland.
  • One function of Wnt proteins is self-renewal of adult tissue stem cells, suggesting that progesterone may exert its effects within the breast, at least partly, by regulating the mammary stem cell population.
  • [MeSH-major] Mammary Glands, Human / growth & development. Mammary Neoplasms, Animal / physiopathology. Progesterone / physiology. Signal Transduction. Wnt Proteins / metabolism

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  • (PMID = 18543432.001).
  • [Journal-full-title] Ernst Schering Foundation symposium proceedings
  • [ISO-abbreviation] Ernst Schering Found Symp Proc
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] Germany
  • [Chemical-registry-number] 0 / Wnt Proteins; 4G7DS2Q64Y / Progesterone
  • [Number-of-references] 97
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24. Karayannopoulou M, Kaldrymidou E, Constantinidis TC, Dessiris A: Histological grading and prognosis in dogs with mammary carcinomas: application of a human grading method. J Comp Pathol; 2005 Nov;133(4):246-52

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Histological grading and prognosis in dogs with mammary carcinomas: application of a human grading method.
  • The human "Elston and Ellis grading method" was used in dogs with mammary carcinoma to examine its relation to prognosis in this species, based on a 2-year follow-up period.
  • Of the 85 cases examined, 27(31.8%) had well-differentiated (grade I), 28 (32.9%) had moderately differentiated (grade II) and 30 (35.3%) had poorly differentiated (grade III) carcinomas.
  • Two years after mastectomy, significant differences in survival between cases with different tumour grade were found; thus, survival was worse in dogs with grade III carcinomas than in those with grade II (P<0.05) or grade I (P<0.001) tumours.
  • However, in dogs with simple carcinomas which had a less favourable prognosis than that of other carcinomas (P<0.001), there was no significant difference in survival between grade II and grade III cases (P=0.878), both having a very poor prognosis.
  • Undifferentiated (grade III) carcinoma cases had a 21-fold increased risk of death as compared with differentiated (grade I and II) carcinoma cases.
  • An increased risk (about 10-fold) was also associated with undifferentiated simple carcinomas as compared with differentiated ones.
  • Routine use of this human grading method would help the clinician to make a more accurate prognosis in the interests of post-surgical management in dogs with mammary carcinomas.
  • [MeSH-major] Dog Diseases / pathology. Mammary Neoplasms, Animal / pathology

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  • (PMID = 16202421.001).
  • [ISSN] 0021-9975
  • [Journal-full-title] Journal of comparative pathology
  • [ISO-abbreviation] J. Comp. Pathol.
  • [Language] eng
  • [Publication-type] Journal Article; Validation Studies
  • [Publication-country] England
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25. Iizuka D, Imaoka T, Takabatake T, Nishimura M, Kakinuma S, Nishimura Y, Shimada Y: DNA copy number aberrations and disruption of the p16Ink4a/Rb pathway in radiation-induced and spontaneous rat mammary carcinomas. Radiat Res; 2010 Aug;174(2):206-15
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  • [Title] DNA copy number aberrations and disruption of the p16Ink4a/Rb pathway in radiation-induced and spontaneous rat mammary carcinomas.
  • To clarify how ionizing radiation induces mammary carcinogenesis, we characterized genomic copy number aberrations for gamma-ray-induced rat mammary carcinomas using microarray-based comparative genomic hybridization.
  • We examined 14 carcinomas induced by gamma radiation (2 Gy) and found 26 aberrations, including trisomies of chromosomes 4 and 10 for three and one carcinomas, respectively, an amplification of the chromosomal region 1q12 in two carcinomas, and deletions of the chromosomal regions 3q35q36, 5q32 and 7q11 in two, two and four carcinomas, respectively.
  • These aberrations were not observed in seven spontaneous mammary carcinomas.
  • The expression of p16Ink4a and p19Arf, which are located in the chromosomal region 5q32, was always up-regulated except for a carcinoma with a homozygous deletion of region 5q32.
  • However, the amounts of Rb and its mRNA were down-regulated in these carcinomas, indicating a disruption of the p16Ink4a/Rb pathway.
  • This is the first report of array CGH analysis for radiation-induced mammary tumors, which reveals that they show distinct DNA copy number aberration patterns that are different from those of spontaneous tumors and those reported previously for chemically induced tumors.
  • [MeSH-major] Chromosome Aberrations. Cyclin-Dependent Kinase Inhibitor p16 / genetics. DNA, Neoplasm / genetics. Gene Expression Regulation, Neoplastic / radiation effects. Mammary Neoplasms, Animal / genetics. Mammary Neoplasms, Animal / radionuclide imaging

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  • (PMID = 20681787.001).
  • [ISSN] 1938-5404
  • [Journal-full-title] Radiation research
  • [ISO-abbreviation] Radiat. Res.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Cyclin-Dependent Kinase Inhibitor p16; 0 / DNA Primers; 0 / DNA, Neoplasm; 0 / RNA, Neoplasm
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26. Vasiljeva O, Korovin M, Gajda M, Brodoefel H, Bojic L, Krüger A, Schurigt U, Sevenich L, Turk B, Peters C, Reinheckel T: Reduced tumour cell proliferation and delayed development of high-grade mammary carcinomas in cathepsin B-deficient mice. Oncogene; 2008 Jul 10;27(30):4191-9
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  • [Title] Reduced tumour cell proliferation and delayed development of high-grade mammary carcinomas in cathepsin B-deficient mice.
  • Expression levels of the papain-like cysteine protease cathepsin B (Ctsb) have been positively correlated with mammary tumour progression and metastasis; however, its roles in the hallmark processes of malignant growth remain poorly defined.
  • Using Ctsb-deficient mice we investigated tumour cell differentiation, proliferation and apoptosis in the Tg(MMTV-PyMT) mouse mammary cancer model.
  • Absence of Ctsb significantly impaired development of high-grade invasive ductal carcinomas and reduced the metastatic burden in the lungs.
  • Mice lacking Ctsb exhibited reduced cell proliferation in mammary carcinomas and their lung metastases.
  • Notably, intravenous injection of primarily isolated, Ctsb-expressing tumour cells into congenic Ctsb-deficient mice revealed impaired cell proliferation in the resulting experimental lung metastases, providing evidence for the involvement of Ctsb in paracrine regulation of cancer cell proliferation.
  • No Ctsb genotype-dependent difference in tumour cell death was observed in vivo or by treatment of isolated PyMT cancer cells with tumour necrosis factor-alpha.
  • However, cancer cells lacking Ctsb exhibited significantly higher resistance to apoptosis induction by the lysosomotropic agent Leu-Leu-OMe.
  • Thus, our results indicate an in vivo role for Ctsb in promoting cellular anaplasia in mammary cancers and proliferation in lung metastases.
  • [MeSH-major] Carcinoma / genetics. Cathepsin B / genetics. Cell Proliferation. Immunity, Innate / genetics. Mammary Neoplasms, Animal / genetics. Tumor Burden / genetics

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  • (PMID = 18345026.001).
  • [ISSN] 1476-5594
  • [Journal-full-title] Oncogene
  • [ISO-abbreviation] Oncogene
  • [Language] eng
  • [Publication-type] Comparative Study; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] EC 3.4.22.1 / Cathepsin B
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27. Qiu C, Shan L, Yu M, Snyderwine EG: Steroid hormone receptor expression and proliferation in rat mammary gland carcinomas induced by 2-amino-1-methyl-6-phenylimidazo[4,5-b]pyridine. Carcinogenesis; 2005 Apr;26(4):763-9
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  • [Title] Steroid hormone receptor expression and proliferation in rat mammary gland carcinomas induced by 2-amino-1-methyl-6-phenylimidazo[4,5-b]pyridine.
  • 2-Amino-1-methyl-6-phenylimidazo[4,5-b]pyridine (PhIP) is a mammary gland carcinogen present in the human diet.
  • Herein, the expression of estrogen receptor alpha (ERalpha), estrogen receptor beta (ER beta) and progesterone receptor (PR) was examined in mammary gland carcinomas induced by PhIP in female Sprague-Dawley rats.
  • Quantitative real-time polymerase chain reaction demonstrated that ER alpha, ER beta and PR were statistically elevated by 3-, 4- and 8-fold in carcinomas compared with normal mammary glands.
  • By immunohistochemistry, carcinomas showed statistically higher nuclear expression of all three steroid receptors with the majority of carcinomas showing at least 10% of epithelial cells stained for ER alpha (49/55, 89%), ER beta (41/55, 75%) and PR (48/55, 87%).
  • Furthermore, the level of expression of the three steroid hormone receptors was positively correlated with each other across the bank of carcinomas (Spearman analysis, P < 0.05).
  • The expression of ER alpha in carcinomas was associated with tumor grade, extent of nuclear pleomorphism and cellular proliferation as measured by proliferating cell nuclear antigen (PCNA) and phospho-Rb immunostaining (Spearman analysis, P < 0.05).
  • Colocalization of the receptors, and the colocalization of the receptors with PCNA and cyclin D1 was strikingly higher in carcinomas than in the normal mammary gland.
  • In carcinoma cells, 37% of ER alpha positive epithelial cells were colocalized with PCNA in contrast to just 0.25% of cells in the normal mammary gland.
  • The findings from this study indicate that ER alpha, ER beta and PR were co-upregulated and nuclear localized in epithelial cells from rat mammary carcinomas compared with normal mammary glands, and that the co-upregulation was positively correlated with proliferation and cell cycle progression in carcinomas.
  • [MeSH-major] Carcinogens / toxicity. Cell Proliferation / drug effects. Estrogen Receptor alpha / metabolism. Estrogen Receptor beta / metabolism. Imidazoles / toxicity. Mammary Neoplasms, Experimental / metabolism. Receptors, Progesterone / metabolism
  • [MeSH-minor] Animals. Cell Cycle / drug effects. Cell Nucleus / metabolism. Cyclin D1 / metabolism. Epithelial Cells / ultrastructure. Female. Immunoenzyme Techniques. Mammary Glands, Animal / metabolism. Mammary Glands, Animal / pathology. Proliferating Cell Nuclear Antigen / metabolism. RNA, Messenger / genetics. RNA, Messenger / metabolism. Rats. Rats, Sprague-Dawley. Retinoblastoma Protein / metabolism. Reverse Transcriptase Polymerase Chain Reaction

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  • (PMID = 15637090.001).
  • [ISSN] 0143-3334
  • [Journal-full-title] Carcinogenesis
  • [ISO-abbreviation] Carcinogenesis
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, U.S. Gov't, Non-P.H.S.; Research Support, U.S. Gov't, P.H.S.
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Carcinogens; 0 / Estrogen Receptor alpha; 0 / Estrogen Receptor beta; 0 / Imidazoles; 0 / Proliferating Cell Nuclear Antigen; 0 / RNA, Messenger; 0 / Receptors, Progesterone; 0 / Retinoblastoma Protein; 136601-57-5 / Cyclin D1; 909C6UN66T / 2-amino-1-methyl-6-phenylimidazo(4,5-b)pyridine
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28. Klopfleisch R, Hvid H, Klose P, da Costa A, Gruber AD: Insulin receptor is expressed in normal canine mammary gland and benign adenomas but decreased in metastatic canine mammary carcinomas similar to human breast cancer. Vet Comp Oncol; 2010 Dec;8(4):293-301
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  • [Title] Insulin receptor is expressed in normal canine mammary gland and benign adenomas but decreased in metastatic canine mammary carcinomas similar to human breast cancer.
  • Insulin receptor (INSR) or insulin-like growth factor (IGF) signalling is speculated to be involved in mammary tumour development.
  • Expression levels of members of the insulin receptor family (INSR, IGF1R, IGF2R, GHR) and their ligands IGF1and IGF2 were quantified in macro- and microdissected tissue samples of normal canine mammary gland, adenomas, carcinomas and their lymph node metastases to evaluate their potential impact on the carcinogenesis of canine mammary tumours.
  • Normal mammary gland and adenomas had strong INSR expression, while carcinomas and metastases had significantly decreased expression.
  • IGF1, IGF2 and GHR mRNA expressions were strongly decreased in adenomas, carcinomas and metastases.
  • However, decreased INSR expression carcinomas and their metastases render questionable its impact at late stages of carcinogenesis.
  • [MeSH-major] Adenoma / veterinary. Carcinoma / veterinary. Dog Diseases / metabolism. Mammary Glands, Animal / metabolism. Mammary Neoplasms, Animal / metabolism. Receptor, Insulin / metabolism

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  • [Copyright] © 2010 Blackwell Publishing Ltd.
  • (PMID = 21062411.001).
  • [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 / RNA, Messenger; EC 2.7.10.1 / Receptor, Insulin
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29. Woditschka S, Haag JD, Sullivan R, Gould MN: A short-term rat mammary carcinogenesis model for the prevention of hormonally responsive and nonresponsive in situ carcinomas. Cancer Prev Res (Phila); 2009 Feb;2(2):153-60
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  • [Title] A short-term rat mammary carcinogenesis model for the prevention of hormonally responsive and nonresponsive in situ carcinomas.
  • We developed a novel, short-term prevention model, which is particularly useful for assessing the efficacy of a compound to prevent hormonally responsive and nonresponsive in situ carcinomas.
  • The multiplicity and size of the resulting in situ carcinomas are scored in whole-mounted, aluminum carmine-stained mammary glands at 15 days postinfusion.
  • These in situ carcinomas represent a distinct biological time point in the development of neu-induced mammary cancer in the rat.
  • They are characterized by high rates of proliferation (40.0%; P < 0.0001) and apoptosis (2.8%; P < 0.005) compared with mammary carcinomas.
  • The majority of in situ carcinomas regress spontaneously after 20 days postinfusion.
  • The in situ carcinomas at 15 days postinfusion exhibit hormonal responsiveness.
  • The effects of the chemoprevention agents tamoxifen, celecoxib, and targretin on hormonally responsive and nonresponsive in situ carcinomas recapitulate those observed on mammary carcinomas at 12 and 18 weeks postinfusion for intact and ovariectomized rats, respectively.
  • Neu-induced in situ carcinomas in the rat represent etiologically relevant intermediate time points of mammary carcinogenesis.
  • Our prevention model represents a cost-efficient in vivo system to determine whether the preventive effects of a compound extend to hormonally nonresponsive mammary lesions, for which new chemoprevention approaches are needed.

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  • (PMID = 19196722.001).
  • [ISSN] 1940-6215
  • [Journal-full-title] Cancer prevention research (Philadelphia, Pa.)
  • [ISO-abbreviation] Cancer Prev Res (Phila)
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / R01-CA101201; United States / NCI NIH HHS / CA / P30 CA014520; United States / NCI NIH HHS / CA / P30-CA014520; United States / NCI NIH HHS / CA / R01 CA101201; United States / NCI NIH HHS / CA / R01 CA101201-05; United States / NCI NIH HHS / CA / CA101201-05
  • [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 / Anticarcinogenic Agents; 0 / Antineoplastic Agents, Hormonal; 0 / Cyclooxygenase Inhibitors; 0 / Pyrazoles; 0 / Sulfonamides; 0 / Tetrahydronaphthalenes; 094ZI81Y45 / Tamoxifen; A61RXM4375 / bexarotene; JCX84Q7J1L / Celecoxib
  • [Other-IDs] NLM/ NIHMS199061; NLM/ PMC2881640
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30. Nair P, O'Donnell CM, Janasek K, Sajduk MK, Smith EA, Golden JM, Vasta CA, Huggins AB, Kurt RA: Lipopolysacchride-treated mammary carcinomas secrete proinflammatory chemokines and exhibit reduced growth rates in vivo, but not in vitro. Immunol Invest; 2009;38(8):730-48
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  • [Title] Lipopolysacchride-treated mammary carcinomas secrete proinflammatory chemokines and exhibit reduced growth rates in vivo, but not in vitro.
  • Here we report that the murine mammary carcinoma 4T1 constitutively expressed genes encoding TLR2, 3, 4 and 5.
  • Analysis of 3 additional murine mammary carcinomas revealed that they also secreted CCL2, CCL5 and CXCL1 in response to TLR agonist treatment, and LPS treated 168 and SM1 tumors exhibited decreased growth rates in vivo, but not in vitro.
  • These data indicated that 4 out of 4 murine mammary carcinomas secreted proinflammatory chemokines following treatment with TLR agonists, and 3 out of 4 of the mammary carcinomas responded to LPS treatment in a manner that decreased tumor growth in vivo.
  • [MeSH-major] Cell Nucleus / metabolism. Chemokines / metabolism. Lipopolysaccharides / pharmacology. Mammary Neoplasms, Animal / metabolism. NF-kappa B / metabolism

