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1. 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
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  • [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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2. Stein T, Price KN, Morris JS, Heath VJ, Ferrier RK, Bell AK, Pringle MA, Villadsen R, Petersen OW, Sauter G, Bryson G, Mallon EA, Gusterson BA: Annexin A8 is up-regulated during mouse mammary gland involution and predicts poor survival in breast cancer. Clin Cancer Res; 2005 Oct 1;11(19 Pt 1):6872-9
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  • [Title] Annexin A8 is up-regulated during mouse mammary gland involution and predicts poor survival in breast cancer.
  • We assessed Annexin A8's contribution to the overall prognosis and its expression in normal, benign, and cancerous tissue and addressed Annexin A8's physiologic role in the mammary gland.
  • EXPERIMENTAL DESIGN: Using microarrays and reverse transcription-PCR, the Annexin A8 expression was studied during mouse mammary gland development and in isolated mammary structures.
  • Annexin A8's prognostic relevance and its coexpression with CK5 were assessed on tissue arrays of 1,631 cases of invasive breast cancer.
  • RESULTS: Annexin A8 was up-regulated during mouse mammary gland involution and in pubertal ductal epithelium.
  • Hyperplasias and in situ carcinomas showed a strong staining of basal cells.
  • CONCLUSION: Annexin A8 is involved in mouse mammary gland involution.
  • In humans, it is a luminally expressed protein with basal expression in cell culture and in hyperplasia/ductal carcinoma in situ.
  • Expression in invasive breast carcinomas has a significant effect on survival (P = 0.03) but is not independent of grade or CK5.
  • [MeSH-major] Annexins / biosynthesis. Breast Neoplasms / metabolism. Breast Neoplasms / mortality. Gene Expression Regulation, Neoplastic. Mammary Glands, Animal / metabolism. Mammary Glands, Animal / pathology. Up-Regulation
  • [MeSH-minor] Animals. Apoptosis. Carcinoma / metabolism. Carcinoma / pathology. Carcinoma, Intraductal, Noninfiltrating / pathology. Cohort Studies. Female. Genes, BRCA1. Humans. Immunohistochemistry. Keratins / biosynthesis. Mice. Mutation. Oligonucleotide Array Sequence Analysis. Oligonucleotides / chemistry. Phenotype. Polymerase Chain Reaction. Prognosis. RNA / chemistry. Reverse Transcriptase Polymerase Chain Reaction. Time Factors. Treatment Outcome

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  • (PMID = 16203777.001).
  • [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
  • [Grant] United States / NCI NIH HHS / CA / CA-75362
  • [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] United States
  • [Chemical-registry-number] 0 / Annexins; 0 / Oligonucleotides; 63231-63-0 / RNA; 68238-35-7 / Keratins
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3. Petterino C, Ratto A, Podestà G, Drigo M, Pellegrino C: Immunohistochemical evaluation of STAT3-p-tyr705 expression in feline mammary gland tumours and correlation with histologic grade. Res Vet Sci; 2007 Apr;82(2):218-24
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  • [Title] Immunohistochemical evaluation of STAT3-p-tyr705 expression in feline mammary gland tumours and correlation with histologic grade.
  • The expression of STAT3 phosphorylated on tyrosine 705 (STAT3-p-tyr705) in normal, hyperplastic and neoplastic feline mammary gland tissue was assessed by immunohistochemistry in 45 cats.
  • The samples included 4 normal mammary non-lactating tissues, 9 hyperplastic tissues (5 fibroepithelial hyperplasia and 4 lobular epithelial hyperplasia), 2 benign tumours (1 complex adenoma, and 1 simple adenoma), and 30 carcinomas (18 simple tubular papillary, 6 simple tubular, 2 simple solid, 3 cribriform, and 1 adenosquamous carcinoma).
  • Normal non-lactating mammary tissue showed a low number of positive cells, similar to hyperplastic tissue.
  • These results confirm previous our data and reinforce the potential role of STAT3 in malignancy as reported for human breast cancer and other sporadic tumours.
  • [MeSH-major] Carcinoma / veterinary. Cat Diseases / metabolism. Mammary Neoplasms, Animal / metabolism. STAT3 Transcription Factor / biosynthesis

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  • (PMID = 16934302.001).
  • [ISSN] 0034-5288
  • [Journal-full-title] Research in veterinary science
  • [ISO-abbreviation] Res. Vet. Sci.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / STAT3 Transcription Factor; 42HK56048U / Tyrosine
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4. von Euler HP, Ohrvik AB, Eriksson SK: A non-radiometric method for measuring serum thymidine kinase activity in malignant lymphoma in dogs. Res Vet Sci; 2006 Feb;80(1):17-24
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  • Apart from 37 dogs with ML, four normal dogs as well as two dogs with mammary carcinomas, one dog with bladder carcinoma, and one dog with malignant fibrous histiocytoma were included.

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  • (PMID = 16140350.001).
  • [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 / Biomarkers, Tumor; EC 2.7.1.21 / Thymidine Kinase
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5. Montesano R: Bone morphogenetic protein-4 abrogates lumen formation by mammary epithelial cells and promotes invasive growth. Biochem Biophys Res Commun; 2007 Feb 16;353(3):817-22
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  • [Title] Bone morphogenetic protein-4 abrogates lumen formation by mammary epithelial cells and promotes invasive growth.
  • Bone morphogenetic proteins (BMPs) are multifunctional cytokines that regulate key developmental processes, but are also overexpressed in many carcinomas.
  • To assess whether BMPs would influence the three-dimensional architecture of epithelial structures, we took advantage of an in vitro model in which mammary epithelial cells form alveolar-like spherical cysts in collagen gels.
  • The finding that BMP-4 subverts the ability of mammary epithelial cells to form polarized lumen-containing structures and endows them with invasive properties supports the involvement of this cytokine in the progression of breast cancer.
  • [MeSH-major] Bone Morphogenetic Proteins / pharmacology. Mammary Glands, Animal / cytology. Neoplasm Invasiveness / physiopathology

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  • (PMID = 17189614.001).
  • [ISSN] 0006-291X
  • [Journal-full-title] Biochemical and biophysical research communications
  • [ISO-abbreviation] Biochem. Biophys. Res. Commun.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Anthracenes; 0 / BMP4 protein, human; 0 / Bmp4 protein, mouse; 0 / Bone Morphogenetic Protein 4; 0 / Bone Morphogenetic Proteins; 0 / Butadienes; 0 / Imidazoles; 0 / Nitriles; 0 / PD 169316; 0 / U 0126; 0 / anthra(1,9-cd)pyrazol-6(2H)-one; EC 2.7.11.24 / Mitogen-Activated Protein Kinases
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6. Bertagnolli AC, Soares P, van Asch B, Amorim A, Cirnes L, Máximo V, Cassali GD: An assessment of the clonality of the components of canine mixed mammary tumours by mitochondrial DNA analysis. Vet J; 2009 Nov;182(2):269-74
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  • [Title] An assessment of the clonality of the components of canine mixed mammary tumours by mitochondrial DNA analysis.
  • The aim of this study was to investigate if mutations in the mitochondrial DNA (mtDNA) D-loop fragment control region of canine mammary mixed tumours could be used as clonal markers that identified the cell population of origin.
  • Ten benign mixed mammary tumours and nine carcinomas arising from benign mixed tumours were microdissected and DNA from epithelial and mesenchymal tumour cells and from normal mammary tissue was examined for sequence variations in a fragment of the hypervariable control region.
  • Identical sequence variants in both the epithelial and mesenchymal components (as well as in the corresponding normal tissue) were found in 80% of the benign mixed tumours and in 89% of the carcinomas arising from benign mixed tumours suggesting a shared clonal origin.
  • The distinctive sequence alterations identified in the epithelial and mesenchymal components of 15.8% of all 19 tumours examined, suggests the possibility that a minority of mammary tumours are polyclonal in origin or that early clonal divergence occurs.
  • [MeSH-major] DNA, Mitochondrial / genetics. Dog Diseases / genetics. Dog Diseases / pathology. Mammary Neoplasms, Animal / genetics. Mammary Neoplasms, Animal / pathology

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  • (PMID = 18752974.001).
  • [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 / DNA, Mitochondrial; 0 / DNA, Neoplasm
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7. Klinakis A, Szabolcs M, Chen G, Xuan S, Hibshoosh H, Efstratiadis A: Igf1r as a therapeutic target in a mouse model of basal-like breast cancer. Proc Natl Acad Sci U S A; 2009 Feb 17;106(7):2359-64
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  • [Title] Igf1r as a therapeutic target in a mouse model of basal-like breast cancer.
  • Considering the strong association between dysregulated insulin-like growth factor (IGF) signaling and various human cancers, we have used an expedient combination of genetic analysis and pharmacological treatment to evaluate the potential of the type 1 IGF receptor (Igf1r) for targeted anticancer therapy in a mouse model of mammary tumorigenesis.
  • In this particular strain of genetically modified animals, histopathologically heterogeneous invasive carcinomas exhibiting up-regulation of the Igf1r gene developed extremely rapidly by mammary gland-specific overexpression of constitutively active oncogenic Kras* (mutant Kras(G12D)).
  • Conditional ablation of Igf1r in the mouse mammary epithelium increased the latency of Kras*-induced tumors very significantly (approximately 11-fold in comparison with the intact model), whereas treatment of tumor-bearing animals by administration of picropodophyllin (PPP), a specific Igf1r inhibitor, resulted in a dramatic decrease in tumor mass of the main forms of basal-like carcinomas.
  • PPP also was effective against xenografts of the human basal-like cancer cell line MDA-MB-231, which carries a KRAS(G13D) mutation.

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  • (PMID = 19174523.001).
  • [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 / 1 P01 CA97403
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0F35AOI227 / picropodophyllin; EC 2.7.10.1 / Receptor, IGF Type 1; EC 3.6.5.2 / ras Proteins; L36H50F353 / Podophyllotoxin
  • [Other-IDs] NLM/ PMC2650161
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8. 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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  • [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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9. Derksen PW, Liu X, Saridin F, van der Gulden H, Zevenhoven J, Evers B, van Beijnum JR, Griffioen AW, Vink J, Krimpenfort P, Peterse JL, Cardiff RD, Berns A, Jonkers J: Somatic inactivation of E-cadherin and p53 in mice leads to metastatic lobular mammary carcinoma through induction of anoikis resistance and angiogenesis. Cancer Cell; 2006 Nov;10(5):437-49
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  • [Title] Somatic inactivation of E-cadherin and p53 in mice leads to metastatic lobular mammary carcinoma through induction of anoikis resistance and angiogenesis.
  • Metastatic disease is the primary cause of death in breast cancer, the most common malignancy in Western women.
  • Loss of E-cadherin is associated with tumor metastasis, as well as with invasive lobular carcinoma (ILC), which accounts for 10%-15% of all breast cancers.
  • Combined loss of E-cadherin and p53 resulted in accelerated development of invasive and metastatic mammary carcinomas, which show strong resemblance to human ILC.
  • Our results suggest that loss of E-cadherin contributes to both mammary tumor initiation and metastasis.
  • [MeSH-major] Anoikis / physiology. Breast Neoplasms / metabolism. Cadherins / metabolism. Carcinoma, Lobular / metabolism. Gene Silencing. Tumor Suppressor Protein p53 / metabolism
  • [MeSH-minor] Animals. Disease Models, Animal. Female. Humans. Mammary Glands, Human / anatomy & histology. Mammary Glands, Human / metabolism. Mammary Glands, Human / pathology. Mice. Mice, Inbred BALB C. Neoplasm Metastasis. Neovascularization, Pathologic. Skin Neoplasms / metabolism. Skin Neoplasms / pathology. Survival Rate. Tumor Cells, Cultured


10. 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
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  • [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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11. 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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12. Yan H, Blackburn AC, McLary SC, Tao L, Roberts AL, Xavier EA, Dickinson ES, Seo JH, Arenas RB, Otis CN, Cao QJ, Lawlor RG, Osborne BA, Kittrell FS, Medina D, Jerry DJ: Pathways contributing to development of spontaneous mammary tumors in BALB/c-Trp53+/- mice. Am J Pathol; 2010 Mar;176(3):1421-32
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  • [Title] Pathways contributing to development of spontaneous mammary tumors in BALB/c-Trp53+/- mice.
  • Here we use BALB/c-Trp53+/- mice as a model to examine the sequence of events leading to mammary tumors.
  • Mammary gland proliferation rates were similar in both BALB/c-Trp53+/- mice and wild-type controls.
  • In addition, sporadic mammary hyperplasias were rare in BALB/c-Trp53+/- mice and not detectably different from those of wild-type controls.
  • Among the 28 mammary tumors collected from BALB/c-Trp53+/- mice, loss of heterozygosity for Trp53 was detected in more than 90% of invasive mammary tumors.
  • Transplantation of Trp53+/- ductal hyperplasias also indicated an association between loss of the wild-type allele of Trp53 and progression to invasive carcinomas.
  • Moreover, expression of biomarkers such as estrogen receptor alpha, progesterone receptor, Her2/Neu, and activated Notch1 varied among mammary tumors, suggesting that multiple oncogenic lesions collaborate with loss of p53 function.
  • Overall, this panel of transplantable tumors provides a resource for detailed evaluation of the cell lineages undergoing transformation and preclinical testing of therapeutic agents targeting a variety of oncogenic pathways including cancer stem cells.