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  • (PMID = 19860585.001).
  • [ISSN] 1532-4311
  • [Journal-full-title] Immunological investigations
  • [ISO-abbreviation] Immunol. Invest.
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / R15CA137858
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Chemokines; 0 / Lipopolysaccharides; 0 / NF-kappa B; 0 / Peptidoglycan; 0 / Toll-Like Receptors; 24939-03-5 / Poly I-C
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31. Klopfleisch R, Klose P, da Costa A, Brunnberg L, Gruber AD: HEPACAM1 and 2 are differentially regulated in canine mammary adenomas and carcinomas and its lymph node metastases. BMC Vet Res; 2010;6:15
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  • [Title] HEPACAM1 and 2 are differentially regulated in canine mammary adenomas and carcinomas and its lymph node metastases.
  • HEPACAM1 is involved in negative cell cycle regulation via p53, p21 and p27 signalling but also mediates increased human breast cancer cell spread.
  • In the present study we quantified gene expression levels of HEPACAM1 and 2 to evaluate their possible role during the carcinogenesis of canine mammary tumours.
  • RESULTS: Adenomas displayed increased HEPACAM1 and 2 mRNA expression levels and decreased HEPACAM1 protein expression levels when compared to normal gland, carcinomas and lymph node metastases.
  • In contrast, metastatic carcinomas, intravascular tumour cells and lymph node metastases had HEPACAM 1 protein and mRNA expression levels similar to normal gland but decreased HEPACAM2 mRNA expression when compared to normal gland of the same dog.
  • CONCLUSIONS: HEPACAM1 and 2 seem to be important for cell-cell adhesion of normal and neoplastic canine mammary cells.
  • The loss of HEPACAM1 protein expression in adenomas but not in carcinomas questions its role as a tumour suppressor at late stages of malignant transformation and indicates that it might rather be involved in physiologic mammary cell adhesion and canine mammary tumour metastasis.
  • Furthermore, it can be speculated, whether HEPACAM2 plays a different role in malignancy and metastasis of canine mammary tumours since its transcriptional levels are different in carcinomas and their lymph node metastases when compared to HEPACAM1.
  • [MeSH-major] Adenoma / physiopathology. Dog Diseases / physiopathology. Gene Expression Regulation, Neoplastic. Mammary Glands, Animal / physiopathology. Mammary Neoplasms, Animal / physiopathology. Proteins / metabolism

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  • (PMID = 20226097.001).
  • [ISSN] 1746-6148
  • [Journal-full-title] BMC veterinary research
  • [ISO-abbreviation] BMC Vet. Res.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Proteins
  • [Other-IDs] NLM/ PMC2842258
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32. Spadaro M, Ambrosino E, Iezzi M, Di Carlo E, Sacchetti P, Curcio C, Amici A, Wei WZ, Musiani P, Lollini PL, Cavallo F, Forni G: Cure of mammary carcinomas in Her-2 transgenic mice through sequential stimulation of innate (neoadjuvant interleukin-12) and adaptive (DNA vaccine electroporation) immunity. Clin Cancer Res; 2005 Mar 1;11(5):1941-52
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  • [Title] Cure of mammary carcinomas in Her-2 transgenic mice through sequential stimulation of innate (neoadjuvant interleukin-12) and adaptive (DNA vaccine electroporation) immunity.
  • PURPOSE: Whereas neoadjuvant therapy is emerging as a treatment option in early primary breast cancer, no data are available on the use of antiangiogenic and immunomodulatory agents in a neoadjuvant setting.
  • In a model of Her-2 spontaneous mammary cancer, we investigated the efficacy of neoadjuvant interleukin 12 (IL-12) followed by "immune-surgery" of the residual tumor.
  • EXPERIMENTAL DESIGN: Female BALB/c mice transgenic for the rat Her-2 oncogene inexorably develop invasive carcinomas in all their mammary glands by the 23rd week of age.
  • Mice with multifocal in situ carcinomas received four weekly i.p. injections of 100 ng IL-12 followed by a 3-week rest.
  • [MeSH-major] Cancer Vaccines. Carcinoma / genetics. Carcinoma / immunology. Electroporation. Genes, erbB-2. Interleukin-12 / pharmacology. Mammary Neoplasms, Animal / genetics. Mammary Neoplasms, Animal / immunology

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  • (PMID = 15756020.001).
  • [ISSN] 1078-0432
  • [Journal-full-title] Clinical cancer research : an official journal of the American Association for Cancer Research
  • [ISO-abbreviation] Clin. Cancer Res.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Cancer Vaccines; 187348-17-0 / Interleukin-12
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33. Estrela-Lima A, Araújo MS, Costa-Neto JM, Teixeira-Carvalho A, Barrouin-Melo SM, Cardoso SV, Martins-Filho OA, Serakides R, Cassali GD: Immunophenotypic features of tumor infiltrating lymphocytes from mammary carcinomas in female dogs associated with prognostic factors and survival rates. BMC Cancer; 2010;10:256

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Immunophenotypic features of tumor infiltrating lymphocytes from mammary carcinomas in female dogs associated with prognostic factors and survival rates.
  • The goal of this study was to characterize the clinical-pathological status and the immunophenotyping profile of tumor infiltrating lymphocytes and their association with the animal survival rates in canine mammary carcinomas.
  • METHODS: Fifty-one animals with mammary carcinomas, classified as carcinomas in mixed tumors-MC-BMT = 31 and carcinomas-MC = 20 were submitted to systematic clinical-pathological analysis (tumor size; presence of lymph node and pulmonary metastasis; clinical stage; histological grade; inflammatory distribution and intensity as well as the lymphocytic infiltrate intensity) and survival rates.
  • CONCLUSION: The intensity of lymphocytic infiltrate and probably the relative abundance of the CD4+ and CD8+ T-lymphocytes may represent important survival prognostic biomarkers for canine mammary carcinomas.
  • [MeSH-major] CD4-Positive T-Lymphocytes / immunology. CD8-Positive T-Lymphocytes / immunology. Carcinoma / veterinary. Dog Diseases / immunology. Immunophenotyping / veterinary. Inflammation / veterinary. Lymphocytes, Tumor-Infiltrating / immunology. Mammary Neoplasms, Animal / immunology

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  • (PMID = 20525350.001).
  • [ISSN] 1471-2407
  • [Journal-full-title] BMC cancer
  • [ISO-abbreviation] BMC Cancer
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Other-IDs] NLM/ PMC2894795
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34. Jiang W, Zhu Z, Thompson HJ: Dietary energy restriction modulates the activity of AMP-activated protein kinase, Akt, and mammalian target of rapamycin in mammary carcinomas, mammary gland, and liver. Cancer Res; 2008 Jul 1;68(13):5492-9
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  • [Title] Dietary energy restriction modulates the activity of AMP-activated protein kinase, Akt, and mammalian target of rapamycin in mammary carcinomas, mammary gland, and liver.
  • Dietary energy restriction (DER) inhibits mammary carcinogenesis, yet mechanisms accounting for its protective activity have not been fully elucidated.
  • In this study, we tested the hypothesis that DER exerts effects on intracellular energy sensing pathways, resulting in alterations of phosphorylated proteins that play a key role in the regulation of cancer.
  • Experiments were conducted using the 1-methyl-1-nitrosourea-induced mammary cancer model in which rats were 0%, 20%, or 40% energy restricted during the postinitiation stage of carcinogenesis.
  • In a DER dose-dependent manner, levels of Thr(172) phosphorylated AMP-activated protein kinase (AMPK) increased in mammary carcinomas with a concomitant increase in phosphorylated acetyl-CoA-carboxylase, a direct target of AMPK, the phosphorylation of which is regarded as an indicator of AMPK activity.
  • Similar patterns were observed in mammary glands and livers of non-carcinogen-treated rats.

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  • (PMID = 18593953.001).
  • [ISSN] 1538-7445
  • [Journal-full-title] Cancer research
  • [ISO-abbreviation] Cancer Res.
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / CA52626; United States / NCI NIH HHS / CA / CA052626-16; United States / NCI NIH HHS / CA / R01 CA100693; United States / NCI NIH HHS / CA / R01 CA052626-16; United States / NCI NIH HHS / CA / R01 CA052626
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Carrier Proteins; 0 / Eif4ebp1 protein, rat; 0 / Multienzyme Complexes; 0 / Phosphoproteins; EC 2.7.- / Protein Kinases; EC 2.7.1.1 / TOR Serine-Threonine Kinases; EC 2.7.1.1 / mTOR protein, rat; EC 2.7.11.1 / AMP-Activated Protein Kinases; EC 2.7.11.1 / Oncogene Protein v-akt; EC 2.7.11.1 / Protein-Serine-Threonine Kinases; EC 2.7.11.1 / Ribosomal Protein S6 Kinases, 70-kDa
  • [Other-IDs] NLM/ NIHMS54517; NLM/ PMC2587286
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35. Adamovic T, McAllister D, Guryev V, Wang X, Andrae JW, Cuppen E, Jacob HJ, Sugg SL: Microalterations of inherently unstable genomic regions in rat mammary carcinomas as revealed by long oligonucleotide array-based comparative genomic hybridization. Cancer Res; 2009 Jun 15;69(12):5159-67
Hazardous Substances Data Bank. 7,12-DIMETHYLBENZ(A)ANTHRACENE .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Microalterations of inherently unstable genomic regions in rat mammary carcinomas as revealed by long oligonucleotide array-based comparative genomic hybridization.
  • The presence of copy number variants in normal genomes poses a challenge to identify small genuine somatic copy number changes in high-resolution cancer genome profiling studies due to the use of unpaired reference DNA.
  • We here show real gains of the IgG heavy chain V gene region in carcinogen-induced rat mammary tumor samples after normalization to paired mammary gland, a tissue without lymphocyte infiltration.
  • We further show that the segmental duplication region encompassing the IgG heavy chain V genes is a copy number variant between the susceptible (SS) and the resistant (BN) to mammary tumor development inbred rat strains.
  • Our data suggest that the already inherently unstable genomic region is a convenient target for additional structural rearrangements (gains) at the somatic level when exposed to a carcinogen (7,12-dimethylbenz[a]anthracene), which subsequently seem to benefit tumor development in the mammary gland of the susceptible strain.
  • Thus, the selection of an appropriate reference DNA enabled us to identify immunoglobulin genes as novel cancer targets playing a role in mammary tumor development.
  • We conclude that control DNA in array-based comparative genomic hybridization experiments should be selected with care, and DNA from pooled spleen (contains immature lymphocytes and is used as reference in animal studies) or blood may not be the ideal control in the study of primary tumors.
  • [MeSH-major] Adenocarcinoma / genetics. Mammary Neoplasms, Experimental / genetics. Nucleic Acid Hybridization / methods. Oligonucleotide Array Sequence Analysis

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  • (PMID = 19509235.001).
  • [ISSN] 1538-7445
  • [Journal-full-title] Cancer research
  • [ISO-abbreviation] Cancer Res.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Carcinogens; 0 / DNA Primers; 57-97-6 / 9,10-Dimethyl-1,2-benzanthracene
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36. Simeonov R, Simeonova G: Nuclear cytomorphometry in feline mammary gland epithelial tumours. Vet J; 2009 Feb;179(2):296-300

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Nuclear cytomorphometry in feline mammary gland epithelial tumours.
  • Stained cytological specimens from 35 feline mammary gland epithelial tumours (4 adenomas, 11 tubulopapillary carcinomas 13 solid carcinomas and 7 cribriform carcinomas) were analysed by computer-assisted nuclear morphometry.
  • The study aimed to evaluate (1) the possibility of using nuclear cytomorphometry as an auxiliary diagnostic method to differentiate between benign and malignant feline mammary gland epithelial tumours, and (2) the prognostic value of nuclear morphometry in feline mammary carcinomas.
  • The results indicated that MNA, MNP, MND and NR could be a useful adjunct in diagnosis but are not reliable prognostic indicators for feline mammary gland carcinomas.
  • [MeSH-major] Cat Diseases / diagnosis. Cell Nucleus / pathology. Cytological Techniques / veterinary. Mammary Glands, Animal / cytology. Mammary Neoplasms, Animal / diagnosis
  • [MeSH-minor] Adenoma / diagnosis. Adenoma / pathology. Adenoma / veterinary. Animals. Automation. Carcinoma / diagnosis. Carcinoma / pathology. Carcinoma / veterinary. Cats. Diagnosis, Differential. Female

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  • (PMID = 17959399.001).
  • [ISSN] 1090-0233
  • [Journal-full-title] Veterinary journal (London, England : 1997)
  • [ISO-abbreviation] Vet. J.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] England
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37. Yuri T, Tsukamoto R, Uehara N, Matsuoka Y, Tsubura A: Effects of different durations of estrogen and progesterone treatment on development of N-methyl-N-nitrosourea-induced mammary carcinomas in female Lewis rats. In Vivo; 2006 Nov-Dec;20(6B):829-36
Hazardous Substances Data Bank. N-NITROSO-N-METHYLUREA .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Effects of different durations of estrogen and progesterone treatment on development of N-methyl-N-nitrosourea-induced mammary carcinomas in female Lewis rats.
  • BACKGROUND: There have been no precise evaluations of the effects of different durations of exposure to estrogen and progesterone pregnancy levels on mammary carcinogenesis risk.
  • We examined such effects on the development of N-methyl-N-nitrosourea (MNU)-induced rat mammary carcinoma.
  • Circulating 17beta-estradiol and progesterone levels in the serum, and expression of estrogen receptor (ER) a and progesterone receptor (PgR) in the normal mammary gland were measured.
  • The rats were sacrificed when they developed a mammary tumor with a diameter of > or =1 cm, or when they reached the age of 29 weeks.
  • In normal mammary glands of rats sacrificed at 29 weeks of age, both long- and short-term E/P treatment decreased the percentage of ERalpha- and PgR-positive cells.
  • Rats that received long- or short-term E/P treatment had a decreased incidence of mammary carcinoma with a diameter of > or =1 cm, compared to control rats.
  • Although short-term E/P treatment significantly suppressed mammary carcinomas of all sizes, long-term E/P treatment had no cancer-suppressing effect.
  • CONCLUSION: The duration of E/P treatment is an essential factor for the suppression of mammary carcinogenesis.
  • [MeSH-major] Estrogens / therapeutic use. Mammary Neoplasms, Experimental / prevention & control. Methylnitrosourea / toxicity. Progesterone / therapeutic use
  • [MeSH-minor] Animals. Body Weight / drug effects. Drug Implants. Estradiol / administration & dosage. Estradiol / blood. Estradiol / therapeutic use. Estrogen Receptor alpha / metabolism. Female. Injections, Intraperitoneal. Mammary Glands, Animal / drug effects. Mammary Glands, Animal / metabolism. Mammary Glands, Animal / pathology. Rats. Rats, Inbred Lew. Receptors, Progesterone / metabolism. Time Factors

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  • (PMID = 17203775.001).
  • [ISSN] 0258-851X
  • [Journal-full-title] In vivo (Athens, Greece)
  • [ISO-abbreviation] In Vivo
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Greece
  • [Chemical-registry-number] 0 / Drug Implants; 0 / Estrogen Receptor alpha; 0 / Estrogens; 0 / Receptors, Progesterone; 4G7DS2Q64Y / Progesterone; 4TI98Z838E / Estradiol; 684-93-5 / Methylnitrosourea
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38. Ninomiya K, Kawaguchi H, Souda M, Taguchi S, Funato M, Umekita Y, Yoshida H: Effects of neonatally administered diethylstilbestrol on induction of mammary carcinomas induced by 7, 12-dimethylbenz(a)anthracene in female rats. Toxicol Pathol; 2007 Oct;35(6):813-8
Hazardous Substances Data Bank. 7,12-DIMETHYLBENZ(A)ANTHRACENE .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Effects of neonatally administered diethylstilbestrol on induction of mammary carcinomas induced by 7, 12-dimethylbenz(a)anthracene in female rats.
  • The incidence of mammary carcinomas (MCs) were 50, 54, 91, 39, 19% at 175 days after birth, and 77, 87, 100, 85, 75% at necropsy in the 0, 0.1, 1, 10, 100 microg groups, respectively.
  • [MeSH-major] Diethylstilbestrol / toxicity. Mammary Neoplasms, Experimental / chemically induced
  • [MeSH-minor] 9,10-Dimethyl-1,2-benzanthracene. Animals. Animals, Newborn. Corpus Luteum / abnormalities. Estrus / drug effects. Female. Ki-67 Antigen / analysis. Mammary Glands, Animal / pathology. Rats. Rats, Sprague-Dawley

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  • (PMID = 17943655.001).
  • [ISSN] 0192-6233
  • [Journal-full-title] Toxicologic pathology
  • [ISO-abbreviation] Toxicol Pathol
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Ki-67 Antigen; 57-97-6 / 9,10-Dimethyl-1,2-benzanthracene; 731DCA35BT / Diethylstilbestrol
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39. Umesako S, Iiga S, Takahashi M, Imura K, Mori N, Hong DP, Song CW, Niwa O, Okumoto M: Distinct pattern of allelic loss and inactivation of cadherin 1 and 5 genes in mammary carcinomas arising in p53(+/-) mice. J Radiat Res; 2007 Mar;48(2):143-52
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Distinct pattern of allelic loss and inactivation of cadherin 1 and 5 genes in mammary carcinomas arising in p53(+/-) mice.
  • p53 is one of the most frequently mutated genes in mammary carcinomas (MCs).
  • To detect tumor suppressor genes cooperating with a hetero-deficient p53 gene in mammary carcinogenesis, we first examined allelotypes in MCs from (BALB/cHeA x MSM/Ms) F(1)- p53(+/-) and (BALB/cHeA x 129/SvEv) F(1)- p53(+/-) female mice, and then surveyed down-regulated genes in the allelic loss regions.
  • Thus, inactivation of Cdh1 and Cdh5 is likely to cooperate with the loss of p53, suggesting a possible tumor suppressive function of these genes in mammary carcinogenesis.
  • [MeSH-major] Alleles. Antigens, CD / genetics. Cadherins / genetics. Gene Expression Regulation, Neoplastic. Genes, p53. Loss of Heterozygosity. Mammary Neoplasms, Animal / genetics

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  • (PMID = 17327688.001).
  • [ISSN] 0449-3060
  • [Journal-full-title] Journal of radiation research
  • [ISO-abbreviation] J. Radiat. Res.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Japan
  • [Chemical-registry-number] 0 / Antigens, CD; 0 / Cadherins; 0 / cadherin 5
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40. Wicha MS: Identification of murine mammary stem cells: implications for studies of mammary development and carcinogenesis. Breast Cancer Res; 2006;8(5):109
COS Scholar Universe. author profiles.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Identification of murine mammary stem cells: implications for studies of mammary development and carcinogenesis.
  • The epithelial components of the mammary gland are thought to arise from a stem cell capable of both self-renewal and multi-lineage differentiation.
  • Furthermore, there is increasing evidence that mammary carcinomas originate in these cells or their immediate progeny.
  • The recent identification of murine mammary stem cells should facilitate their molecular characterization and help to elucidate their role in mammary carcinogenesis.
  • In addition, an understanding of the biology of these cells including the pathways that regulate their self-renewal and differentiation may suggest new approaches for the prevention and treatment of breast cancer.