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  • (PMID = 20110418.001).
  • [ISSN] 1525-2191
  • [Journal-full-title] The American journal of pathology
  • [ISO-abbreviation] Am. J. Pathol.
  • [Language] ENG
  • [Grant] United States / NIEHS NIH HHS / ES / R01 ES015739; United States / NCI NIH HHS / CA / R01-CA105452; United States / NCI NIH HHS / CA / R01 CA095164; United States / NCI NIH HHS / CA / R01 CA105452; United States / NCI NIH HHS / CA / R01-CA095164; United States / NIEHS NIH HHS / ES / R01-ES015739
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Receptors, Estrogen; 0 / Receptors, Notch; 0 / Receptors, Progesterone; 0 / Tumor Suppressor Protein p53; 68238-35-7 / Keratins; EC 2.7.10.1 / Erbb2 protein, mouse; EC 2.7.10.1 / Receptor, ErbB-2
  • [Other-IDs] NLM/ PMC2832161
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13. Gonzalez ME, Li X, Toy K, DuPrie M, Ventura AC, Banerjee M, Ljungman M, Merajver SD, Kleer CG: Downregulation of EZH2 decreases growth of estrogen receptor-negative invasive breast carcinoma and requires BRCA1. Oncogene; 2009 Feb 12;28(6):843-53
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  • [Title] Downregulation of EZH2 decreases growth of estrogen receptor-negative invasive breast carcinoma and requires BRCA1.
  • Increased levels of enhancer of zeste homolog 2 (EZH2), a critical regulator of cellular memory, are associated with negative estrogen receptor (ER) expression and disease progression in breast cancer.
  • High levels of EZH2 signal the presence of metastasis and poor outcome in breast cancer patients.
  • To test the hypothesis that deregulation of EZH2 contributes to ER-negative breast cancer progression, EZH2 expression was inhibited in ER-negative breast cancer cells MDA-MB-231 and CAL51 using a lentivirus system.
  • Invasive ER-negative breast carcinomas show significant overexpression of EZH2 and downregulation of BRCA1 proteins.
  • Taken together, we show that EZH2 is important in ER-negative breast cancer growth in vivo and in vitro, and that BRCA1 is required for the proliferative effects of EZH2.
  • Blockade of EZH2 may provide a prime target to prevent and/or halt ER-negative breast cancer progression.

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  • (PMID = 19079346.001).
  • [ISSN] 1476-5594
  • [Journal-full-title] Oncogene
  • [ISO-abbreviation] Oncogene
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / R01 CA107469-01A1; United States / NCI NIH HHS / CA / R01 CA077612-09; United States / NCI NIH HHS / CA / R01 CA077612; None / None / / R01 CA077612-09; United States / NCI NIH HHS / CA / CA77612; United States / NCI NIH HHS / CA / R01 CA107469; United States / NCI NIH HHS / CA / K08 CA090876; United States / NCI NIH HHS / CA / CA107469; United States / NCI NIH HHS / CA / CA090876
  • [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 / BRCA1 Protein; 0 / BRCA1 protein, human; 0 / DNA-Binding Proteins; 0 / Receptors, Estrogen; 0 / Transcription Factors; EC 2.1.1.43 / EZH2 protein, human; EC 2.1.1.43 / Polycomb Repressive Complex 2
  • [Other-IDs] NLM/ NIHMS76277; NLM/ PMC2643353
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14. 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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15. Kossoy G, Anisimov VN, Ben-Hur H, Kossoy N, Zusman I: Effect of the synthetic pineal peptide epitalon on spontaneous carcinogenesis in female C3H/He mice. In Vivo; 2006 Mar-Apr;20(2):253-7
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  • Spontaneous tumors of the reproductive organs (mammary glands and ovaries) were predominant in both groups of mice (control and experimental).
  • The mammary gland tumors were different variants of invasive ductal carcinomas.
  • [MeSH-major] Antineoplastic Agents / pharmacology. Carcinoma, Intraductal, Noninfiltrating / drug therapy. Mammary Neoplasms, Animal / drug therapy. Neoplasm Metastasis / drug therapy. Neoplasms / drug therapy. Oligopeptides / pharmacology

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  • (PMID = 16634527.001).
  • [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 / Antineoplastic Agents; 0 / Oligopeptides; O65P17785G / alanyl-glutamyl-aspartyl-glycine
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16. Blanchard A, Iwasiow B, Yarmill A, Fresnosa A, Silha J, Myal Y, Murphy LC, Chrétien M, Seidah N, Shiu RP: Targeted production of proprotein convertase PC1 enhances mammary development and tumorigenesis in transgenic mice. Can J Physiol Pharmacol; 2009 Oct;87(10):831-8
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  • [Title] Targeted production of proprotein convertase PC1 enhances mammary development and tumorigenesis in transgenic mice.
  • Elevated production of proprotein convertases (PCs), proteolytic enzymes that posttranslationally modify the biological activities of diverse groups of cellular proteins, is a common occurrence in human breast carcinomas.
  • Mammary epithelium-specific and early expression of PC1 was targeted by the use of the mouse mammary tumor virus promoter/enhancer.
  • Whole-mount examinations revealed that the mammary glands of 83-day-old virgin PC1 transgenic mice exhibited an accelerated lobuloalveolar development compared with that of age-matched wild-type mice (p < 0.001).
  • Pathway analysis of PC1-induced alterations in gene expression has revealed possible mechanism of action of PC1 in the mammary gland.
  • PC1 expression alone, however, did not promote spontaneous mammary tumorigenesis in the transgenic mice.
  • PC1 transgene expression resulted in a significantly higher incidence (p = 0.008) and accelerated growth (p = 0.023) of 7,12-dimethylbenz[a]anthracene (DMBA)-induced mammary adenocarcinomas.
  • The present study therefore shows that PC1 expression can promote normal and neoplastic mammary development and growth and suggests that proprotein convertases may be important etiological factors in human breast neoplasia.
  • [MeSH-major] Mammary Glands, Animal / growth & development. Mammary Neoplasms, Experimental / genetics. Mammary Neoplasms, Experimental / pathology. Proprotein Convertase 1 / biosynthesis. Proprotein Convertase 1 / genetics

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  • (PMID = 20052009.001).
  • [ISSN] 1205-7541
  • [Journal-full-title] Canadian journal of physiology and pharmacology
  • [ISO-abbreviation] Can. J. Physiol. Pharmacol.
  • [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] Canada
  • [Chemical-registry-number] 0 / Carcinogens; 0 / DNA, Complementary; 57-97-6 / 9,10-Dimethyl-1,2-benzanthracene; EC 3.4.21.93 / Proprotein Convertase 1
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17. 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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18. 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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19. Ordás J, Millán Y, Dios R, Reymundo C, de Las Mulas JM: Proto-oncogene HER-2 in normal, dysplastic and tumorous feline mammary glands: an immunohistochemical and chromogenic in situ hybridization study. BMC Cancer; 2007;7:179
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  • [Title] Proto-oncogene HER-2 in normal, dysplastic and tumorous feline mammary glands: an immunohistochemical and chromogenic in situ hybridization study.
  • BACKGROUND: Feline mammary carcinoma has been proposed as a natural model of highly aggressive, hormone-independent human breast cancer.
  • METHODS: Formalin-fixed, paraffin-embedded tissue samples from 30 invasive carcinomas, 7 benign lesions and two normal mammary glands were analyzed.
  • RESULTS: Immunohistochemical HER-2 protein overexpression was found in 40% of feline mammary carcinomas, a percentage higher to that observed in human breast carcinoma.
  • However, amplification of HER-2 was detected in 16% of carcinomas with protein overexpression, a percentage much lower than that observed in their human counterpart.
  • CONCLUSION: Feline mammary carcinoma would be a suitable natural model of that subset of human breast carcinomas with HER-2 protein overexpression without gene amplification.
  • [MeSH-major] Fluorescent Dyes. In Situ Hybridization. Mammary Glands, Animal / chemistry. Mammary Neoplasms, Animal / enzymology. Mammary Neoplasms, Animal / genetics. Receptor, ErbB-2 / analysis