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  • (PMID = 16934104.001).
  • [ISSN] 1465-542X
  • [Journal-full-title] Breast cancer research : BCR
  • [ISO-abbreviation] Breast Cancer Res.
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / P30 CA046592; United States / NCI NIH HHS / CA / R01 CA101860; United States / NCI NIH HHS / CA / 5P53CA46592; United States / NCI NIH HHS / CA / CA101860
  • [Publication-type] Editorial; Research Support, N.I.H., Extramural; Research Support, U.S. Gov't, Non-P.H.S.
  • [Publication-country] England
  • [Other-IDs] NLM/ PMC1779494
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41. Klopfleisch R, Lenze D, Hummel M, Gruber AD: Metastatic canine mammary carcinomas can be identified by a gene expression profile that partly overlaps with human breast cancer profiles. BMC Cancer; 2010;10:618
SciCrunch. ArrayExpress: Data: Microarray .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Metastatic canine mammary carcinomas can be identified by a gene expression profile that partly overlaps with human breast cancer profiles.
  • BACKGROUND: Similar to human breast cancer mammary tumors of the female dog are commonly associated with a fatal outcome due to the development of distant metastases.
  • However, the molecular defects leading to metastasis are largely unknown and the value of canine mammary carcinoma as a model for human breast cancer is unclear.
  • In this study, we analyzed the gene expression signatures associated with mammary tumor metastasis and asked for parallels with the human equivalent.
  • METHODS: Messenger RNA expression profiles of twenty-seven lymph node metastasis positive or negative canine mammary carcinomas were established by microarray analysis.
  • The findings were also correlated with published data on human breast cancer.
  • RESULTS: Metastatic canine mammary carcinomas had 1,011 significantly differentially expressed genes when compared to non-metastatic carcinomas.
  • Metastatic carcinomas had a significant up-regulation of genes associated with cell cycle regulation, matrix modulation, protein folding and proteasomal degradation whereas cell differentiation genes, growth factor pathway genes and regulators of actin organization were significantly down-regulated.
  • Interestingly, 265 of the 1,011 differentially expressed canine genes are also related to human breast cancer and, vice versa, parts of a human prognostic gene signature were identified in the expression profiles of the metastatic canine tumors.
  • CONCLUSIONS: Metastatic canine mammary carcinomas can be discriminated from non-metastatic carcinomas by their gene expression profiles.
  • More than one third of the differentially expressed genes are also described of relevance for human breast cancer.
  • [MeSH-major] Breast Neoplasms / genetics. Breast Neoplasms / metabolism. Gene Expression Regulation, Neoplastic. Mammary Neoplasms, Animal / genetics. Mammary Neoplasms, Animal / metabolism

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  • (PMID = 21062462.001).
  • [ISSN] 1471-2407
  • [Journal-full-title] BMC cancer
  • [ISO-abbreviation] BMC Cancer
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Intercellular Signaling Peptides and Proteins; 0 / RNA, Messenger
  • [Other-IDs] NLM/ PMC2994823
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42. Schug TT, Berry DC, Toshkov IA, Cheng L, Nikitin AY, Noy N: Overcoming retinoic acid-resistance of mammary carcinomas by diverting retinoic acid from PPARbeta/delta to RAR. Proc Natl Acad Sci U S A; 2008 May 27;105(21):7546-51
NCI CPTC Antibody Characterization Program. NCI CPTC Antibody Characterization Program .

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  • [Title] Overcoming retinoic acid-resistance of mammary carcinomas by diverting retinoic acid from PPARbeta/delta to RAR.
  • Here, we show that, in the RA-resistant mouse model of breast cancer MMTV-neu, RA indeed activates the nonclassical RA receptor PPARbeta/delta.
  • Decreasing this ratio in mammary tissue diverted RA from PPARbeta/delta to RAR and suppressed tumor growth.

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  • (PMID = 18495924.001).
  • [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 / NCRR NIH HHS / RR / K26 RR017595; United States / NCI NIH HHS / CA / 5T32CA009682; United States / NCI NIH HHS / CA / R01 CA96823; United States / NCI NIH HHS / CA / R01 CA096823; United States / NCI NIH HHS / CA / T32 CA009682; United States / NCI NIH HHS / CA / R01 CA107013
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / Fabp5 protein, mouse; 0 / Fatty Acid-Binding Proteins; 0 / Neoplasm Proteins; 0 / PPAR delta; 0 / PPAR-beta; 0 / Receptors, Retinoic Acid; 0 / retinoic acid binding protein II, cellular; 5688UTC01R / Tretinoin
  • [Other-IDs] NLM/ PMC2396692
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43. Martinez-Ruzafa I, Dominguez PA, Dervisis NG, Sarbu L, Newman RG, Cadile CD, Kitchell BE: Tolerability of gemcitabine and carboplatin doublet therapy in cats with carcinomas. J Vet Intern Med; 2009 May-Jun;23(3):570-7
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  • [Title] Tolerability of gemcitabine and carboplatin doublet therapy in cats with carcinomas.
  • BACKGROUND: This study was performed to determine the toxicity of gemcitabine-carboplatin doublet therapy in cats with carcinomas.
  • ANIMALS: Twenty cats with spontaneously occurring carcinomas.
  • RESULTS: Cats in the 1st cohort received a median of 3.75 cycles per animal (range, 1-6).
  • Cats in the 2nd cohort received a median of 2 cycles per animal (range, 0.5-10).
  • In the 2nd cohort, of 11 cats with measurable tumors, there was 1 complete response (pancreatic carcinoma) and 1 partial response (squamous cell carcinoma, receiving concurrent nonsteroidal anti-inflammatory drugs).

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  • (PMID = 19298611.001).
  • [ISSN] 0891-6640
  • [Journal-full-title] Journal of veterinary internal medicine
  • [ISO-abbreviation] J. Vet. Intern. Med.
  • [Language] ENG
  • [Publication-type] Clinical Trial; Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0W860991D6 / Deoxycytidine; B76N6SBZ8R / gemcitabine; BG3F62OND5 / Carboplatin
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44. Shibata MA, Ito Y, Morimoto J, Kusakabe K, Yoshinaka R, Otsuki Y: In vivo electrogene transfer of interleukin-12 inhibits tumor growth and lymph node and lung metastases in mouse mammary carcinomas. J Gene Med; 2006 Mar;8(3):335-52
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  • [Title] In vivo electrogene transfer of interleukin-12 inhibits tumor growth and lymph node and lung metastases in mouse mammary carcinomas.
  • BACKGROUND: Human breast cancer metastasizes mainly to lymph nodes, lungs, liver, and bone; in the majority of cases, it is the development of metastases which leads to death.
  • In order to suppress mammary cancer metastasis, we applied in vivo electrogene transfer (non-viral method) as a means of interleukin-12 (IL-12) gene therapy on highly metastatic murine mammary cancer model.
  • METHODS: Metastatic mammary tumors induced by inoculation in BALB/c female mice were treated by intratumoral injections of either a plasmid vector containing IL-12 or empty vector and then subjected to in vivo electrogene transfer once a week for 8 weeks.
  • RESULTS: Treatment with IL-12 resulted in elevation of both IL-12 and IFNgamma levels in mammary tumors and in serum and intratumoral levels of CD4 and CD8 proteins were also increased.
  • [MeSH-major] Gene Transfer Techniques. Interleukin-12 / genetics. Lung Neoplasms / secondary. Mammary Neoplasms, Animal / genetics. Mammary Neoplasms, Animal / therapy

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  • (PMID = 16345101.001).
  • [ISSN] 1099-498X
  • [Journal-full-title] The journal of gene medicine
  • [ISO-abbreviation] J Gene Med
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 187348-17-0 / Interleukin-12; EC 2.7.10.1 / Vascular Endothelial Growth Factor Receptor-3
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45. Park JM, Terabe M, Sakai Y, Munasinghe J, Forni G, Morris JC, Berzofsky JA: Early role of CD4+ Th1 cells and antibodies in HER-2 adenovirus vaccine protection against autochthonous mammary carcinomas. J Immunol; 2005 Apr 1;174(7):4228-36
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  • [Title] Early role of CD4+ Th1 cells and antibodies in HER-2 adenovirus vaccine protection against autochthonous mammary carcinomas.
  • HER-2 is an oncogenic tumor-associated Ag that is overexpressed in several human tumors including breast and ovarian cancer.
  • The efficacy and mechanism of a HER-2-expressing recombinant adenoviral vaccine to protect against tumorigenesis was examined using HER-2 transgenic (BALB-neuT) mice, which develop spontaneous breast tumors in all 10 mammary glands, and also using a transplantable mouse tumor model.
  • Vaccination beginning at 6-8 wk of age (through 19 wk of age) prevented development of spontaneous mammary tumors even after 50 wk, whereas the animals in the control groups had tumors in all mammary glands by 25 wk.
  • Anti-HER-2 serum not only inhibited growth of mammary tumor cell lines expressing HER-2 in vitro but also protected mice from tumors in vivo, suggesting a direct action of Ab on the tumor cells.
  • [MeSH-major] Cancer Vaccines / administration & dosage. Mammary Neoplasms, Animal / prevention & control. Receptor, ErbB-2 / administration & dosage. Th1 Cells / immunology

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  • (PMID = 15778385.001).
  • [ISSN] 0022-1767
  • [Journal-full-title] Journal of immunology (Baltimore, Md. : 1950)
  • [ISO-abbreviation] J. Immunol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antigens, Neoplasm; 0 / Cancer Vaccines; 0 / Immunoglobulin G; EC 2.7.10.1 / Receptor, ErbB-2
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46. Döpke C, Fehr M, Thiele A, Pohlenz J, Wohlsein P: Morphological and immunohistochemical characterization of spontaneous mammary tumours in European hedgehogs (Erinaceus europaeus). J Comp Pathol; 2007 Jul;137(1):22-9
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  • [Title] Morphological and immunohistochemical characterization of spontaneous mammary tumours in European hedgehogs (Erinaceus europaeus).
  • Mammary tumour samples (11 surgical and five post-mortem) from 16 adult European hedgehogs submitted between 1980 and 2004 were examined.
  • Histologically, the tumours were classified as simple tubulo-papillary carcinomas with local invasive growth.
  • CK expression did not differ from that in normal mammary gland tissue.
  • CK20 was expressed in the mammary tissue of hedgehogs, in contrast to that of dogs and cats; CK7 immunolabelling, however, which commonly occurs in mammary epithelial cells, was negative.
  • CK20 expression, together with the lack of CK7 as determined by a protein-specific antibody, represented an important difference from the CK profile shown by mammary epithelial cells of other mammalian species, including the dog and cat.
  • [MeSH-major] Adenocarcinoma / veterinary. Carcinoma, Papillary / veterinary. Hedgehogs. Mammary Neoplasms, Animal / pathology

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  • (PMID = 17467727.001).
  • [ISSN] 0021-9975
  • [Journal-full-title] Journal of comparative pathology
  • [ISO-abbreviation] J. Comp. Pathol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 68238-35-7 / Keratins
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47. Illera JC, Pérez-Alenza MD, Nieto A, Jiménez MA, Silvan G, Dunner S, Peña L: Steroids and receptors in canine mammary cancer. Steroids; 2006 Jul;71(7):541-8
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  • [Title] Steroids and receptors in canine mammary cancer.
  • The aims of this study were to investigate the serum and tissue content of androgens and estrogens in canine inflammatory mammary carcinomas (IMC) as well as in non-inflammatory malignant mammary tumors (MMT), and assessed the immunoexpression of estrogen and androgen receptors using immunohistochemistry.
  • Profiles for the androgens dehydroepiandrosterone (DHEA), androstenedione (A4), and testosterone (T), and for the estrogens 17beta estradiol (E2) and estrone-sulphate (SO4E1) were measured both in tissue homogenates and in serum of MMT and IMC by EIA techniques in 42 non-inflammatory malignant mammary tumors (MMT) and in 14 inflammatory mammary carcinomas (IMC), prospectively collected from 56 female dogs.
  • ERbeta and AR were intensely expressed in highly malignant inflammatory mammary carcinoma cells.
  • To our knowledge, this is the first report relative to AR immunohistochemistry in canine mammary cancer and to estrogens or androgens in serum of dogs with benign or malignant mammary tumors.
  • [MeSH-major] Androgens / metabolism. Estrogens / metabolism. Mammary Neoplasms, Animal / metabolism. Receptors, Androgen / metabolism. Receptors, Estrogen / metabolism

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  • (PMID = 16631217.001).
  • [ISSN] 0039-128X
  • [Journal-full-title] Steroids
  • [ISO-abbreviation] Steroids
  • [Language] eng
  • [Publication-type] Comparative Study; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Androgens; 0 / Estrogens; 0 / Receptors, Androgen; 0 / Receptors, Estrogen
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48. Fusaro L, Panarese S, Brunetti B, Zambelli D, Benazzi C, Sarli G: Quantitative analysis of telomerase in feline mammary tissues. J Vet Diagn Invest; 2009 May;21(3):369-73
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  • [Title] Quantitative analysis of telomerase in feline mammary tissues.
  • TRAP-enzyme-linked immunosorbent assay (ELISA) reactivity was compared with telomerase reverse transcription (TERT) IHC staining in 22 feline mammary tissues (6 normal mammary glands, 2 dysplastic mammary glands, 1 fibroadenoma, and 13 malignant neoplasms [6 solid mammary carcinomas, 2 squamous-cell carcinomas, 4 tubulopapillary mammary carcinomas, and 1 mammary carcinosarcoma]).
  • With TERT IHC staining, the absolute number and percentage of cells with positive nuclei and nucleoli within the same cell were the variables with the greatest discrimination between benign and malignant mammary lesions (analysis of variance [ANOVA], average P < 0.0001; percentage P < 0.001).
  • For TRAP-ELISA-positive versus TRAP-ELISA-negative tissues, a positive test result provided greater differentiation between malignant versus benign mammary lesions (ANOVA, average P = 0.00038; percentage P = 0.0022).
  • [MeSH-major] Immunohistochemistry / veterinary. Mammary Glands, Animal / enzymology. Mammary Neoplasms, Animal / diagnosis. Telomerase / analysis. Telomerase / metabolism
  • [MeSH-minor] Animals. Carcinoma / enzymology. Carcinoma / veterinary. Cats. Gene Expression Regulation, Enzymologic / physiology. Gene Expression Regulation, Neoplastic / physiology

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  • (PMID = 19407092.001).
  • [ISSN] 1040-6387
  • [Journal-full-title] Journal of veterinary diagnostic investigation : official publication of the American Association of Veterinary Laboratory Diagnosticians, Inc
  • [ISO-abbreviation] J. Vet. Diagn. Invest.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] EC 2.7.7.49 / Telomerase
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49. Pagani IS, Terrinoni A, Marenghi L, Zucchi I, Chiaravalli AM, Serra V, Rovera F, Sirchia S, Dionigi G, Miozzo M, Frattini A, Ferrari A, Capella C, Pasquali F, Lo Curto F, Albertini A, Melino G, Porta G: The mammary gland and the homeobox gene Otx1. Breast J; 2010 Sep-Oct;16 Suppl 1:S53-6
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  • [Title] The mammary gland and the homeobox gene Otx1.
  • The mammary gland, the unique organ that primarily form at puberty, is an ideal model to study the functions of homeobox (HB) genes in both development and tumorigenesis.
  • In the normal mammary gland, homeobox genes are involved in ductal formation, epithelial branching, and lobulo-alveolar development by regulating epithelial proliferation and differentiation.
  • When homeobox genes are misexpressed in animal models, different defects are displayed in mammary gland development.
  • Aberrant expression of homeobox genes, overexpressed or downregulated, is found in primary carcinomas and in breast cancer.
  • During cyclical development of mammary gland, the Otx1 gene is overexpressed in lactation, confirming a role of this transcription factor in cell differentiation.
  • Recent studies report that Otx1 is overexpressed in breast cancer.
  • [MeSH-minor] Animals. Epithelial Cells / metabolism. Female. Humans. Mammary Glands, Animal / embryology. Mammary Glands, Human / embryology. Neoplastic Stem Cells

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  • [Copyright] © 2010 Wiley Periodicals, Inc.
  • [ErratumIn] Breast J. 2011 Sep-Oct;17(5):568. Mozzo, Monica [corrected to Miozzo, Monica]; Curto, Francesco L [corrected to Lo Curto, Francesco]
  • (PMID = 21050313.001).
  • [ISSN] 1524-4741
  • [Journal-full-title] The breast journal
  • [ISO-abbreviation] Breast J
  • [Language] eng
  • [Grant] United Kingdom / Medical Research Council / / MRC/ MC/ U132670600
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / OTX1 protein, human; 0 / Otx Transcription Factors
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50. Paltian V, Alldinger S, Baumgärtner W, Wohlsein P: Expression of CD44 in canine mammary tumours. J Comp Pathol; 2009 Nov;141(4):237-47
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  • [Title] Expression of CD44 in canine mammary tumours.
  • In human breast cancer, the interaction of tumour cells with the ECM via CD44 is favoured as a major candidate for tumour progression and metastasis.
  • The present study was designed to investigate immunohistochemically the expression of the standard form of CD44 in normal, hyperplastic and neoplastic canine mammary tissue.
  • CD44 was expressed in normal and hyperplastic mammary tissue predominantly by ductal and alveolar epithelial cells and to a minor extent by myoepithelial cells.
  • In simple and complex adenomas and benign mixed tumours there was significant up-regulation of CD44 expression in alveolar epithelial cells compared with adjacent non-neoplastic mammary tissue.
  • Peripheral epithelial cells of simple and complex adenomas, benign mixed tumours and complex carcinomas expressed significantly more CD44 compared with adjacent non-neoplastic mammary tissue.
  • Peripheral epithelial cells of simple adenomas revealed a significantly higher CD44 expression compared with simple carcinomas.
  • A statistical trend to greater CD44 expression was found in peripheral epithelial cells of complex adenomas, benign mixed tumours and complex carcinomas compared with simple carcinomas.
  • Up-regulation of CD44 therefore appears to be associated with benign or relatively benign biological behaviour of canine mammary tumours.
  • [MeSH-major] Adenoma / metabolism. Antigens, CD44 / metabolism. Carcinoma / metabolism. Dog Diseases. Mammary Neoplasms, Animal / metabolism
  • [MeSH-minor] Analysis of Variance. Animals. Dogs. Female. Immunohistochemistry. Mammary Glands, Animal / metabolism. Mammary Glands, Animal / pathology. Neoplasm Staging. Statistics, Nonparametric

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  • (PMID = 19592009.001).
  • [ISSN] 1532-3129
  • [Journal-full-title] Journal of comparative pathology
  • [ISO-abbreviation] J. Comp. Pathol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Antigens, CD44
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51. Boggs RM, Wright ZM, Stickney MJ, Porter WW, Murphy KE: MicroRNA expression in canine mammary cancer. Mamm Genome; 2008 Aug;19(7-8):561-9
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] MicroRNA expression in canine mammary cancer.
  • Furthermore, because the dog presents with distinct, spontaneously occurring mammary tumors, it may serve as a model for genetic analysis and treatments of humans with malignant breast tumors.
  • Because miRNAs have been found to act as both tumor suppressors and oncogenes in several different cancers, expression patterns of ten miRNAs (miR-15a, miR-16, miR-17-5p, miR-21, miR-29b, miR-125b, miR-145, miR-155, miR-181b, let-7f) known to be associated with human breast cancers were compared to malignant canine mammary tumors (n = 6) and normal canine mammary tissue (n = 10).
  • In addition, when analyzed according to specific cancer phenotypes, miR-15a and miR-16 show a significant downregulation in canine ductal carcinomas while miRsR-181b, -21, -29b, and let-7f show a significant upregulation in canine tubular papillary carcinomas.
  • [MeSH-major] Gene Expression Regulation, Neoplastic. Mammary Neoplasms, Animal / genetics. MicroRNAs / genetics
  • [MeSH-minor] Animals. Disease Models, Animal. Dogs. Female. Humans

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  • (PMID = 18665421.001).
  • [ISSN] 0938-8990
  • [Journal-full-title] Mammalian genome : official journal of the International Mammalian Genome Society
  • [ISO-abbreviation] Mamm. Genome
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / MicroRNAs
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52. Teulière J, Faraldo MM, Deugnier MA, Shtutman M, Ben-Ze'ev A, Thiery JP, Glukhova MA: Targeted activation of beta-catenin signaling in basal mammary epithelial cells affects mammary development and leads to hyperplasia. Development; 2005 Jan;132(2):267-77
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  • [Title] Targeted activation of beta-catenin signaling in basal mammary epithelial cells affects mammary development and leads to hyperplasia.
  • In the mammary gland, constitutive activation of Wnt/beta-catenin signaling in luminal secretory cells results in precocious lobuloalveolar differentiation and induces adenocarcinomas, whereas the impact of this signaling pathway on the function of the second major mammary epithelial cell lineage, the basal myoepithelial cells, has not been analyzed.
  • We have used the keratin (K) 5 promoter to target the expression of stabilized N-terminally truncated beta-catenin to the basal cell layer of mouse mammary epithelium.
  • The transgenic mice presented an abnormal mammary phenotype: precocious lateral bud formation, increased proliferation and premature differentiation of luminal epithelium in pregnancy, persistent proliferation in lactation and accelerated involution.
  • Nulliparous transgenic females developed mammary hyperplasia that comprised undifferentiated basal (K5/14-positive, K8- and alpha-smooth muscle-actin-negative) cells.
  • Multiparous mice, in addition, developed invasive basal-type carcinomas.
  • Thus, activation of beta-catenin signaling in basal mammary epithelial cells affects the entire process of mammary gland development and induces amplification of basal-type cells that lack lineage markers, presumably, a subpopulation of mammary progenitors able to give rise to tumors.
  • [MeSH-major] Cytoskeletal Proteins / genetics. Cytoskeletal Proteins / metabolism. Epithelial Cells / metabolism. Gene Expression Regulation, Developmental. Mammary Glands, Animal / metabolism. Trans-Activators / genetics. Trans-Activators / metabolism

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  • (PMID = 15590737.001).
  • [ISSN] 0950-1991
  • [Journal-full-title] Development (Cambridge, England)
  • [ISO-abbreviation] Development
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / CTNNB1 protein, mouse; 0 / Cytoskeletal Proteins; 0 / DNA Primers; 0 / Phosphoproteins; 0 / RNA, Messenger; 0 / Trans-Activators; 0 / Trp63 protein, mouse; 0 / beta Catenin
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53. Bultman SJ, Herschkowitz JI, Godfrey V, Gebuhr TC, Yaniv M, Perou CM, Magnuson T: Characterization of mammary tumors from Brg1 heterozygous mice. Oncogene; 2008 Jan 17;27(4):460-8
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  • [Title] Characterization of mammary tumors from Brg1 heterozygous mice.
  • Mammalian SWI/SNF-related complexes have been implicated in cancer based on some of the subunits physically interacting with retinoblastoma (RB) and other proteins involved in carcinogenesis.
  • Here, we demonstrate that Brg1 heterozygotes are susceptible to mammary tumors that are fundamentally different than Snf5 tumors.
  • First, mammary tumors are carcinomas not sarcomas.
  • These findings demonstrate that BRG1 and SNF5 are not functionally equivalent but protect against cancer in different ways.
  • We also demonstrate that Brg1+/- mammary tumors have relatively heterogeneous gene expression profiles with similarities and differences compared to other mouse models of breast cancer.
  • The Brg1+/- expression profiles are not particularly similar to mammary tumors from Wap-T121 transgenic line where RB is perturbed.
  • [MeSH-major] Adenocarcinoma / genetics. DNA Helicases / genetics. Heterozygote. Mammary Neoplasms, Experimental / genetics. Nuclear Proteins / genetics. Transcription Factors / genetics
  • [MeSH-minor] Animals. Cluster Analysis. Disease Models, Animal. Female. Gene Expression Profiling. Genomic Instability / physiology. Loss of Heterozygosity. Male. Mice. Mutation, Missense. Oligonucleotide Array Sequence Analysis. Penetrance. Phenotype. Retinoblastoma Protein / genetics

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  • (PMID = 17637742.001).
  • [ISSN] 1476-5594
  • [Journal-full-title] Oncogene
  • [ISO-abbreviation] Oncogene
  • [Language] eng
  • [Grant] United States / NICHD NIH HHS / HD / R01 HD036655
  • [Publication-type] Comparative Study; Journal Article; Research Support, N.I.H., Extramural
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Nuclear Proteins; 0 / Retinoblastoma Protein; 0 / Transcription Factors; EC 3.6.1.- / SMARCA4 protein, human; EC 3.6.4.- / DNA Helicases
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54. Rodo A, Malicka E: E-cadherin immunohistochemical expression in mammary gland neoplasms in bitches. Pol J Vet Sci; 2008;11(1):47-54
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  • [Title] E-cadherin immunohistochemical expression in mammary gland neoplasms in bitches.
  • Material for the investigation comprised mammary gland tumours, collected from dogs, the patients of veterinary clinics, during surgical procedures and archival samples.
  • All together 21 adenomas, 32 complex carcinomas, 35 simple carcinomas and 13 solid carcinomas were qualified for further investigation.
  • E-cadherin expression was higher in adenomas as compared with carcinomas but lower in solid carcinomas as compared with simple and complex carcinomas.
  • [MeSH-major] Adenoma / veterinary. Cadherins / metabolism. Carcinoma / veterinary. Dog Diseases / metabolism. Mammary Neoplasms, Animal / enzymology

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  • (PMID = 18540208.001).
  • [ISSN] 1505-1773
  • [Journal-full-title] Polish journal of veterinary sciences
  • [ISO-abbreviation] Pol J Vet Sci
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Poland
  • [Chemical-registry-number] 0 / Cadherins
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55. Lubet RA, Boring D, Steele VE, Ruppert JM, Juliana MM, Grubbs CJ: Lack of efficacy of the statins atorvastatin and lovastatin in rodent mammary carcinogenesis. Cancer Prev Res (Phila); 2009 Feb;2(2):161-7
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  • [Title] Lack of efficacy of the statins atorvastatin and lovastatin in rodent mammary carcinogenesis.
  • Recently, there has been conflicting epidemiologic data indicating that statins decrease the incidence of certain types of cancer, including breast cancer.
  • Atorvastatin and lovastatin, statins with different lipophicilities, were administered in diet either as single agents or in combination with suboptimal doses of tamoxifen or the retinoid X receptor agonist bexarotene were evaluated for prevention of estrogen receptor-positive mammary cancers induced in the rat with methylnitrosourea.
  • Atorvastatin (125 or 500 mg/kg diet) alone did not significantly alter cancer incidence or multiplicity.
  • Suboptimal doses of tamoxifen (0.4 mg/kg diet) or bexarotene (80 mg/kg diet) reduced cancer multiplicity from 3.8 (control) to 2.9 and 0.9, respectively.
  • Thus, the statins had minimal activity in this model of mammary cancer in which approximately half of the cancers are mutated in the Ha Ras oncogene.
  • Similarly, atorvastatin failed to alter the development of estrogen receptor-negative mammary carcinomas in a new animal model using bitransgenic mice (MMTV-Neu(+/-)/p53KO(+/-)), whereas bexarotene (250 mg/kg diet) was effective.
  • [MeSH-major] Anticholesteremic Agents / therapeutic use. Disease Models, Animal. Heptanoic Acids / therapeutic use. Lovastatin / therapeutic use. Mammary Neoplasms, Experimental / drug therapy. Mammary Neoplasms, Experimental / pathology. Pyrroles / therapeutic use

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  • (PMID = 19196723.001).
  • [ISSN] 1940-6215
  • [Journal-full-title] Cancer prevention research (Philadelphia, Pa.)
  • [ISO-abbreviation] Cancer Prev Res (Phila)
  • [Language] eng
  • [Grant] United States / PHS HHS / / HHSN261200433001C; United States / NCI NIH HHS / CA / R01 CA127405
  • [Publication-type] Comparative Study; Journal Article; Research Support, N.I.H., Extramural
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Alkylating Agents; 0 / Anticarcinogenic Agents; 0 / Anticholesteremic Agents; 0 / Antineoplastic Agents, Hormonal; 0 / Heptanoic Acids; 0 / Pyrroles; 0 / Receptors, Estrogen; 0 / Retinoid X Receptors; 0 / Tetrahydronaphthalenes; 0 / Tumor Suppressor Protein p53; 094ZI81Y45 / Tamoxifen; 48A5M73Z4Q / Atorvastatin Calcium; 684-93-5 / Methylnitrosourea; 9LHU78OQFD / Lovastatin; A61RXM4375 / bexarotene
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56. Millanta F, Silvestri G, Vaselli C, Citi S, Pisani G, Lorenzi D, Poli A: The role of vascular endothelial growth factor and its receptor Flk-1/KDR in promoting tumour angiogenesis in feline and canine mammary carcinomas: a preliminary study of autocrine and paracrine loops. Res Vet Sci; 2006 Dec;81(3):350-7

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] The role of vascular endothelial growth factor and its receptor Flk-1/KDR in promoting tumour angiogenesis in feline and canine mammary carcinomas: a preliminary study of autocrine and paracrine loops.
  • Vascular Endothelial Growth Factor (VEGF) and its receptor KDR are involved in the regulation of angiogenesis and are up-regulated in a number of tumours in humans and in particular, breast cancer.
  • We therefore evaluated the prognostic potential of the angiogenetic process in feline and canine mammary carcinomas by the immunohistochemical assessment of VEGF expression and micro vessel density (MVD) quantification and examined the interplay between VEGF and KDR.
  • VEGF and KDR were found to be detected on the epithelial, and/or endothelial and/or stromal cells of the carcinomas in both species, suggesting indications for some possible autocrine and paracrine loops.
  • Our results encourage further studies on the possible prognostic role of VEGF and MVD in canine and feline mammary tumours and on the role of growth factors and their receptors in promoting tumour proliferation and an "angiogenetic shift".
  • [MeSH-major] Carcinoma / veterinary. Mammary Neoplasms, Animal / metabolism. Neovascularization, Pathologic / veterinary. Vascular Endothelial Growth Factor A / metabolism. Vascular Endothelial Growth Factor Receptor-2 / metabolism

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  • (PMID = 16556453.001).
  • [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 / Vascular Endothelial Growth Factor A; EC 2.7.10.1 / Vascular Endothelial Growth Factor Receptor-2
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57. Wood CE, Usborne AL, Starost MF, Tarara RP, Hill LR, Wilkinson LM, Geisinger KR, Feiste EA, Cline JM: Hyperplastic and neoplastic lesions of the mammary gland in macaques. Vet Pathol; 2006 Jul;43(4):471-83
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  • [Title] Hyperplastic and neoplastic lesions of the mammary gland in macaques.
  • Macaques provide an important animal model for the study of hormonal agents and their effects on risk biomarkers for breast cancer.
  • A common criticism of this model is that spontaneous breast cancer has rarely been described in these animals.
  • In this report, we characterize 35 mammary gland lesions ranging from ductal hyperplasia to carcinoma in situ and invasive ductal carcinoma in cynomolgus and rhesus macaques.
  • Based on a retrospective analysis, we estimated the lifetime incidence of mammary gland neoplasia in aged female macaques to be about 6%.
  • In situ carcinomas (n = 8) included solid, comedo, cribriform, and micropapillary elements, encompassing 4 of the major architectural patterns seen in human lesions.
  • Invasive ductal carcinomas (n = 8) were generally solid, with prominent central necrosis and mineralization, often on a background of micropapillary ductal hyperplasia and in situ carcinoma.
  • Axillary lymph-node metastases were confirmed in 5 of the 8 invasive carcinomas.
  • On immunohistochemistry, intraductal and invasive carcinomas had increased Ki67/MIB1 and HER2 expression and selective loss of estrogen and progesterone receptors.
  • These findings suggest that breast cancer is an underreported lesion in macaques and highlight unique morphologic and molecular similarities in breast cancer between human and macaque species.
  • [MeSH-major] Carcinoma in Situ / veterinary. Carcinoma, Ductal / veterinary. Macaca fascicularis. Macaca mulatta. Mammary Neoplasms, Animal / pathology. Monkey Diseases / pathology
  • [MeSH-minor] Animals. Female. Gene Expression. Genes, erbB-2. Immunohistochemistry / veterinary. Ki-67 Antigen / metabolism. Male. Mammary Glands, Animal / metabolism. Mammary Glands, Animal / pathology. Oncogenes. Receptors, Estrogen / biosynthesis. Receptors, Progesterone / biosynthesis. Retrospective Studies