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  • (PMID = 17880730.001).
  • [ISSN] 1471-2407
  • [Journal-full-title] BMC cancer
  • [ISO-abbreviation] BMC Cancer
  • [Language] eng
  • [Publication-type] Comparative Study; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Fluorescent Dyes; EC 2.7.10.1 / Receptor, ErbB-2
  • [Other-IDs] NLM/ PMC2045669
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20. Liu T, Niu Y, Yu Y, Liu Y, Zhang F: Increased gamma-tubulin expression and P16INK4A promoter methylation occur together in preinvasive lesions and carcinomas of the breast. Ann Oncol; 2009 Mar;20(3):441-8
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  • [Title] Increased gamma-tubulin expression and P16INK4A promoter methylation occur together in preinvasive lesions and carcinomas of the breast.
  • BACKGROUND: Loss of p16(INK4A) due to promoter hypermethylation is correlated with the ability to acquire centrosomal abnormalities in variant human mammary epithelial cells. gamma-Tubulin is a highly conserved component of centrosome in most animal cells and gamma-tubulin protein overexpression could lead to centrosome aberration.
  • MATERIALS AND METHODS: A large series of breast premalignant lesions and carcinoma was analyzed.
  • RESULTS: gamma-Tubulin protein expression was concordant with gene amplification; both of them were found to increase with atypical ductal hyperplasia-carcinoma sequence.
  • CONCLUSION: gamma-Tubulin gene amplification and the concomitant protein overexpression present not only in invasive carcinoma but also in a significant fraction of atypical hyperplasia and in situ carcinomas.

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  • (PMID = 19131428.001).
  • [ISSN] 1569-8041
  • [Journal-full-title] Annals of oncology : official journal of the European Society for Medical Oncology
  • [ISO-abbreviation] Ann. Oncol.
  • [Language] ENG
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / DNA Primers; 0 / Tubulin
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21. Kawaguchi H, Umekita Y, Souda M, Gejima K, Kawashima H, Yoshikawa T, Yoshida H: Effects of neonatally administered high-dose diethylstilbestrol on the induction of mammary tumors induced by 7,12-dimethylbenz[a]anthracene in female rats. Vet Pathol; 2009 Jan;46(1):142-50
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  • [Title] Effects of neonatally administered high-dose diethylstilbestrol on the induction of mammary tumors induced by 7,12-dimethylbenz[a]anthracene in female rats.
  • The aim of this study was to investigate the effects of neonatal administration of a relatively high dose of diethylstilbestrol (DES) on the induction of mammary carcinomas (MCs) and benign proliferative lesions (PLs) induced by 7,12-dimethylbenz[a]anthracene (DMBA) in female rats.
  • [MeSH-major] 9,10-Dimethyl-1,2-benzanthracene / toxicity. Breast Neoplasms / chemically induced. Breast Neoplasms / pathology. Carcinogens / toxicity. Diethylstilbestrol / toxicity. Disease Models, Animal

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  • (PMID = 19112128.001).
  • [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 / Carcinogens; 0 / Gonadal Steroid Hormones; 57-97-6 / 9,10-Dimethyl-1,2-benzanthracene; 731DCA35BT / Diethylstilbestrol
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22. 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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  • [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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23. 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
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  • [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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24. Ressel L, Millanta F, Caleri E, Innocenti VM, Poli A: Reduced PTEN protein expression and its prognostic implications in canine and feline mammary tumors. Vet Pathol; 2009 Sep;46(5):860-8
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  • [Title] Reduced PTEN protein expression and its prognostic implications in canine and feline mammary tumors.
  • PTEN-negative status occurred in 33% of canine and 76% of feline mammary carcinomas.
  • In canine mammary carcinomas, there was a significant (P < .05) correlation between loss of PTEN protein expression and simple carcinoma histotype, lymphatic vessel invasion, lymph node metastases, distant organ metastases, tumor dedifferentiation, tumor recurrence, and shorter overall survival.
  • In feline mammary tumors, a significant correlation between loss of PTEN protein expression and lymphatic vessel invasion was found.
  • Loss of PTEN expression could be a useful prognostic marker in canine mammary carcinomas.
  • [MeSH-major] Carcinoma / veterinary. Cat Diseases / metabolism. Dog Diseases / metabolism. Mammary Neoplasms, Animal / metabolism. PTEN Phosphohydrolase / metabolism

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  • (PMID = 19429983.001).
  • [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 3.1.3.67 / PTEN Phosphohydrolase
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25. 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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  • [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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26. Millanta F, Calandrella M, Vannozzi I, Poli A: Steroid hormone receptors in normal, dysplastic and neoplastic feline mammary tissues and their prognostic significance. Vet Rec; 2006 Jun 17;158(24):821-4
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  • [Title] Steroid hormone receptors in normal, dysplastic and neoplastic feline mammary tissues and their prognostic significance.
  • The expression of oestrogen-alpha and progesterone receptors was determined in 13 normal, 21 dysplastic and 53 neoplastic feline mammary tissues.
  • The expression of oestrogen receptors was significantly higher in healthy tissues and in adenosis than in neoplastic lesions, and the levels of progesterone receptors increased in fibroadenomatous changes and in "in situ" carcinomas but decreased in invasive carcinomas.
  • The oestrogen and progesterone receptor status of the invasive carcinomas did not correlate either with the histological parameters or with the overall survival of the cats, although the oestrogen receptor-negative tumours had a poor prognosis.
  • [MeSH-major] Carcinoma / veterinary. Cat Diseases / metabolism. Mammary Glands, Animal / metabolism. Mammary Neoplasms, Animal / metabolism. Receptors, Estrogen / analysis. Receptors, Progesterone / analysis