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  • (PMID = 16846989.001).
  • [ISSN] 0300-9858
  • [Journal-full-title] Veterinary pathology
  • [ISO-abbreviation] Vet. Pathol.
  • [Language] eng
  • [Grant] United States / NCCIH NIH HHS / AT / AT00639; United States / NCRR NIH HHS / RR / P51RR000167; United States / NCRR NIH HHS / RR / P51RR000169; United States / NCRR NIH HHS / RR / T32 RR07009
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Ki-67 Antigen; 0 / Receptors, Estrogen; 0 / Receptors, Progesterone
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58. Meijer J, Ogink J, Kreike B, Nuyten D, de Visser KE, Roos E: The chemokine receptor CXCR6 and its ligand CXCL16 are expressed in carcinomas and inhibit proliferation. Cancer Res; 2008 Jun 15;68(12):4701-8
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  • [Title] The chemokine receptor CXCR6 and its ligand CXCL16 are expressed in carcinomas and inhibit proliferation.
  • However, we detected both in all of 170 human primary mammary carcinomas and at similar levels in all 8 human mammary carcinoma cell lines tested by microarray analysis.
  • CXCR6 and CXCL16 were also detected in several mouse and human mammary, colon, and pancreatic carcinoma cell lines.
  • The transmembrane form is present on the surface of the carcinoma cells.
  • It is remarkable that both CXCR6 and CXCL16 are expressed by all mammary carcinomas because cells that lose either acquire a growth advantage and should be selected during tumor progression.
  • [MeSH-minor] Animals. Cells, Cultured. Colonic Neoplasms / genetics. Colonic Neoplasms / metabolism. Colonic Neoplasms / pathology. Flow Cytometry. Gene Expression Profiling. Humans. Luminescent Measurements. Mammary Glands, Animal / cytology. Mammary Glands, Animal / metabolism. Mice. Mice, Inbred BALB C. Mice, Nude. Neoplasm Recurrence, Local / metabolism. Neoplasm Recurrence, Local / pathology. Oligonucleotide Array Sequence Analysis. Pancreatic Neoplasms / genetics. Pancreatic Neoplasms / metabolism. Pancreatic Neoplasms / pathology. Pertussis Toxin / pharmacology. Receptors, G-Protein-Coupled / metabolism

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  • [RetractionIn] Ogink J, Kreike B, Nuyten D, de Visser KE, Roos E. Cancer Res. 2011 Feb 1;71(3):1196 [21245092.001]
  • (PMID = 18559516.001).
  • [ISSN] 1538-7445
  • [Journal-full-title] Cancer research
  • [ISO-abbreviation] Cancer Res.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't; Retracted Publication
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / CXCL16 protein, human; 0 / CXCR6 protein, human; 0 / Chemokine CXCL6; 0 / Chemokines, CXC; 0 / Cxcl16 protein, mouse; 0 / Cxcr6 protein, mouse; 0 / Receptors, CXCR; 0 / Receptors, Chemokine; 0 / Receptors, G-Protein-Coupled; 0 / Receptors, Scavenger; 0 / Receptors, Virus; EC 2.4.2.31 / Pertussis Toxin
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59. Picco G, Julien S, Brockhausen I, Beatson R, Antonopoulos A, Haslam S, Mandel U, Dell A, Pinder S, Taylor-Papadimitriou J, Burchell J: Over-expression of ST3Gal-I promotes mammary tumorigenesis. Glycobiology; 2010 Oct;20(10):1241-50
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  • [Title] Over-expression of ST3Gal-I promotes mammary tumorigenesis.
  • In breast carcinomas, the O-linked glycans are frequently truncated, often as a result of premature sialylation.
  • The sialyltransferase ST3Gal-I adds sialic acid to the galactose residue of core 1 (Galbeta1,3GalNAc) O-glycans and this enzyme is over-expressed in breast cancer resulting in the expression of sialylated core 1 glycans.
  • In order to study the role of ST3Gal-I in mammary tumor development, we developed transgenic mice that over-express the sialyltransferase under the control of the human membrane-bound mucin 1 promoter.
  • These mice were then crossed with PyMT mice that spontaneously develop mammary tumors.
  • As expected, ST3Gal-I transgenic mice showed increased activity and expression of the enzyme in the pregnant and lactating mammary glands, the stomach, lungs and intestine.
  • Although no obvious defects were observed in the fully developed mammary gland, when these mice were crossed with PyMT mice, a highly significant decrease in tumor latency was observed compared to the PyMT mice on an identical background.
  • These results indicate that ST3Gal-I is acting as a tumor promoter in this model of breast cancer.

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  • (PMID = 20534593.001).
  • [ISSN] 1460-2423
  • [Journal-full-title] Glycobiology
  • [ISO-abbreviation] Glycobiology
  • [Language] ENG
  • [Grant] United Kingdom / Cancer Research UK / / ; United Kingdom / Department of Health / /
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Antigens, Polyomavirus Transforming; 0 / Mucin-1; 0 / RNA, Messenger; EC 2.4.99.- / Sialyltransferases; EC 2.4.99.4 / beta-galactoside alpha-2,3-sialyltransferase; GZP2782OP0 / N-Acetylneuraminic Acid; X2RN3Q8DNE / Galactose
  • [Other-IDs] NLM/ PMC2934706
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60. Weng D, Cunin MC, Song B, Price BD, Eller MS, Gilchrest BA, Calderwood SK, Gong J: Radiosensitization of mammary carcinoma cells by telomere homolog oligonucleotide pretreatment. Breast Cancer Res; 2010;12(5):R71

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Radiosensitization of mammary carcinoma cells by telomere homolog oligonucleotide pretreatment.
  • INTRODUCTION: Ionizing radiation (IR) is a widely used approach to cancer therapy, ranking second only to surgery in rate of utilization.
  • Responses of cancer patients to radiotherapy depend in part on the intrinsic radiosensitivity of the tumor cells.
  • METHODS: Mammary tumor cells were treated by a 16-base phosphodiester-linked oligonucleotide homologous to the telomere G-rich sequence TTAGGG (T-oligo: GGTTAGGTGTAGGTTT) or a control-oligo (the partial complement, TAACCCTAACCCTAAC) followed by IR.
  • The efficacy of the combined treatment was assessed in a spontaneous murine mammary tumor model.
  • T-oligo also caused radiosensitization in two in vivo mammary tumor models.
  • Of further significance, treatment with T-oligo and IR led to synergistic inhibition of the growth of spontaneous mammary carcinomas.
  • CONCLUSIONS: Pretreatment with T-oligo sensitizes mammary tumor cells to radiation in both in vitro and in vivo settings with minimal or no normal tissue side effects.
  • [MeSH-major] Mammary Neoplasms, Animal / radiotherapy. Oligonucleotides / pharmacology. Radiation Tolerance / drug effects. Radiation-Sensitizing Agents / pharmacology

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  • (PMID = 20846433.001).
  • [ISSN] 1465-542X
  • [Journal-full-title] Breast cancer research : BCR
  • [ISO-abbreviation] Breast Cancer Res.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Galactosides; 0 / H2AX protein, mouse; 0 / Histones; 0 / Oligonucleotides; 0 / Radiation-Sensitizing Agents; 0 / beta-galactoside
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61. Macejova D, Radikova Z, Macho L, Liska J, Brtko J: MNU-induced carcinogenesis of rat mammary gland: effect of thyroid hormone on expression of retinoic acid receptors in tumours of mammary gland. Mol Cell Endocrinol; 2005 Dec 1;244(1-2):47-56
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  • [Title] MNU-induced carcinogenesis of rat mammary gland: effect of thyroid hormone on expression of retinoic acid receptors in tumours of mammary gland.
  • The rat model of N-methyl-N-nitrosourea (MNU)-induced mammary carcinomas is well-established animal model for breast cancer.
  • This study was carried out to investigate whether hypothyroid (thyroidectomy or PTU treatment) or hyperthyroid status of female rats would affect MNU-induced mammary carcinogenesis with specific focus on both retinoid and rexinoid receptor expression in mammary tumours.
  • Application of PTU before and during MNU-induced mammary gland carcinogenesis yielded in a marked decrease of the number and volume of tumours per animal, however, there was no effect of hypothyroid state in thyroidectomized rats as well as hyperthyroid state concerning the number and volume of tumours.
  • Mammary tumours of in euthyroid group of MNU animals showed that there was no tumour, in which all of subtypes of retinoid and rexinoid receptors were expressed.
  • A different pattern of expression of retinoid or rexinoid receptors was found either in MNU-induced mammary carcinomas in both hypothyroid and hyperthyroid rats.
  • [MeSH-major] Mammary Neoplasms, Experimental / metabolism. Receptors, Retinoic Acid / metabolism. Thyroid Hormones / physiology

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  • (PMID = 16219415.001).
  • [ISSN] 0303-7207
  • [Journal-full-title] Molecular and cellular endocrinology
  • [ISO-abbreviation] Mol. Cell. Endocrinol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Ireland
  • [Chemical-registry-number] 0 / Carcinogens; 0 / RNA, Messenger; 0 / Receptors, Retinoic Acid; 0 / Thyroid Hormones; 684-93-5 / Methylnitrosourea; 721M9407IY / Propylthiouracil
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62. Radaelli E, Arnold A, Papanikolaou A, Garcia-Fernandez RA, Mattiello S, Scanziani E, Cardiff RD: Mammary tumor phenotypes in wild-type aging female FVB/N mice with pituitary prolactinomas. Vet Pathol; 2009 Jul;46(4):736-45
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  • [Title] Mammary tumor phenotypes in wild-type aging female FVB/N mice with pituitary prolactinomas.
  • Prolactin-secreting pituitary proliferations play a significant role in mouse mammary tumorigenesis generally producing adenosquamous carcinomas.
  • Since genetically engineered FVB mice are frequently used to study mammary tumor biology, we have examined a cohort of 64 aging wild-type FVB/N females to establish the prevalence and the nature of spontaneous mammary and pituitary tumors.
  • Tissues from mammary and pituitary glands were studied by histopathology and immunohistochemistry.
  • Of the 64 examined mice, 20 had pituitary tumors and 20 had mammary tumors.
  • Mammary and pituitary tumors were associated in 17 mice.
  • Fourteen mammary tumors, including 12 cases with and 2 without concurrent prolactinomas, were adenocarcinomas with different combinations of epithelial growth patterns.
  • Five mice with prolactinomas had mammary tumors characterized by the epithelial-mesenchymal transition (EMT) phenotype.
  • Estrogen receptor alpha (ERalpha)-positivity was observed for 14 of the 18 mammary tumors tested, including both adenocarcinomas with nuclear immunoreactivity and EMT-phenotype tumors with both nuclear and cytoplasmic immunoreactivity.
  • This study confirms that spontaneous prolactinomas and mammary tumors are both common and significantly associated lesions in FVB mice.
  • Compared with previous reports, prolactinoma-associated mammary tumors displayed a broader morphologic spectrum, including cases with the EMT phenotype.
  • The elevated number of prolactinoma-associated and ERalpha-positive mammary tumors opens intriguing possibilities concerning the role of ERalpha cytoplasmic localization during EMT tumorigenesis.

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  • (PMID = 19276050.001).
  • [ISSN] 1544-2217
  • [Journal-full-title] Veterinary pathology
  • [ISO-abbreviation] Vet. Pathol.
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / U01 CA141582; United States / NCI NIH HHS / CA / CA55909
  • [Publication-type] Case Reports; Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
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63. Simeonov R, Simeonova G: Fractal dimension of canine mammary gland epithelial tumors on cytologic smears. Vet Clin Pathol; 2006 Dec;35(4):446-8
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  • [Title] Fractal dimension of canine mammary gland epithelial tumors on cytologic smears.
  • OBJECTIVE: The aim of this study was to define whether the fractal dimension parameter could be used on cytologic specimens to differentiate benign from malignant canine mammary gland epithelial tumors.
  • METHODS: The fractal dimension of nuclear surface was determined by computer-assisted morphometry on Hemacolor-stained cytologic smears obtained by fine needle aspiration of normal canine mammary gland epithelial cells, and cells in mammary adenomas, tubulopapillary carcinomas, solid carcinomas, and anaplastic carcinomas.
  • RESULTS: Significant differences (P <.001) were observed in mean fractal dimension among all tumor types and in comparison with normal canine mammary gland epithelial cells (except for the fractal dimension between solid carcinomas and anaplastic carcinomas).
  • CONCLUSION: The morphometric parameter, fractal dimension, could help in the diagnostic discrimination between benign and malignant canine mammary gland epithelial tumors on cytologic specimens.

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  • (PMID = 17123252.001).
  • [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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64. Sassi F, Sarli G, Brunetti B, Morandi F, Benazzi C: Immunohistochemical characterization of mammary squamous cell carcinoma of the dog. J Vet Diagn Invest; 2008 Nov;20(6):766-73
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  • [Title] Immunohistochemical characterization of mammary squamous cell carcinoma of the dog.
  • Squamous cell carcinoma of the mammary gland is rare in both veterinary and human medicine.
  • Whereas human metaplastic and squamous variants are known, the objectives of the current study were to ascertain the presence of such entities in canine mammary tumors and to distinguish them from other (epidermal, sweat gland) squamous tumors that may develop in the same area.
  • A panel of antibodies (anti-cytokeratin [CK] 19, CK 14, CK 5/6, pancytokeratin, and vimentin) was used on 18 mammary gland malignancies with squamous features and 16 malignant skin tumors (11 squamous cell carcinomas of the skin and 5 sweat glands).
  • Fifteen of the 18 mammary carcinomas were classified as metaplastic carcinomas, and the remaining 3 were classified as squamous cell carcinomas.
  • The 2 most useful markers to establish the histogenesis of mammary tumors were pancytokeratin and CK 19.
  • The antibody panel discriminated primary epidermal squamous tumors (pancytokeratin positive and CK 19 negative) from gland-derived squamous neoplasms (pancytokeratin positive and CK 19 positive) but failed to distinguish primary mammary tumors from other squamous tumors of glandular origin.
  • [MeSH-major] Carcinoma, Squamous Cell / veterinary. Dog Diseases / pathology. Mammary Glands, Animal / pathology. Neoplasms / veterinary. Skin Neoplasms / veterinary

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  • (PMID = 18987226.001).
  • [ISSN] 1040-6387
  • [Journal-full-title] Journal of veterinary diagnostic investigation : official publication of the American Association of Veterinary Laboratory Diagnosticians, Inc
  • [ISO-abbreviation] J. Vet. Diagn. Invest.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Neoplasm Proteins; 0 / Vimentin; 68238-35-7 / Keratins
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65. Andrechek ER, White D, Muller WJ: Targeted disruption of ErbB2/Neu in the mammary epithelium results in impaired ductal outgrowth. Oncogene; 2005 Jan 27;24(5):932-7
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  • [Title] Targeted disruption of ErbB2/Neu in the mammary epithelium results in impaired ductal outgrowth.
  • The ErbB2 receptor tyrosine kinase has been implicated as a critical growth factor receptor in both normal development and cancer.
  • Studies with transgenic mice have established that elevated expression of erbB2 in mammary epithelium can directly induce mammary carcinomas.
  • Although these studies confirmed a role for ErbB2 in breast cancer induction, the precise role of ErbB2 in normal mammary gland development remained to be elucidated due to the embryonic lethality associated with the null mutation.
  • Here, we demonstrate that the mammary-specific ablation of erbB2 through Cre-mediated recombination leads to a striking ductal elongation defect.
  • In addition to the observed elongation defect, we noted that branching in the adult mammary gland was also reduced.
  • Despite these perturbations in virgin mammary gland morphogenesis, targeted disruption of erbB2 had little impact on the ability of these animals to lactate.
  • Taken together, these observations indicate that erbB2 plays a critical role in the initial stages of mammary gland morphogenesis.
  • [MeSH-major] Epithelial Cells / cytology. Mammary Glands, Animal / cytology. Receptor, ErbB-2 / deficiency

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  • (PMID = 15580295.001).
  • [ISSN] 0950-9232
  • [Journal-full-title] Oncogene
  • [ISO-abbreviation] Oncogene
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't; Research Support, U.S. Gov't, Non-P.H.S.
  • [Publication-country] England
  • [Chemical-registry-number] EC 2.7.10.1 / Receptor, ErbB-2
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66. Bar-Sinai A, Bassa N, Fischette M, Gottesman MM, Love DC, Hanover JA, Hochman J: Mouse mammary tumor virus Env-derived peptide associates with nucleolar targets in lymphoma, mammary carcinoma, and human breast cancer. Cancer Res; 2005 Aug 15;65(16):7223-30
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  • [Title] Mouse mammary tumor virus Env-derived peptide associates with nucleolar targets in lymphoma, mammary carcinoma, and human breast cancer.
  • We have previously shown that the leader peptide (p14) of the Env-precursor of mouse mammary tumor virus is translocated into the nucleoli of murine T cell lymphomas that harbor this virus.
  • Using a polyclonal antibody against recombinant p14, we show here that p14 is also localized to the nucleoli of murine mammary carcinomas and some human breast cancer samples.
  • Taken together, these findings point towards a more general involvement of p14 in lymphomagenesis and mammary carcinogenesis.
  • [MeSH-major] Breast Neoplasms / virology. Cell Nucleolus / virology. Lymphoma, T-Cell / virology. Mammary Neoplasms, Experimental / metabolism. Mammary Tumor Virus, Mouse / metabolism. Viral Envelope Proteins / metabolism

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  • (PMID = 16103073.001).
  • [ISSN] 0008-5472
  • [Journal-full-title] Cancer research
  • [ISO-abbreviation] Cancer Res.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antibodies, Viral; 0 / Viral Envelope Proteins
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67. Jacobs TM, Hoppe BR, Poehlmann CE, Ferracone JD, Sorenmo KU: Mammary adenocarcinomas in three male cats exposed to medroxyprogesterone acetate (1990-2006). J Feline Med Surg; 2010 Feb;12(2):169-74
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  • [Title] Mammary adenocarcinomas in three male cats exposed to medroxyprogesterone acetate (1990-2006).
  • All three cats subsequently developed multiple recurrent mammary adenocarcinomas and underwent numerous surgical resections.
  • This report describes the clinical, histopathological and immunohistochemical findings in these three cats and highlights the potential for mammary carcinomas to develop in male cats years after receiving MPA injections.
  • Extended survival times and a long delay between the administration of the progestin injections and the onset of mammary neoplasia are noted.
  • Estrogen and progesterone receptor staining was performed on some of the tumors and the complex role of hormones in the pathogenesis and the prognosis of feline mammary carcinoma is discussed.
  • Clinicians using MPA should institute life-long surveillance of their feline patients for mammary tumors.
  • [MeSH-major] Adenocarcinoma / veterinary. Cat Diseases / chemically induced. Mammary Neoplasms, Animal / chemically induced. Medroxyprogesterone Acetate / adverse effects

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  • [Copyright] Copyright 2009 ESFM and AAFP. Published by Elsevier Ltd. All rights reserved.
  • (PMID = 19818661.001).
  • [ISSN] 1532-2750
  • [Journal-full-title] Journal of feline medicine and surgery
  • [ISO-abbreviation] J. Feline Med. Surg.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] England
  • [Chemical-registry-number] C2QI4IOI2G / Medroxyprogesterone Acetate
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68. 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

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [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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69. 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

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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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70. Tsubura A, Yoshizawa K, Uehara N, Yuri T, Matsuoka Y: Multistep mouse mammary tumorigenesis through pre-neoplasia to neoplasia and acquisition of metastatic potential. Med Mol Morphol; 2007 Mar;40(1):9-17
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  • [Title] Multistep mouse mammary tumorigenesis through pre-neoplasia to neoplasia and acquisition of metastatic potential.
  • Human breast tissue can give rise to hyperplasias, atypical hyperplasias, and in situ carcinomas originating in a terminal duct-lobular unit (TDLU).
  • These entities are associated with increased risk of subsequent development of invasive carcinoma.
  • Human breast carcinomas arise via intermediate steps known as precursor or premalignant lesions.
  • However, it is difficult to perform stepwise observation of the progression of human breast cancer.
  • Mouse mammary tissue can give rise to several characteristic types of premalignant hyperplasia and tumor, originating in a duct or acinus, that progress to carcinoma.
  • Three specific types of mouse mammary lesion with premalignant potential have been identified: hyperplastic alveolar nodule (HAN), plaque (PLQ), and ductal hyperplasia (DH).
  • Some invasive breast carcinomas acquire metastatic potential and may cause the death of the patient.
  • Mouse mammary carcinomas rarely metastasize, but there exist mouse models of metastasis of mammary carcinoma.
  • [MeSH-major] Mammary Neoplasms, Animal / pathology. Neoplasm Metastasis / pathology. Precancerous Conditions / pathology
  • [MeSH-minor] Adenocarcinoma / secondary. Animals. Disease Models, Animal. Female. Mammary Glands, Animal / pathology. Mammary Neoplasms, Experimental / etiology. Mammary Neoplasms, Experimental / pathology. Mice

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  • (PMID = 17384984.001).
  • [ISSN] 1860-1480
  • [Journal-full-title] Medical molecular morphology
  • [ISO-abbreviation] Med Mol Morphol
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't; Review
  • [Publication-country] Japan
  • [Number-of-references] 51
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71. Queiroga FL, Pérez-Alenza D, Silvan G, Peña L, Illera JC: Positive correlation of steroid hormones and EGF in canine mammary cancer. J Steroid Biochem Mol Biol; 2009 May;115(1-2):9-13
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  • [Title] Positive correlation of steroid hormones and EGF in canine mammary cancer.
  • There are no published studies focused on the potential crosstalk between steroid hormones and EGF in canine mammary tumourigenesis.
  • The objective was to investigate the role of EGF in canine mammary tumours (CMT) and the relationship with steroid hormones.
  • Sixty-three CMT (39 malignant including 10 inflammatory mammary carcinomas (IMC); 19 benign and 5 dysplasias), and 13 normal mammary glands from dogs without history of neoplastic disease were analysed.
  • Levels of EGF were significantly higher in malignant compared with benign tumours, dysplasias and normal mammary glands (p<0.001).
  • Steroid hormone levels were also significantly higher in malignant tumours compared with benign tumours, dysplasias and normal mammary glands (p<0.001).
  • These results suggest that EGF is implicated in canine mammary tumourigenesis.
  • [MeSH-major] Epidermal Growth Factor / analysis. Mammary Neoplasms, Animal / etiology. Steroids / analysis

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  • (PMID = 19429455.001).
  • [ISSN] 1879-1220
  • [Journal-full-title] The Journal of steroid biochemistry and molecular biology
  • [ISO-abbreviation] J. Steroid Biochem. Mol. Biol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Steroids; 409J2J96VR / Androstenedione; 459AG36T1B / Dehydroepiandrosterone; 4G7DS2Q64Y / Progesterone; 4TI98Z838E / Estradiol; 62229-50-9 / Epidermal Growth Factor
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72. Klopfleisch R, Schütze M, Gruber AD: Loss of p27 expression in canine mammary tumors and their metastases. Res Vet Sci; 2010 Apr;88(2):300-3
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  • [Title] Loss of p27 expression in canine mammary tumors and their metastases.
  • We have previously shown a significant reduction of p27 mRNA expression level in laser-microdissected mammary carcinomas and their lymph node metastases when compared to non-neoplastic mammary gland of the same dog.
  • Here, p27 expression was analyzed on the protein level in non-neoplastic mammary gland, primary mammary carcinomas, their lymph node metastases and intravascular tumor cells of 49 dogs, adenomas of 49 dogs and non-neoplastic mammary gland of 98 dogs by immunohistochemistry.
  • A significantly (p0.05) decreased percentage of p27 positive tissue samples was found when normal gland was compared with adenomas, carcinomas and lymph node metastases.
  • In contrast, only 22% of the adenomas, 20% of carcinomas, 12% of lymph node metastases and 32% of intravascular tumor cells had p27 reactivity.
  • Cell cycle control by p27 is therefore lost in the majority of canine mammary tumors.
  • The lack of significant differences between benign and malignant mammary tumors indicates that decreased p27 expression is an early step in carcinogenesis of canine mammary tumors and hinders the use of p27 as a marker of malignancy for this tumor type.
  • [MeSH-major] Dog Diseases / metabolism. Gene Expression Regulation, Neoplastic / physiology. Mammary Neoplasms, Animal / metabolism. Mammary Neoplasms, Animal / pathology. Proliferating Cell Nuclear Antigen / metabolism
  • [MeSH-minor] Adenoma / veterinary. Animals. Carcinoma / secondary. Carcinoma / veterinary. Dogs. Female. Lymph Nodes / pathology

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  • [Copyright] Copyright 2009 Elsevier Ltd. All rights reserved.
  • (PMID = 19748645.001).
  • [ISSN] 1532-2661
  • [Journal-full-title] Research in veterinary science
  • [ISO-abbreviation] Res. Vet. Sci.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Proliferating Cell Nuclear Antigen; 0 / p27 antigen
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73. Munson L, Moresco A: Comparative pathology of mammary gland cancers in domestic and wild animals. Breast Dis; 2007;28:7-21
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  • [Title] Comparative pathology of mammary gland cancers in domestic and wild animals.
  • Mammary cancer occurs among all taxonomic groups, and comparing the disease in animals with breast cancer in women could greatly improve our understanding of the relevant risk factors and genetic profiles for this disease.
  • Differences in cancer prevalence between carnivores and herbivores and between captive and wild carnivores are striking and support the hypotheses that diet and reproductive history are major risk factors.
  • Domestic dogs and cats have a high prevalence of mammary tumors, and the majority of tumors in cats are aggressive cancers.
  • Therefore progesterone appears to be a significant risk factor for cancer development.
  • Supporting this suspicion is the observation that most mammary cancers in zoo cats are in those treated with the potent synthetic progestin contraceptive, melengestrol acetate.
  • The more common morphologic types of mammary cancer in canids and felids include tubulopapillary, solid, cribriform, comedo and anaplastic carcinomas.
  • Dogs also develop complex carcinomas, which likely evolve from the complex adenomas or mixed tumors that are so common in this species and are promoted by exogenous progesterone treatment.
  • Among zoo felids, jaguars are at higher risk for mammary cancer and also have a high prevalence of ovarian papillarycystadenocarcinomas, a profile similar to women with BRCA1 mutations.
  • As for women, estrogen (ER) and progesterone receptor (PR) expression varies in canine and feline mammary cancers.
  • Alterations in molecular controls of cell proliferation or survival in breast cancer, such as cyclin A and p53 expression, have been identified in dog and cat mammary cancers.
  • Overall, spontaneous mammary cancers in cats and dogs make excellent models for human breast cancer, and knowledge of mammary carcinogenesis would be greatly enhanced across all species by a "One Medicine" approach.
  • [MeSH-major] Animals, Domestic. Animals, Wild. Mammary Neoplasms, Animal / pathology

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  • (PMID = 18057539.001).
  • [ISSN] 0888-6008
  • [Journal-full-title] Breast disease
  • [ISO-abbreviation] Breast Dis
  • [Language] eng
  • [Publication-type] Comparative Study; Journal Article; Review
  • [Publication-country] Netherlands
  • [Chemical-registry-number] 0 / Contraceptive Agents, Female; 0 / Gonadal Steroid Hormones; 0 / Progestins; 0 / Receptors, Steroid
  • [Number-of-references] 126
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74. Restucci B, Maiolino P, Martano M, Esposito G, De Filippis D, Borzacchiello G, Lo Muzio L: Expression of beta-catenin, E-cadherin and APC in canine mammary tumors. Anticancer Res; 2007 Sep-Oct;27(5A):3083-9
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Expression of beta-catenin, E-cadherin and APC in canine mammary tumors.
  • BACKGROUND: Mammary tumors are a very common neoplasm in the dog and show histological features and biological behaviour similar to human mammary carcinomas.
  • Recently, a pathway named Wnt-1, involving beta-catenin and APC protein, has emerged as an important player in many human tumor types, including mammary neoplasms.
  • MATERIALS AND METHODS: Thirty-five samples of canine mammary tumors (10 benign and 25 malignant) were studied in order to evaluate the co-expression of beta-catenin, APC protein and E cadherin with confocal laser microscopical observation, by western blot analysis and by correlating data obtained with the histological grade of tumours.
  • CONCLUSION: These results may indicate the multifunctional role played by beta-catenin in canine mammary oncogenesis.
  • [MeSH-major] Adenocarcinoma / metabolism. Adenomatous Polyposis Coli Protein / biosynthesis. Cadherins / biosynthesis. Dog Diseases / metabolism. Mammary Neoplasms, Animal / metabolism. beta Catenin / biosynthesis

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  • (PMID = 17970048.001).
  • [ISSN] 0250-7005
  • [Journal-full-title] Anticancer research
  • [ISO-abbreviation] Anticancer Res.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Greece
  • [Chemical-registry-number] 0 / Adenomatous Polyposis Coli Protein; 0 / Cadherins; 0 / beta Catenin
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75. Suárez-Bonnet A, Martín de Las Mulas J, Millán MY, Herráez P, Rodríguez F, Espinosa de los Monteros A: Morphological and immunohistochemical characterization of spontaneous mammary gland tumors in the guinea pig (Cavia porcellus). Vet Pathol; 2010 Mar;47(2):298-305

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Morphological and immunohistochemical characterization of spontaneous mammary gland tumors in the guinea pig (Cavia porcellus).
  • Ten spontaneous mammary gland tumors affecting guinea pigs (GP) were analyzed histologically and immunohistochemically.
  • Histologically, 3 were benign (2 simple adenomas and 1 benign mixed tumor) and 7 were malignant (1 simple solid carcinoma and 6 simple tubulopapillary carcinomas).
  • This article describes the morphological and immunohistochemical features of the normal mammary gland and spontaneous mammary gland tumors in GP.
  • [MeSH-major] Adenocarcinoma / veterinary. Guinea Pigs. Mammary Neoplasms, Animal / pathology. Rodent Diseases / pathology

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  • (PMID = 20106793.001).
  • [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] 0 / Estrogen Receptor alpha; 0 / Receptors, Progesterone
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76. Triplett AA, Montagna C, Wagner KU: A mammary-specific, long-range deletion on mouse chromosome 11 accelerates Brca1-associated mammary tumorigenesis. Neoplasia; 2008 Dec;10(12):1325-34
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  • [Title] A mammary-specific, long-range deletion on mouse chromosome 11 accelerates Brca1-associated mammary tumorigenesis.
  • We engineered a mammary-specific knockout model for Brca1 deficiency that also lacks the majority of one chromosome 11 to determine whether tumor susceptibility loci reside on this chromosome that cooperate with the loss of Brca1 during mammary cancer formation.
  • Brca1-deficient females that are haploinsufficient in 60 cM of chromosome 11 exhibited accelerated mammary tumorigenesis in comparison to Brca1 conditional knockout mice.
  • Like human BRCA1-associated breast cancers, mammary carcinomas in this new mouse model were ERalpha-negative and of basal epithelial origin.
  • The analysis of the coding sequence and expression pattern of p53 and p21 suggests that loss-of-heterozygosity of Trp53 caused by somatic mutations contributes to accelerated mammary tumorigenesis in this model.
  • [MeSH-major] BRCA1 Protein / genetics. Cyclin-Dependent Kinase Inhibitor p21 / metabolism. Gene Deletion. Mammary Neoplasms, Animal / genetics. Tumor Suppressor Protein p53 / metabolism
  • [MeSH-minor] Animals. Chromosomes / ultrastructure. Disease Progression. Estrogen Receptor alpha / metabolism. Female. Karyotyping. Mammary Glands, Animal / metabolism. Mice. Mice, Knockout. Models, Genetic

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  • (PMID = 19048111.001).
  • [ISSN] 1476-5586
  • [Journal-full-title] Neoplasia (New York, N.Y.)
  • [ISO-abbreviation] Neoplasia
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Canada
  • [Chemical-registry-number] 0 / BRCA1 Protein; 0 / Cdkn1a protein, mouse; 0 / Cyclin-Dependent Kinase Inhibitor p21; 0 / Estrogen Receptor alpha; 0 / Tumor Suppressor Protein p53
  • [Other-IDs] NLM/ PMC2586683
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77. Wensman H, Flama V, Pejler G, Hellmén E: Plasticity of cloned canine mammary spindle cell tumor, osteosarcoma and carcinoma cells. Vet Pathol; 2008 Nov;45(6):803-15
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Plasticity of cloned canine mammary spindle cell tumor, osteosarcoma and carcinoma cells.
  • Female dogs are frequently affected by mammary tumors, both carcinomas and sarcomas.
  • The mechanisms behind mammary-tumor formation and the high degree of heterogeneity are not understood.
  • We studied 3 different tumors (a spindle-cell tumor, an osteosarcoma, and a carcinoma) and followed the change of lineage marker expression between the primary canine mammary tumors, the clones derived from the corresponding tumors and in tumors generated after inoculation of tumor clones into nude mice (n = 75).
  • In contrast to the primary carcinoma, most of the clones derived thereof lacked keratin expression, but keratin expression was recovered in most of the tumors formed after inoculation of clones into nude mice.
  • Moreover, tumors generated from the carcinoma clones, in contrast to the primary tumor, were positive for smooth-muscle-cell markers.
  • Our results point to plasticity in canine mammary tumors, as shown both by morphologic criteria and by expression patterns for lineage specific markers.
  • [MeSH-major] Carcinoma / veterinary. Mammary Neoplasms, Animal. Osteosarcoma / veterinary

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  • (PMID = 18984783.001).
  • [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
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78. Queiroga FL, Alves A, Pires I, Lopes C: Expression of Cox-1 and Cox-2 in canine mammary tumours. J Comp Pathol; 2007 Feb-Apr;136(2-3):177-85

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Expression of Cox-1 and Cox-2 in canine mammary tumours.
  • The aim of this study was to investigate immunohistochemically the expression of cyclooxygenase-1 (Cox-1) and cyclooxygenase-2 (Cox-2) in canine mammary tumours of different histological types.
  • Cox-1 and Cox-2 enzyme expression was evaluated in 70 mammary samples (four normal, six hyperplastic, 60 neoplastic [21 benign and 39 malignant]).
  • Cox-1 expression was identified in all the samples, and Cox-2 in all the mammary lesions except ductal hyperplasia.
  • Two of the four normal mammary gland samples showed focal immunoreactivity for Cox-2.
  • Of the malignant tumours, carcinosarcomas and tubulopapillary and squamous cell carcinomas had the highest Cox-2 scores.
  • This suggests that nonsteroidal anti-inflammatory drugs (NSAIDs), particularly Cox-2 inhibitors, may have a useful role to play in the treatment of canine malignant mammary tumours.
  • [MeSH-major] Adenocarcinoma / veterinary. Adenoma / veterinary. Carcinosarcoma / veterinary. Cyclooxygenase 1 / metabolism. Cyclooxygenase 2 / metabolism. Dog Diseases / enzymology. Mammary Neoplasms, Animal / enzymology
  • [MeSH-minor] Animals. Dogs. Female. Fluorescent Antibody Technique, Indirect / veterinary. Immunoenzyme Techniques / veterinary. Mammary Glands, Animal / enzymology. Mammary Glands, Animal / pathology