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  • (PMID = 16782855.001).
  • [ISSN] 0042-4900
  • [Journal-full-title] The Veterinary record
  • [ISO-abbreviation] Vet. Rec.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Receptors, Estrogen; 0 / Receptors, Progesterone
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27. Rao NA, van Wolferen ME, van den Ham R, van Leenen D, Groot Koerkamp MJ, Holstege FC, Mol JA: cDNA microarray profiles of canine mammary tumour cell lines reveal deregulated pathways pertaining to their phenotype. Anim Genet; 2008 Aug;39(4):333-45
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  • [Title] cDNA microarray profiles of canine mammary tumour cell lines reveal deregulated pathways pertaining to their phenotype.
  • Mammary cancer is the most common type of cancer in female dogs with a lifetime risk of over 24% when dogs are not spayed.
  • The elucidation of the complete canine genome opens new areas for development of cancer therapies.
  • However, to date, no canine mammary cell lines have been characterized by expression profiling.
  • In this study, canine mammary tumour cell lines with histologically distinct primary tumours of origin were characterized using a newly developed canine cDNA microarray.
  • Because these pathways show an overlap at the molecular level with those found in human breast cancer, the expression profiling of spontaneous canine mammary cancer may also function as a biological sieve to identify conserved gene expression or pathway profiles of evolutionary significance that are involved in tumourigenesis.
  • These results are the basis for further characterization of canine mammary carcinomas and development of new therapies directed towards specific pathways.
  • [MeSH-major] Dog Diseases / genetics. Gene Expression Profiling. Gene Expression Regulation, Neoplastic. Mammary Neoplasms, Animal / genetics. Oligonucleotide Array Sequence Analysis. RNA, Neoplasm / genetics

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  • (PMID = 18462483.001).
  • [ISSN] 1365-2052
  • [Journal-full-title] Animal genetics
  • [ISO-abbreviation] Anim. Genet.
  • [Language] eng
  • [Publication-type] Comparative Study; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / RNA, Neoplasm
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28. Cuadros C, Dominguez AL, Lollini PL, Croft M, Mittler RS, Borgström P, Lustgarten J: Vaccination with dendritic cells pulsed with apoptotic tumors in combination with anti-OX40 and anti-4-1BB monoclonal antibodies induces T cell-mediated protective immunity in Her-2/neu transgenic mice. Int J Cancer; 2005 Oct 10;116(6):934-43
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  • One such normal self-protein is the growth factor receptor Her-2/neu, which is overexpressed in 25-35% of all mammary carcinomas in humans.
  • [MeSH-major] Antibodies, Monoclonal / therapeutic use. Antigens, CD / immunology. Cancer Vaccines. Dendritic Cells / immunology. Genes, erbB-2. Mammary Neoplasms, Animal / immunology. Receptors, Nerve Growth Factor / immunology. Receptors, Tumor Necrosis Factor / immunology. T-Lymphocytes / immunology

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  • (PMID = 15856473.001).
  • [ISSN] 0020-7136
  • [Journal-full-title] International journal of cancer
  • [ISO-abbreviation] Int. J. Cancer
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / CA 78579
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, U.S. Gov't, P.H.S.
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antibodies, Monoclonal; 0 / Antigens, CD; 0 / Antigens, CD137; 0 / Antigens, Differentiation; 0 / Cancer Vaccines; 0 / OX40Ig; 0 / Receptors, Nerve Growth Factor; 0 / Receptors, Tumor Necrosis Factor; 0 / TNFRSF9 protein, human; 0 / Tnfrsf9 protein, mouse
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29. Romanucci M, Marinelli A, Sarli G, Della Salda L: Heat shock protein expression in canine malignant mammary tumours. BMC Cancer; 2006;6:171
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  • [Title] Heat shock protein expression in canine malignant mammary tumours.
  • BACKGROUND: Abnormal levels of Heat Shock Proteins (HSPs) have been observed in many human neoplasms including breast cancer and it has been demonstrated that they have both prognostic and therapeutic implications.
  • In this study, we evaluated immunohistochemical expression of HSPs in normal and neoplastic canine mammary glands and confronted these results with overall survival (OS), in order to understand the role of HSPs in carcinogenesis and to establish their potential prognostic and/or therapeutic value.
  • METHODS: Immunohistochemical expression of Hsp27, Hsp72, Hsp73 and Hsp90 was evaluated in 3 normal canine mammary glands and 30 malignant mammary tumours (10 in situ carcinomas, 10 invasive carcinomas limited to local structures without identifiable invasion of blood or lymphatic vessels, 10 carcinomas with invasion of blood or lymphatic vessels and/or metastases to regional lymph nodes).
  • In mammary tumours, a significant increase in Hsp27 (P < 0.01), Hsp72 (P < 0.05) and Hsp90 (P < 0.01) expression was observed as well as a significant reduction in Hsp73 (P < 0.01) immunoreactivity compared to normal mammary gland tissue.
  • CONCLUSION: These results suggest that Hsp27, Hsp72 and Hsp90 are involved in canine mammary gland carcinogenesis.
  • [MeSH-major] Carcinoma / genetics. Dog Diseases / genetics. Heat-Shock Proteins / metabolism. Mammary Neoplasms, Animal / genetics

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  • (PMID = 16803633.001).
  • [ISSN] 1471-2407
  • [Journal-full-title] BMC cancer
  • [ISO-abbreviation] BMC Cancer
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Heat-Shock Proteins
  • [Other-IDs] NLM/ PMC1525201
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30. 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
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  • [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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31. Perk J, Gil-Bazo I, Chin Y, de Candia P, Chen JJ, Zhao Y, Chao S, Cheong W, Ke Y, Al-Ahmadie H, Gerald WL, Brogi E, Benezra R: Reassessment of id1 protein expression in human mammary, prostate, and bladder cancers using a monospecific rabbit monoclonal anti-id1 antibody. Cancer Res; 2006 Nov 15;66(22):10870-7
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  • [Title] Reassessment of id1 protein expression in human mammary, prostate, and bladder cancers using a monospecific rabbit monoclonal anti-id1 antibody.
  • Although the importance of Id1 in tumor endothelial cells is well established, the expression and role of the Id1 protein in human cancer cells is controversial.
  • Our results show that in usual types of human mammary carcinomas, the Id1 protein is expressed exclusively in the endothelium.
  • Interestingly, we detected nuclear expression of the Id1 protein in the tumor cells in 10 of 45 cases of poorly differentiated and highly aggressive carcinoma with metaplastic morphology.
  • Similarly, only 1 of 30 prostate cancer samples showed Id1-positive tumor cells, whereas in almost all, endothelial cells showed high Id1 expression.
  • In contrast to the lack of Id1 expression in the usual types of mammary and prostate cancers, the majority of transitional cell bladder tumors showed Id1 protein expression in both tumor and endothelial cells.
  • [MeSH-minor] Animals. Antibodies, Monoclonal / immunology. Endothelial Cells / pathology. Epithelial Cells / metabolism. Epithelial Cells / pathology. Female. Humans. Immunohistochemistry. Male. Mammary Neoplasms, Animal / metabolism. Mammary Neoplasms, Animal / pathology. Prostatic Neoplasms / metabolism. Prostatic Neoplasms / pathology. Rabbits. Urinary Bladder Neoplasms / metabolism. Urinary Bladder Neoplasms / pathology

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  • (PMID = 17108123.001).
  • [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, Monoclonal; 0 / ID1 protein, human; 0 / Inhibitor of Differentiation Protein 1
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32. Suedmeyer WK, Johnson G: Survey of neoplasia in red kangaroos (Macropus rufus), 1992-2002, in a zoological collection. J Zoo Wildl Med; 2007 Jun;38(2):231-9
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  • Two squamous cell carcinomas of the oral cavity, two mammary gland adenocarcinomas, a multicentric T-cell lymphosarcoma, and one submucosal pyloric lipoma were diagnosed in six of 28 kangaroo deaths.
  • On the basis of these cases and a review of the literature, the most commonly observed neoplasms in red kangaroos are mammary gland adenocarcinomas and oral squamous cell carcinomas.
  • Common denominators were not identified in these cases, although chronic gingivitis could have been a contributing factor in the development of the oral squamous cell carcinomas.
  • [MeSH-major] Lymphoma, Non-Hodgkin / veterinary. Macropodidae. Mammary Neoplasms, Animal / epidemiology. Mouth Neoplasms / veterinary. Stomach Neoplasms / veterinary
  • [MeSH-minor] Adenocarcinoma / epidemiology. Adenocarcinoma / mortality. Adenocarcinoma / pathology. Adenocarcinoma / veterinary. Animals. Animals, Zoo. Carcinoma, Squamous Cell / epidemiology. Carcinoma, Squamous Cell / mortality. Carcinoma, Squamous Cell / pathology. Carcinoma, Squamous Cell / veterinary. Female. Immunohistochemistry / veterinary. Lipoma / epidemiology. Lipoma / mortality. Lipoma / pathology. Lipoma / veterinary. T-Lymphocytes / pathology

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  • (PMID = 17679506.001).
  • [ISSN] 1042-7260
  • [Journal-full-title] Journal of zoo and wildlife medicine : official publication of the American Association of Zoo Veterinarians
  • [ISO-abbreviation] J. Zoo Wildl. Med.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
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33. 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
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  • [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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34. 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
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  • [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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35. Labelle M, Schnittler HJ, Aust DE, Friedrich K, Baretton G, Vestweber D, Breier G: Vascular endothelial cadherin promotes breast cancer progression via transforming growth factor beta signaling. Cancer Res; 2008 Mar 1;68(5):1388-97
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  • [Title] Vascular endothelial cadherin promotes breast cancer progression via transforming growth factor beta signaling.
  • Epithelial-to-mesenchymal transition (EMT) is an important event during carcinoma progression and leads to increased tumor cell malignancy.
  • Here, we show that vascular endothelial (VE)-cadherin is induced during EMT in mammary tumor cells and is aberrantly expressed in invasive human breast carcinomas.
  • Consistently, VE-cadherin expression in malignant fibroblastoid tumor cells promoted the growth of experimental mammary carcinomas in vivo.
  • [MeSH-minor] Animals. Cell Line, Tumor. Disease Progression. Gene Expression Profiling. Humans. Mammary Neoplasms, Animal / pathology. Mice. Mice, Inbred BALB C. Neoplasm Metastasis. Neoplasm Transplantation. Neovascularization, Pathologic. Signal Transduction

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  • (PMID = 18316602.001).
  • [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 / Antigens, CD; 0 / Cadherins; 0 / Transforming Growth Factor beta; 0 / cadherin 5
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36. Sckell A, Klenke FM: The cranial bone window model: studying angiogenesis of primary and secondary bone tumors by intravital microscopy. Methods Mol Biol; 2009;467:343-55
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  • Malignant primary bone tumor growth predominantly occurs in younger people, whereas older people predominantly suffer from secondary bone tumors since up to 85% of the most frequently occurring malignant solid tumors, such as lung, mammary, and prostate carcinomas, metastasize into the bone.
  • Since most physiologic and pathophysiologic processes are active and dynamic events, one of the major strengths of chronic animal models using intravital microscopy is the possibility of monitoring the regions of interest in vivo continuously up to several weeks with high spatial and temporal resolution.
  • [MeSH-minor] Animals. Disease Models, Animal. Mice. Neoplasm Transplantation

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  • (PMID = 19301683.001).
  • [ISSN] 1064-3745
  • [Journal-full-title] Methods in molecular biology (Clifton, N.J.)
  • [ISO-abbreviation] Methods Mol. Biol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
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37. 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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38. 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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  • [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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39. 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


40. Sung YM, Xu X, Sun J, Mueller D, Sentissi K, Johnson P, Urbach E, Seillier-Moiseiwitsch F, Johnson MD, Mueller SC: Tumor suppressor function of Syk in human MCF10A in vitro and normal mouse mammary epithelium in vivo. PLoS One; 2009 Oct 15;4(10):e7445
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  • [Title] Tumor suppressor function of Syk in human MCF10A in vitro and normal mouse mammary epithelium in vivo.
  • The normal function of Syk in epithelium of the developing or adult breast is not known, however, Syk suppresses tumor growth, invasion, and metastasis in breast cancer cells.
  • Here, we demonstrate that in the mouse mammary gland, loss of one Syk allele profoundly increases proliferation and ductal branching and invasion of epithelial cells through the mammary fat pad during puberty.
  • Mammary carcinomas develop by one year.
  • These results support the role of Syk in limiting proliferation and invasion of epithelial cells during normal morphogenesis, and emphasize the critical role of Syk as a tumor suppressor for breast cancer.
  • The question of breast cancer risk following systemic anti-Syk therapy is raised since only partial loss of Syk was sufficient to induce mammary carcinomas.

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  • (PMID = 19829710.001).
  • [ISSN] 1932-6203
  • [Journal-full-title] PloS one
  • [ISO-abbreviation] PLoS ONE
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / 9R01 CA 112673; United States / NCRR NIH HHS / RR / S10 RR019291; United States / NCRR NIH HHS / RR / 1 S10 RR019291-01A2; United States / NCATS NIH HHS / TR / UL1 TR000101; United States / NCI NIH HHS / CA / P30 CA051008; United States / NCI NIH HHS / CA / R01 CA112673; United States / NCI NIH HHS / CA / 1P30-CA-51008; United States / NCRR NIH HHS / RR / 1S10 RR15768-01
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't; Research Support, U.S. Gov't, Non-P.H.S.
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antigens, CD44; 0 / Integrin alpha6; 0 / Intracellular Signaling Peptides and Proteins; EC 2.7.10.1 / Protein-Tyrosine Kinases; EC 2.7.10.1 / Syk kinase; EC 3.4.24.80 / Matrix Metalloproteinase 14
  • [Other-IDs] NLM/ PMC2759536
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41. Bastid J, Bouchet BP, Ciancia C, Pourchet J, Audoynaud C, Grelier G, Puisieux A, Ansieau S: The SNAIL family member SCRATCH1 is not expressed in human tumors. Oncol Rep; 2010 Feb;23(2):523-9
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  • To further explore this possibility, we assessed SNAI1 (SNAIL), SNAI2 (SLUG) and SCRT1 (SCRATCH1) expression in a wide panel of human and murine tumors encompassing 151 primary tumors and 6 different cancer types, including melanomas and multiple different carcinomas.
  • [MeSH-minor] Animals. Carcinoma / genetics. Female. Gene Expression Regulation, Neoplastic. Humans. Mammary Neoplasms, Animal / genetics. Melanoma / genetics. Mice