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  • (PMID = 17416236.001).
  • [ISSN] 0021-9975
  • [Journal-full-title] Journal of comparative pathology
  • [ISO-abbreviation] J. Comp. Pathol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] EC 1.14.99.1 / Cyclooxygenase 1; EC 1.14.99.1 / Cyclooxygenase 2
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79. Coletta RD, McCoy EL, Burns V, Kawakami K, McManaman JL, Wysolmerski JJ, Ford HL: Characterization of the Six1 homeobox gene in normal mammary gland morphogenesis. BMC Dev Biol; 2010 Jan 14;10:4
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Characterization of the Six1 homeobox gene in normal mammary gland morphogenesis.
  • BACKGROUND: The Six1 homeobox gene is highly expressed in the embryonic mammary gland, continues to be expressed in early postnatal mammary development, but is lost when the mammary gland differentiates during pregnancy.
  • However, Six1 is re-expressed in breast cancers, suggesting that its re-instatement in the adult mammary gland may contribute to breast tumorigenesis via initiating a developmental process out of context.
  • Indeed, recent studies demonstrate that Six1 overexpression in the adult mouse mammary gland is sufficient for initiating invasive carcinomas, and that its overexpression in xenograft models of mammary cancer leads to metastasis.
  • However, because Six1 is highly expressed in the developing mammary gland, and because it has been implicated in the expansion of mammary stem cells, targeting Six1 as an anti-cancer therapy may have unwanted side effects in the breast.
  • RESULTS: We sought to determine the role of Six1 in mammary development using two independent mouse models.
  • To study the effect of Six1 loss in early mammary development when Six1 is normally expressed, Six1-/- embryonic mammary glands were transplanted into Rag1-/- mice.
  • In addition, to determine whether Six1 downregulation is required during later stages of development to allow for proper differentiation, we overexpressed Six1 during adulthood using an inducible, mammary-specific transgenic mouse model.
  • Morphogenesis of the mammary gland occurred normally in animals transplanted with Six1-/- embryonic mammary glands, likely through the redundant functions of other Six family members such as Six2 and Six4, whose expression was increased in response to Six1 loss.
  • Surprisingly, inappropriate expression of Six1 in the adult mammary gland, when levels are normally low to absent, did not inhibit normal mammary differentiation during pregnancy or lactation.
  • CONCLUSIONS: Six1 is not critical for normal mammary gland development, since neither loss nor inappropriate overexpression of Six1 adversely affects normal mammary gland development or function.
  • However, as both Six2 and Six4 levels are increased in Six1-/- mammary glands, we postulate that these Six family members are functionally redundant in the gland, as is true of many homeobox gene families.
  • This data, in conjunction with recent findings that Six1 is capable of promoting breast cancer initiation and progression, suggest that Six1 may serve as a reasonable chemotherapeutic target in a clinical setting, particularly for those women diagnosed with breast cancer in their childbearing years.

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  • (PMID = 20074369.001).
  • [ISSN] 1471-213X
  • [Journal-full-title] BMC developmental biology
  • [ISO-abbreviation] BMC Dev. Biol.
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / R01 CA095277; United States / NICHD NIH HHS / HD / R01 HD045965; United States / NCI NIH HHS / CA / 2R01-CA095277
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't; Research Support, U.S. Gov't, Non-P.H.S.
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Homeodomain Proteins; 0 / Six1 protein, mouse; 0 / Six2 protein, mouse; 0 / Six4 protein, mouse; 0 / Trans-Activators; 0 / Transcription Factors
  • [Other-IDs] NLM/ PMC2823684
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80. Pereira PD, Lopes CC, Matos AJ, Cortez PP, Gärtner F, Medeiros R, Lopes C: Caveolin-1 in diagnosis and prognosis of canine mammary tumours: comparison of evaluation systems. J Comp Pathol; 2010 Aug-Oct;143(2-3):87-93

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Caveolin-1 in diagnosis and prognosis of canine mammary tumours: comparison of evaluation systems.
  • In recent years there has been some controversy regarding the distribution of Cav-1 in normal and neoplastic mammary cell types, which may be attributed to different scoring systems adopted in different studies.
  • The present study compares Cav-1 immunoexpression in normal (n=17) and neoplastic (n=79) canine mammary tissues assessed by two different scoring methods (previously reported by others with conflicting results) and associates Cav-1 expression with metastasis and overall survival (OS).
  • The data suggest that Cav-1 expression is associated with highly malignant subtypes of mammary tumours (i.e. basal-like carcinoma), invasion and metastasis, thus supporting the hypothesis that it may play a major role in the epithelial-mesenchymal transition process.
  • Furthermore, one of the scoring systems employed associated Cav-1 expression with unfavourable prognosis in canine mammary carcinomas, showing a strong correlation between Cav-1-positive carcinomas and shorter OS.
  • [MeSH-major] Biomarkers, Tumor / metabolism. Carcinoma / veterinary. Caveolin 1 / metabolism. Dog Diseases / diagnosis. Mammary Glands, Animal / metabolism. Mammary Neoplasms, Animal / diagnosis

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  • [Copyright] Copyright 2010 Elsevier Ltd. All rights reserved.
  • (PMID = 20153868.001).
  • [ISSN] 1532-3129
  • [Journal-full-title] Journal of comparative pathology
  • [ISO-abbreviation] J. Comp. Pathol.
  • [Language] eng
  • [Publication-type] Comparative Study; Journal Article
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Biomarkers, Tumor; 0 / Caveolin 1
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81. Gama A, Alves A, Schmitt F: Expression and prognostic significance of CK19 in canine malignant mammary tumours. Vet J; 2010 Apr;184(1):45-51

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Expression and prognostic significance of CK19 in canine malignant mammary tumours.
  • Expression of the luminal cytokeratin CK19 was examined in 102 canine mammary carcinomas by immunohistochemical analysis and associated with known expression of oestrogen receptor (ER), basal/myoepithelial cell markers, proliferation and survival.
  • Reduced expression of CK19 in canine mammary carcinomas is related to an aggressive phenotype and may play a role in tumour progression.
  • [MeSH-major] Dog Diseases / metabolism. Dog Diseases / pathology. Keratin-19 / metabolism. Mammary Neoplasms, Animal / metabolism. Mammary Neoplasms, Animal / pathology

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  • [Copyright] Copyright 2009 Elsevier Ltd. All rights reserved.
  • [CommentIn] Vet J. 2010 Apr;184(1):3-4 [19713137.001]
  • (PMID = 19264518.001).
  • [ISSN] 1532-2971
  • [Journal-full-title] Veterinary journal (London, England : 1997)
  • [ISO-abbreviation] Vet. J.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Biomarkers, Tumor; 0 / Keratin-19; 0 / Receptors, Estrogen
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82. Espinosa de los Monteros A, Millán MY, Ramírez GA, Ordás J, Reymundo C, Martín de las Mulas J: Expression of maspin in mammary gland tumors of the dog. Vet Pathol; 2005 May;42(3):250-7

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Expression of maspin in mammary gland tumors of the dog.
  • Maspin is a serine protease inhibitor that inhibits tumor invasion and metastasis in human breast cancer and is consistently expressed by mammary myoepithelial cells (MECs).
  • To analyze the value of maspin as a marker of the MEC layer of the normal and tumoral canine mammary gland, the immunohistochemical expression of maspin was studied in formalin-fixed tissues from 55 benign and malignant tumors (40 tumors also contained the surrounding normal mammary gland) using a commercially available monoclonal antibody.
  • Periacinar and periductal MECs of all 40 normal mammary glands were stained by the anti-human maspin monoclonal antibody, and immunoreactivity was observed in the nucleus and cytoplasm of these cells.
  • The relationship between maspin expression in different cellular compartments of canine mammary carcinomas and the biologic aggressiveness of the disease remains to be elucidated.
  • [MeSH-major] Dog Diseases / metabolism. Mammary Neoplasms, Animal / metabolism. Myoepithelioma / veterinary. Serpins / metabolism

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  • (PMID = 15872371.001).
  • [ISSN] 0300-9858
  • [Journal-full-title] Veterinary pathology
  • [ISO-abbreviation] Vet. Pathol.
  • [Language] eng
  • [Publication-type] Comparative Study; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antibodies, Monoclonal; 0 / SERPIN-B5; 0 / Serpins
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83. Al Masri A, Gendler SJ: Muc1 affects c-Src signaling in PyV MT-induced mammary tumorigenesis. Oncogene; 2005 Sep 1;24(38):5799-808
NCI CPTC Antibody Characterization Program. NCI CPTC Antibody Characterization Program .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Muc1 affects c-Src signaling in PyV MT-induced mammary tumorigenesis.
  • Overexpression of aberrantly glycosylated MUC1 is a hallmark of many carcinomas including 90% of breast carcinomas.
  • MUC1 has been shown to bind to c-Src tyrosine kinase in vitro, whereby c-Src phosphorylates the MUC1 cytoplasmic domain at a YEKV motif. c-Src is an extensively studied nonreceptor tyrosine kinase implicated in mammary tumorigenesis.
  • Previously, mouse mammary tumor virus-driven polyoma middle T-antigen (MMTV-PyV MT) transgenic mice crossed onto a Muc1 null background exhibited a significant delay in tumor progression. c-Src has been shown to interact with PyV MT, and to play an integral and indispensable role in MMTV-PyV MT-induced mammary tumorigenesis.
  • [MeSH-major] Antigens, Polyomavirus Transforming / physiology. Genes, src / physiology. Mammary Neoplasms, Experimental / genetics. Models, Biological. Mucin-1 / metabolism
  • [MeSH-minor] Animals. Cell Transformation, Neoplastic. Disease Models, Animal. Female. Humans. Mammary Tumor Virus, Mouse. Mice. Mice, Transgenic

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  • (PMID = 15897873.001).
  • [ISSN] 0950-9232
  • [Journal-full-title] Oncogene
  • [ISO-abbreviation] Oncogene
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / R01CA64389
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't; Research Support, U.S. Gov't, P.H.S.
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Antigens, Polyomavirus Transforming; 0 / Mucin-1
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84. Wensman H, Göransson H, Leuchowius KJ, Strömberg S, Pontén F, Isaksson A, Rutteman GR, Heldin NE, Pejler G, Hellmén E: Extensive expression of craniofacial related homeobox genes in canine mammary sarcomas. Breast Cancer Res Treat; 2009 Nov;118(2):333-43
NCI CPTC Antibody Characterization Program. NCI CPTC Antibody Characterization Program .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Extensive expression of craniofacial related homeobox genes in canine mammary sarcomas.
  • The global gene expression in three types of canine mammary tumors: carcinoma, fibrosarcoma and osteosarcoma were investigated by Affymetrix gene array technology.
  • Unsupervised clustering analysis revealed a close clustering of the respective tumor types, with fibrosarcomas clustering close to the osteosarcomas and the carcinomas clustering closer to non-malignant mammary tissues (NMTs).
  • A number of epithelial markers were expressed in both carcinomas and NMTs, whereas the sarcomas expressed genes related to mesenchymal differentiation.
  • A comparison of the gene expression profile of the sarcomas versus carcinoma/NMTs revealed that the sarcomas, in particular the osteosarcomas, showed a striking upregulation of a panel of homeobox genes previously linked to craniofacial bone formation.
  • These findings suggest that the development of mammary sarcomas specifically involves triggering of a set of homeobox genes related to neural crest and craniofacial bone development.
  • [MeSH-major] Gene Expression Profiling. Genes, Homeobox / genetics. Mammary Neoplasms, Animal / genetics. Sarcoma / genetics

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  • (PMID = 19048371.001).
  • [ISSN] 1573-7217
  • [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
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85. Badowska-Kozakiewicz AM, Malicka E: Expression of cyclooxygenase-2 in neoplasms of the mammary gland in bitches. Pol J Vet Sci; 2010;13(2):337-42
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Expression of cyclooxygenase-2 in neoplasms of the mammary gland in bitches.
  • Material for the investigation comprised mammary gland tumours, collected from dogs, the patients of veterinary clinics, during surgical procedures.
  • All together 14 adenomas, 66 complex carcinomas, 47 simple carcinomas and 6 solid carcinomas were studied.
  • [MeSH-major] Cyclooxygenase 2 / metabolism. Dog Diseases / metabolism. Gene Expression Regulation, Enzymologic / physiology. Gene Expression Regulation, Neoplastic / physiology. Mammary Neoplasms, Animal / enzymology
  • [MeSH-minor] Adenoma / enzymology. Animals. Carcinoma / enzymology. Dogs. Female

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  • (PMID = 20731190.001).
  • [ISSN] 1505-1773
  • [Journal-full-title] Polish journal of veterinary sciences
  • [ISO-abbreviation] Pol J Vet Sci
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Poland
  • [Chemical-registry-number] EC 1.14.99.1 / Cyclooxygenase 2
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86. 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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87. Badowska-Kozakiewicz AM, Malicka E: Evaluation of immunohistochemical expression of P-glycoprotein in neoplasms of the mammary gland in bitches. Pol J Vet Sci; 2010;13(2):343-7

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Evaluation of immunohistochemical expression of P-glycoprotein in neoplasms of the mammary gland in bitches.
  • Material for the investigation comprised 50 tumours of the mammary gland collected from bitches during surgical procedures performed in Warsaw Veterinary Clinics and Small Animal Clinic of the Department of Clinical Sciences, Faculty of Veterinary Medicine, Warsaw University of Life Sciences - SGGW.
  • All together 8 adenomas, 22 complex carcinomas, 15 simple carcinomas and 5 solid carcinomas.
  • Complex carcinomas were the biggest group among the cancer types which demonstrated positive reaction of P-gp.
  • In bitches aged 9 through 12 years, the cancers featuring a positive reaction of P-gp constituted the most numerous group (63.2%); on the other hand, this cancer type barely appeared in the oldest bitches (10.5%).
  • [MeSH-major] Dog Diseases / metabolism. Gene Expression Regulation, Enzymologic / physiology. Gene Expression Regulation, Neoplastic / physiology. Mammary Neoplasms, Animal / enzymology. P-Glycoprotein / metabolism
  • [MeSH-minor] Adenoma / enzymology. Animals. Carcinoma / enzymology. Dogs. Female

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  • (PMID = 20731191.001).
  • [ISSN] 1505-1773
  • [Journal-full-title] Polish journal of veterinary sciences
  • [ISO-abbreviation] Pol J Vet Sci
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Poland
  • [Chemical-registry-number] 0 / P-Glycoprotein
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88. Planas-Silva MD, Rutherford TM, Stone MC: Prevention of age-related spontaneous mammary tumors in outbred rats by late ovariectomy. Cancer Detect Prev; 2008;32(1):65-71
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Prevention of age-related spontaneous mammary tumors in outbred rats by late ovariectomy.
  • BACKGROUND: Breast cancer prevention trials have shown that the antiestrogen tamoxifen inhibits development of estrogen receptor (ER)-positive tumors.
  • In Sprague-Dawley rats, removal of ovarian function in young animals can reduce the incidence of spontaneous age-dependent mammary tumors.
  • However, it is not known whether removal of ovaries late in life, before middle age onset, can still prevent mammary tumor development.
  • METHODS: In this study we used Hsd:Sprague-Dawley SD (Hsd) rats to determine the effect of late ovariectomy on mammary tumor development.
  • RESULTS: Removal of ovaries before middle age onset ( approximately 5-7 months) inhibited development of spontaneous mammary tumors by 95%.
  • Only one mammary tumor was observed in 19 late ovariectomized animals while 47 total tumors developed in 42 non-ovariectomized animals.
  • The frequency of mammary carcinomas in non-ovariectomized virgin female rats was one in eight rats.
  • Spontaneous rat carcinomas expressed ER and other biomarkers, such as cyclin D1.
  • CONCLUSION: Late ovariectomy prevents spontaneous mammary tumor development in Hsd rats.
  • This animal model may be useful for evaluating novel interventions in breast cancer prevention.
  • [MeSH-major] Mammary Neoplasms, Experimental / prevention & control. Mammary Neoplasms, Experimental / surgery. Ovariectomy

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  • (PMID = 18407436.001).
  • [ISSN] 1525-1500
  • [Journal-full-title] Cancer detection and prevention
  • [ISO-abbreviation] Cancer Detect. Prev.
  • [Language] eng
  • [Publication-type] Comparative Study; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
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89. Seixas F, Palmeira C, Pires MA, Lopes C: Mammary invasive micropapillary carcinoma in cats: clinicopathologic features and nuclear DNA content. Vet Pathol; 2007 Nov;44(6):842-8

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Mammary invasive micropapillary carcinoma in cats: clinicopathologic features and nuclear DNA content.
  • Invasive micropapillary carcinoma (IMC) is a variant of infiltrating ductal carcinoma of the breast associated with poor outcome.
  • In this study, we report 16 carcinomas of the feline mammary gland displaying histologic features that correspond to IMC of the breast in women.
  • The clinicopathologic findings, overall survival time, disease-free survival time, and nuclear DNA content of these cats were compared with 65 more common invasive mammary carcinomas (other feline mammary carcinoma [FMC]) of nonspecified type.
  • [MeSH-major] Carcinoma, Papillary / pathology. Cat Diseases / pathology. Mammary Neoplasms, Animal / pathology
  • [MeSH-minor] Animals. Cats. DNA. Female. Lymph Nodes / pathology. Lymphoma. Mammary Glands, Animal / pathology