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  • (PMID = 20043117.001).
  • [ISSN] 1791-2431
  • [Journal-full-title] Oncology reports
  • [ISO-abbreviation] Oncol. Rep.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Greece
  • [Chemical-registry-number] 0 / SCRATCH1 protein, human; 0 / Transcription Factors; 0 / snail family transcription factors
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42. 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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43. di Bari MG, Ginsburg E, Plant J, Strizzi L, Salomon DS, Vonderhaar BK: Msx2 induces epithelial-mesenchymal transition in mouse mammary epithelial cells through upregulation of Cripto-1. J Cell Physiol; 2009 Jun;219(3):659-66
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  • [Title] Msx2 induces epithelial-mesenchymal transition in mouse mammary epithelial cells through upregulation of Cripto-1.
  • Epithelial-mesenchymal transition (EMT) is a process occurring during both embryogenesis and early stages of invasive cancer.
  • Herein we assess EMT induction in a mouse mammary epithelial cell line driven by Msx2, a homeobox-containing transcription factor important during mammary gland development.
  • NMuMG cells, a normal mouse mammary epithelial cell line, stably transfected with a Msx2 cDNA showed downregulation of an epithelial marker E-cadherin and upregulation of the mesenchymal markers vimentin and N-cadherin.
  • Moreover, immunohistochemistry of human infiltrating breast carcinomas showed positive staining for Msx2 only in the infiltrating tumor cells while the non-infiltrating tumor cells were negative.
  • [MeSH-major] Epidermal Growth Factor / metabolism. Homeodomain Proteins / metabolism. Mammary Glands, Animal / cytology. Mammary Glands, Animal / metabolism. Membrane Glycoproteins / metabolism. Neoplasm Proteins / metabolism
  • [MeSH-minor] Animals. Base Sequence. Breast Neoplasms / genetics. Breast Neoplasms / metabolism. Breast Neoplasms / pathology. Carcinoma, Ductal, Breast / genetics. Carcinoma, Ductal, Breast / metabolism. Carcinoma, Ductal, Breast / pathology. Cell Line. DNA Primers / genetics. Epithelial Cells / cytology. Epithelial Cells / metabolism. Female. Humans. Mesoderm / cytology. Mesoderm / metabolism. Mice. Neoplasm Invasiveness / genetics. Neoplasm Invasiveness / pathology. Neoplasm Invasiveness / physiopathology. Protein-Tyrosine Kinases / metabolism. RNA, Small Interfering / genetics. Recombinant Proteins / genetics. Recombinant Proteins / metabolism. Signal Transduction. Transfection. Up-Regulation. src-Family Kinases

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  • (PMID = 19170109.001).
  • [ISSN] 1097-4652
  • [Journal-full-title] Journal of cellular physiology
  • [ISO-abbreviation] J. Cell. Physiol.
  • [Language] eng
  • [Grant] United States / Intramural NIH HHS / / Z01 BC008226-31
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, N.I.H., Intramural
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / DNA Primers; 0 / Homeodomain Proteins; 0 / MSX2 protein; 0 / Membrane Glycoproteins; 0 / Neoplasm Proteins; 0 / RNA, Small Interfering; 0 / Recombinant Proteins; 0 / Tdgf1 protein, mouse; 62229-50-9 / Epidermal Growth Factor; EC 2.7.10.1 / Protein-Tyrosine Kinases; EC 2.7.10.2 / CSK tyrosine-protein kinase; EC 2.7.10.2 / src-Family Kinases
  • [Other-IDs] NLM/ NIHMS144958; NLM/ PMC2753837
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44. Bowen TJ, Yakushiji H, Montagna C, Jain S, Ried T, Wynshaw-Boris A: Atm heterozygosity cooperates with loss of Brca1 to increase the severity of mammary gland cancer and reduce ductal branching. Cancer Res; 2005 Oct 1;65(19):8736-46
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  • [Title] Atm heterozygosity cooperates with loss of Brca1 to increase the severity of mammary gland cancer and reduce ductal branching.
  • The role of homozygous ataxia telangiectasia mutated (ATM) mutations in familial and sporadic forms of cancer is well established, but the contribution of ATM heterozygosity to mammary gland and other cancers has been controversial.
  • To test the effect of Atm heterozygosity on mammary gland cancer, mice with complete loss of exon 11 of Brca1 specifically in mammary epithelium (Brca1-MG-Deltaex11) were studied in either Atm heterozygous or Atm wild-type backgrounds.
  • Targeted deletion of Brca1 in mammary epithelium resulted in carcinomas and adenocarcinomas of varying histology with long (>9 months) latency.
  • However, the mice displayed variable tumor severity and differences in mammary tissue development.
  • Mammary tumors from Brca1-MG-Deltaex11;Atm heterozygous mice were anaplastic and undifferentiated in all 20 tumors tested, whereas tumors from mice that were Brca1-MG-Deltaex11 but wild-type for Atm displayed variable histologic profiles, with some anaplastic tumors and other differentiated and less invasive tumor types.
  • Our results provide evidence that Atm heterozygosity influences severity of mammary gland tumors in the Brca1-MG-Deltaex11 tumor-prone mouse and suggest that this mutation leads to a newly characterized developmental defect during glandular maturation.
  • [MeSH-major] Cell Cycle Proteins / genetics. DNA-Binding Proteins / genetics. Genes, BRCA1 / physiology. Mammary Neoplasms, Experimental / genetics. Protein-Serine-Threonine Kinases / genetics. Tumor Suppressor Proteins / genetics
  • [MeSH-minor] Animals. Apoptosis / genetics. Ataxia Telangiectasia Mutated Proteins. Cell Differentiation / genetics. Cell Growth Processes / genetics. Cell Transformation, Neoplastic / genetics. Exons. Female. Heterozygote. Inbreeding. Male. Mammary Glands, Animal / abnormalities. Mammary Glands, Animal / pathology. Mammary Glands, Animal / physiology. Mice. Mice, Knockout. Neoplasm Invasiveness. Pregnancy