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  • [CommentIn] Vet Pathol. 2008 Jul;45(4):600-1 [18587110.001]
  • [CommentIn] Vet Pathol. 2008 Sep;45(5):723 [18725480.001]
  • (PMID = 18039897.001).
  • [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] 9007-49-2 / DNA
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90. Rodo A, Malicka E: Immunohistochemical expression of protein p53 in neoplasms of the mammary gland in bitches. Pol J Vet Sci; 2008;11(2):89-95
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Immunohistochemical expression of protein p53 in neoplasms of the mammary gland in bitches.
  • Material for the investigation comprised mammary gland tumours collected from dogs, the patients of veterinary clinics, during surgical procedures, and archival samples.
  • Alltogether 21 adenomas, 31 complex carcinomas, 35 simple carcinomas and 12 solid carcinomas were qualified for further investigation.
  • The highest percent of p53 positive neoplasms was observed in solid carcinomas and neoplasms with the highest degree of histological malignancy.
  • The smallest number showing this expression was observed in adenomas and the highest was characteristic for solid carcinomas.
  • [MeSH-major] Adenoma / veterinary. Carcinoma / veterinary. Dog Diseases / metabolism. Immunohistochemistry / veterinary. Mammary Neoplasms, Animal / metabolism. Tumor Suppressor Protein p53 / metabolism
  • [MeSH-minor] Animals. Cell Division. Dogs. Female. Gene Expression Regulation, Neoplastic. Mammary Glands, Animal. Neoplasm Staging / veterinary

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  • (PMID = 18683536.001).
  • [ISSN] 1505-1773
  • [Journal-full-title] Polish journal of veterinary sciences
  • [ISO-abbreviation] Pol J Vet Sci
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Poland
  • [Chemical-registry-number] 0 / Tumor Suppressor Protein p53
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91. Petterino C, Podestà G, Ratto A, Drigo M, Pellegrino C: Immunohistochemical study of phospho-Stat3-ser727 expression in feline mammary gland tumours. Vet Res Commun; 2007 Feb;31(2):173-84
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Immunohistochemical study of phospho-Stat3-ser727 expression in feline mammary gland tumours.
  • We describe the expression of pStat3-ser727 (signal transducer and activator of transcription 3 phosphorylated on serine 727) in normal, hyperplastic and neoplastic feline mammary gland tissue assessed by immunohistochemistry in 56 cats.
  • The samples included 4 normal mammary non-lactating tissues, 13 hyperplastic lesions (9 lobular and 4 fibroepithelial) and 39 tumours (6 benign and 33 carcinomas).
  • [MeSH-major] Carcinoma / veterinary. Cat Diseases / metabolism. Mammary Neoplasms, Animal / metabolism. STAT3 Transcription Factor / biosynthesis

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  • (PMID = 17186410.001).
  • [ISSN] 0165-7380
  • [Journal-full-title] Veterinary research communications
  • [ISO-abbreviation] Vet. Res. Commun.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Netherlands
  • [Chemical-registry-number] 0 / STAT3 Transcription Factor; 452VLY9402 / Serine
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92. Mack DL, Boulanger CA, Callahan R, Smith GH: Expression of truncated Int6/eIF3e in mammary alveolar epithelium leads to persistent hyperplasia and tumorigenesis. Breast Cancer Res; 2007;9(4):R42
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Expression of truncated Int6/eIF3e in mammary alveolar epithelium leads to persistent hyperplasia and tumorigenesis.
  • Insertion of mouse mammary tumor virus into the Int6 locus creates a C-terminally truncated form of the protein.
  • Expression of the truncated form of Int6 (Int6sh) in stably transfected human and mouse mammary epithelial cell lines leads to cellular transformation.
  • In addition, decreased expression of Int6/eIF3e is observed in approximately one third of all human breast carcinomas.
  • METHODS: To validate that Int6sh has transforming activity in vivo, a transgenic mouse model was designed using the whey acidic protein (Wap) promoter to target expression of truncated Int6 to differentiating alveolar epithelial cells in the mammary gland.
  • RESULTS: Mammary tumors developed in 42% of WapInt6sh heterozygous parous females at an average age of 18 months.
  • In WapInt6sh mice, the contralateral mammary glands from both tumorous and non-tumorous tissues contained widespread focal alveolar hyperplasia.
  • The Wap promoter is active only during estrus in the mammary tissue of cycling non-pregnant mice.
  • Microarray analyses of mammary tissues demonstrated that Int6sh expression in the alveolar tissue altered the mammary transcriptome in a specific manner that was detectable even in the first pregnancy.
  • This Int6sh-specific transcriptome pattern subsequently persisted in both the Int6sh-expressing alveolar hyperplasia and mammary tumors.
  • These observations are consistent with the conclusion that WapInt6sh-expressing alveolar cells survive involution following the cessation of lactation, and subsequently give rise to the mammary tumors that arise in aging multiparous females.
  • CONCLUSION: These observations provide direct in vivo evidence that mammary-specific expression of the Int6sh truncation leads to persistence of alveolar hyperplasia with the accompanying increased predisposition to mammary tumorigenesis.

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  • (PMID = 17626637.001).
  • [ISSN] 1465-542X
  • [Journal-full-title] Breast cancer research : BCR
  • [ISO-abbreviation] Breast Cancer Res.
  • [Language] ENG
  • [Grant] United States / Intramural NIH HHS / /
  • [Publication-type] Journal Article; Research Support, N.I.H., Intramural
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Biomarkers, Tumor; 0 / Eukaryotic Initiation Factor-3; 0 / Milk Proteins; 0 / RNA, Messenger; 0 / whey acidic proteins
  • [Other-IDs] NLM/ PMC2206715
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93. de Oliveira JT, Pinho SS, de Matos AJ, Hespanhol V, Reis CA, Gärtner F: MUC1 expression in canine malignant mammary tumours and relationship to clinicopathological features. Vet J; 2009 Dec;182(3):491-3
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] MUC1 expression in canine malignant mammary tumours and relationship to clinicopathological features.
  • Mucin-1 (MUC1) is over-expressed in human breast carcinomas and is linked to a poorer prognosis.
  • In this study, MUC1 expression in 32 spontaneous canine malignant mammary tumours was characterised in relation to histological type, mode of growth, grade, lymph node metastases and distant metastases.
  • In the normal canine mammary gland, MUC1 was expressed mainly in the apical cellular membrane, while in carcinomas MUC1 was detected in the cytoplasm only (56.3%) or in the cytoplasm with membrane accentuation (43.7%).
  • [MeSH-major] Carcinoma / veterinary. Dog Diseases / metabolism. Gene Expression Regulation, Neoplastic. Mammary Neoplasms, Animal / metabolism. Mucin-1 / metabolism

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  • (PMID = 18948041.001).
  • [ISSN] 1532-2971
  • [Journal-full-title] Veterinary journal (London, England : 1997)
  • [ISO-abbreviation] Vet. J.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Mucin-1
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94. Heller DA, Clifford CA, Goldschmidt MH, Holt DE, Shofer FS, Smith A, Sorenmo KU: Cyclooxygenase-2 expression is associated with histologic tumor type in canine mammary carcinoma. Vet Pathol; 2005 Nov;42(6):776-80

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Cyclooxygenase-2 expression is associated with histologic tumor type in canine mammary carcinoma.
  • The role of COX-2 in canine mammary neoplasia remains to be more clearly elucidated.
  • The goal of the study reported here was to determine whether a direct association between levels of COX-2 expression and tumor histologic subtype exists in canine mammary carcinoma.
  • Anaplastic carcinomas had a significantly higher COX-2 staining distribution, intensity, and index, compared with those for adenocarcinomas (P < 0.0001).
  • To the authors' knowledge, these results indicate, for the first time, a direct association between COX-2 expression and tumor histologic subtype in canine mammary carcinomas.
  • Future research directed at measuring tumor response in canine mammary carcinoma patients treated with a selective COX-2 inhibitor is indicated.
  • [MeSH-major] Adenocarcinoma / veterinary. Carcinoma / veterinary. Cyclooxygenase 2 / metabolism. Dog Diseases / enzymology. Gene Expression Regulation, Neoplastic. Mammary Neoplasms, Animal / enzymology

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  • (PMID = 16301573.001).
  • [ISSN] 0300-9858
  • [Journal-full-title] Veterinary pathology
  • [ISO-abbreviation] Vet. Pathol.
  • [Language] eng
  • [Publication-type] Comparative Study; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] EC 1.14.99.1 / Cyclooxygenase 2
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95. Matsuoka Y, Hamaguchi T, Fukamachi K, Yoshida M, Watanabe G, Taya K, Tsuda H, Tsubura A: Molecular analysis of rat mammary carcinogenesis: an approach from carcinogenesis research to cancer prevention. Med Mol Morphol; 2007 Dec;40(4):185-90

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Molecular analysis of rat mammary carcinogenesis: an approach from carcinogenesis research to cancer prevention.
  • A rat strain carrying the human c-Ha-ras proto-oncogene is highly susceptible to chemically induced mammary carcinogenesis.
  • All the transgenic rats develop preneoplastic mammary lesions within 20 days of an injection of N-methyl-N-nitrosourea, and mammary carcinomas appear within 8 weeks of treatment with a variety of chemical carcinogens.
  • In this review, we summarize molecular aspects of mammary carcinogenesis in transgenic rats and the potential application of this model for studies of breast cancer prevention.
  • [MeSH-major] Mammary Neoplasms, Animal / pathology. Mammary Neoplasms, Animal / prevention & control

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  • (PMID = 18085376.001).
  • [ISSN] 1860-1480
  • [Journal-full-title] Medical molecular morphology
  • [ISO-abbreviation] Med Mol Morphol
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't; Review
  • [Publication-country] Japan
  • [Number-of-references] 37
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96. Jakab C, Halász J, Kiss A, Schaff Z, Szász AM, Rusvai M, Tóth ZA, Kulka J: Evaluation of microvessel density (MVD) in canine mammary tumours by quantitative immunohistochemistry of the claudin-5 molecule. Acta Vet Hung; 2008 Dec;56(4):495-510

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Evaluation of microvessel density (MVD) in canine mammary tumours by quantitative immunohistochemistry of the claudin-5 molecule.
  • In our recent investigation, angiogenesis was evaluated and quantified by immunohistochemical evaluation of microvessel density (MVD) using claudin-5 (CLDN-5) as a marker for vascular endothelium in 67 canine mammary gland tumours.
  • In simple adenomas and grade I tubular-tubulopapillary simple carcinomas the intratumoural microvessels were wide and regular in shape with evident erythrocytes in their lumen.
  • In grade III solid carcinomas the microvessels were smaller, less regular and had irregular shape, often without a distinct lumen, and isolated endothelial cells were frequently present.
  • In the complex carcinomas MVD was low and the intratumoural microvessels were mostly irregular in shape without a distinct lumen.
  • [MeSH-major] Immunohistochemistry / veterinary. Mammary Neoplasms, Animal / blood supply. Membrane Proteins / metabolism. Neovascularization, Pathologic / metabolism
  • [MeSH-minor] Animals. Carcinoma / blood supply. Carcinoma / metabolism. Carcinoma / pathology. Carcinoma / veterinary. Dogs. Female. Gene Expression Regulation, Neoplastic / physiology

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  • (PMID = 19149104.001).
  • [ISSN] 0236-6290
  • [Journal-full-title] Acta veterinaria Hungarica
  • [ISO-abbreviation] Acta Vet. Hung.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Hungary
  • [Chemical-registry-number] 0 / Membrane Proteins
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97. Yang JW, Lee EY, Kang KW: ErbB2 overexpression in p53-inactivated mammary epithelial cells. FEBS Lett; 2006 Nov 27;580(27):6501-8
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  • [Title] ErbB2 overexpression in p53-inactivated mammary epithelial cells.
  • Functional loss of p53 and ErbB2 overexpression are the frequent genetic alterations in human breast carcinomas.
  • Here, we found that ErbB2 expression was upregulated in primary cultured mammary epithelial cells (MECs) isolated from mice with a defect in exons 5 and 6 of the p53 gene (p53(Delta5,6)).
  • [MeSH-major] Epithelial Cells / metabolism. Mammary Glands, Animal / metabolism. Receptor, ErbB-2 / biosynthesis. Tumor Suppressor Protein p53 / deficiency. Up-Regulation

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  • (PMID = 17101136.001).
  • [ISSN] 0014-5793
  • [Journal-full-title] FEBS letters
  • [ISO-abbreviation] FEBS Lett.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Netherlands
  • [Chemical-registry-number] 0 / Transcription Factor AP-2; 0 / Tumor Suppressor Protein p53; EC 2.7.10.1 / Receptor, ErbB-2
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98. Lin DI, Lessie MD, Gladden AB, Bassing CH, Wagner KU, Diehl JA: Disruption of cyclin D1 nuclear export and proteolysis accelerates mammary carcinogenesis. Oncogene; 2008 Feb 21;27(9):1231-42
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  • [Title] Disruption of cyclin D1 nuclear export and proteolysis accelerates mammary carcinogenesis.
  • Inhibition of cyclin D1 proteolysis has been implicated as a causative factor leading to its overexpression in breast and esophageal carcinomas; however, the contribution of stable cyclin D1 to the genesis of such carcinomas has not been evaluated.
  • MMTV-D1T286A mice developed mammary adenocarcinomas at an increased rate relative to MMTV-D1 mice.
  • Collectively, these results suggest that temporal control of cyclin D1 subcellular localization and proteolysis is critical for maintenance of homeostasis within the mammary epithelium.

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  • (PMID = 17724472.001).
  • [ISSN] 1476-5594
  • [Journal-full-title] Oncogene
  • [ISO-abbreviation] Oncogene
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / R01 CA125195-01A1; United States / NCI NIH HHS / CA / CA111360-05; United States / NCI NIH HHS / CA / R01 CA111360; United States / NCI NIH HHS / CA / R01 CA125195; United States / NCI NIH HHS / CA / R01 CA111360-05; United States / NCI NIH HHS / CA / CA125195-01A1; United States / NCI NIH HHS / CA / CA11360
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 136601-57-5 / Cyclin D1
  • [Other-IDs] NLM/ NIHMS482569; NLM/ PMC3733559
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99. Xie L, Xu BJ, Gorska AE, Shyr Y, Schwartz SA, Cheng N, Levy S, Bierie B, Caprioli RM, Moses HL: Genomic and proteomic analysis of mammary tumors arising in transgenic mice. J Proteome Res; 2005 Nov-Dec;4(6):2088-98
Mouse Genome Informatics (MGI). Mouse Genome Informatics (MGI) .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Genomic and proteomic analysis of mammary tumors arising in transgenic mice.
  • The present study was designed to identify differences by cDNA microarray and MALDI-TOF MS analyses in mammary carcinomas with and without TGF-beta signaling.
  • The results demonstrate a significant potential for combination of profiling technologies to further understand the molecular mechanisms of breast cancer.

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  • (PMID = 16335954.001).
  • [ISSN] 1535-3893
  • [Journal-full-title] Journal of proteome research
  • [ISO-abbreviation] J. Proteome Res.
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / CA085492; United States / NIGMS NIH HHS / GM / R01 GM 58008; United States / NCI NIH HHS / CA / T32 CA009592; United States / NCI NIH HHS / CA / R33 CA8243; United States / NCI NIH HHS / CA / CA102162
  • [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 / Biomarkers, Tumor; 0 / DNA, Complementary; 0 / Proteins; 0 / Proteome; 0 / RNA, Messenger; 0 / Transforming Growth Factor beta
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100. Karantza-Wadsworth V, Patel S, Kravchuk O, Chen G, Mathew R, Jin S, White E: Autophagy mitigates metabolic stress and genome damage in mammary tumorigenesis. Genes Dev; 2007 Jul 1;21(13):1621-35
The Lens. Cited by Patents in .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Autophagy mitigates metabolic stress and genome damage in mammary tumorigenesis.
  • Autophagy is also a haploinsufficient tumor suppressor mechanism for mammary tumorigenesis, as the essential autophagy regulator beclin1 is monoallelically deleted in breast carcinomas.
  • However, the mechanism by which autophagy suppresses breast cancer remains elusive.
  • Here we show that allelic loss of beclin1 and defective autophagy sensitized mammary epithelial cells to metabolic stress and accelerated lumen formation in mammary acini.
  • Autophagy defects also activated the DNA damage response in vitro and in mammary tumors in vivo, promoted gene amplification, and synergized with defective apoptosis to promote mammary tumorigenesis.
  • Therefore, we propose that autophagy limits metabolic stress to protect the genome, and that defective autophagy increases DNA damage and genomic instability that ultimately facilitate breast cancer progression.

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  • (PMID = 17606641.001).
  • [ISSN] 0890-9369
  • [Journal-full-title] Genes & development
  • [ISO-abbreviation] Genes Dev.
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / L30 CA116898; United States / NCI NIH HHS / CA / L30 CA116898-01; United States / NCI NIH HHS / CA / CA116898-02; United States / NCI NIH HHS / CA / CA116898-01; United States / NCI NIH HHS / CA / L30 CA116898-02; United States / NCI NIH HHS / CA / T32 CA99946; United States / NCI NIH HHS / CA / T32 CA099946
  • [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 / Apoptosis Regulatory Proteins; 0 / Becn1 protein, mouse; 0 / Proteins
  • [Other-IDs] NLM/ PMC1899472
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