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  • (PMID = 16204043.001).
  • [ISSN] 0008-5472
  • [Journal-full-title] Cancer research
  • [ISO-abbreviation] Cancer Res.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [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
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45. 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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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [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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46. Deeb KK, Michalowska AM, Yoon CY, Krummey SM, Hoenerhoff MJ, Kavanaugh C, Li MC, Demayo FJ, Linnoila I, Deng CX, Lee EY, Medina D, Shih JH, Green JE: Identification of an integrated SV40 T/t-antigen cancer signature in aggressive human breast, prostate, and lung carcinomas with poor prognosis. Cancer Res; 2007 Sep 1;67(17):8065-80
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  • [Title] Identification of an integrated SV40 T/t-antigen cancer signature in aggressive human breast, prostate, and lung carcinomas with poor prognosis.
  • Understanding the genetic architecture of cancer pathways that distinguishes subsets of human cancer is critical to developing new therapies that better target tumors based on their molecular expression profiles.
  • This genetic signature, composed primarily of genes regulating cell replication, proliferation, DNA repair, and apoptosis, is not a general cancer signature.
  • The T/t-antigen signature is highly predictive of human breast cancer prognosis.
  • Because this class of epithelial tumors is generally intractable to currently existing standard therapies, this genetic signature identifies potential targets for novel therapies directed against these lethal forms of cancer.
  • Because these genetic targets have been discovered using mammary, prostate, and lung T/t-antigen mouse cancer models, these models are rationale candidates for use in preclinical testing of therapies focused on these biologically important targets.
  • [MeSH-major] Antigens, Polyomavirus Transforming / genetics. Breast Neoplasms / genetics. Carcinoma / genetics. Lung Neoplasms / genetics. Prostatic Neoplasms / genetics
  • [MeSH-minor] Animals. Cluster Analysis. Female. Gene Expression Profiling. Gene Expression Regulation, Neoplastic. Gene Regulatory Networks. Humans. Male. Mammary Neoplasms, Animal / diagnosis. Mammary Neoplasms, Animal / genetics. Mammary Neoplasms, Animal / pathology. Mice. Mice, Inbred C57BL. Mice, Transgenic. Oligonucleotide Array Sequence Analysis. Prognosis


47. 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
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  • [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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48. Nielsen T, Murata R, Maxwell RJ, Stødkilde-Jørgensen H, Ostergaard L, Ley CD, Kristjansen PE, Horsman MR: Non-invasive imaging of combretastatin activity in two tumor models: Association with invasive estimates. Acta Oncol; 2010 Oct;49(7):906-13
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  • MATERIAL AND METHODS: Mice bearing C3H mammary carcinomas or KHT sarcomas (200 to 800 mm(3)) were intraperitoneally injected with CA4P (100 mg/kg).
  • RESULTS: Initial necrotic fraction was about 10% in both tumor models at 200 mm(3), but only increased significantly with tumor size in the C3H mammary carcinoma.
  • [MeSH-major] Diagnostic Imaging / methods. Mammary Neoplasms, Experimental / diagnosis. Mammary Neoplasms, Experimental / drug therapy. Stilbenes / therapeutic use
  • [MeSH-minor] Animals. Antineoplastic Agents, Phytogenic / pharmacology. Antineoplastic Agents, Phytogenic / therapeutic use. Carcinoma / diagnosis. Carcinoma / drug therapy. Carcinoma / pathology. Cell Line, Tumor. Contrast Media. Disease Models, Animal. Female. Magnetic Resonance Imaging / methods. Mice. Mice, Inbred C3H. Nitric Oxide / metabolism. Sarcoma / diagnosis. Sarcoma / drug therapy. Sarcoma / pathology. Statistics as Topic. Treatment Outcome. Tumor Burden / drug effects

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  • (PMID = 20831477.001).
  • [ISSN] 1651-226X
  • [Journal-full-title] Acta oncologica (Stockholm, Sweden)
  • [ISO-abbreviation] Acta Oncol
  • [Language] eng
  • [Publication-type] Comparative Study; Evaluation Studies; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Antineoplastic Agents, Phytogenic; 0 / Contrast Media; 0 / Stilbenes; 31C4KY9ESH / Nitric Oxide; I5590ES2QZ / fosbretabulin
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49. Ohnishi T, Fukamachi K, Ohshima Y, Jiegou X, Ueda S, Iigo M, Takasuka N, Naito A, Fujita K, Matsuoka Y, Izumi K, Tsuda H: Possible application of human c-Ha-ras proto-oncogene transgenic rats in a medium-term bioassay model for carcinogens. Toxicol Pathol; 2007 Apr;35(3):436-43
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  • With the aim of developing a medium-term assay for screening of environmental carcinogens, we exposed mammary carcinogen sensitive human c-Ha-ras proto-oncogene transgenic (Hras128) rats to various carcinogens, including compounds that do not normally induce mammary tumors.
  • Female Hras128 rats receiving NNK, DEN, or DMA showed a significant increase in mammary tumor incidence and/or multiplicity compared to the respective values with olive oil or deionized distilled water (DDW) vehicles.
  • In male Hras128 rats, a significant increase in mammary tumors was also observed in groups administered 3-MC, B[a]P, anthracene, IQ, and NNK.
  • Thus various carcinogens, not necessarily limited to those normally targeting the breast, were found to induce mammary carcinomas in Hras128 rats, especially in females, pointing to potential use for medium-term screening.
  • [MeSH-major] Biological Assay. Carcinogens / toxicity. Genes, ras. Mammary Neoplasms, Experimental / genetics. Proto-Oncogene Proteins p21(ras) / genetics
  • [MeSH-minor] Animals. Animals, Genetically Modified. DNA Mutational Analysis. Disease Models, Animal. Female. Humans. Male. Rats. Rats, Sprague-Dawley

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  • (PMID = 17474063.001).
  • [ISSN] 0192-6233
  • [Journal-full-title] Toxicologic pathology
  • [ISO-abbreviation] Toxicol Pathol
  • [Language] eng
  • [Publication-type] Comparative Study; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Carcinogens; EC 3.6.5.2 / Proto-Oncogene Proteins p21(ras)
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50. Zhu Z, Jiang W, Sells JL, Neil ES, McGinley JN, Thompson HJ: Effect of nonmotorized wheel running on mammary carcinogenesis: circulating biomarkers, cellular processes, and molecular mechanisms in rats. Cancer Epidemiol Biomarkers Prev; 2008 Aug;17(8):1920-9
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  • [Title] Effect of nonmotorized wheel running on mammary carcinogenesis: circulating biomarkers, cellular processes, and molecular mechanisms in rats.
  • The objective of this experiment was to identify circulating growth factors, hormones, and cellular and molecular mechanisms that account for the effects of physical activity on mammary carcinogenesis.
  • Physical activity reduced mammary cancer incidence (P = 0.015) and cancer multiplicity (P = 0.01).
  • Western blot analyses of mammary carcinomas revealed that proteins involved in cell proliferation were reduced (P < 0.001) and those involved in apoptosis via the mitochondrial pathway were elevated (P < 0.001) by physical activity.
  • Evidence in support of this hypothesis was found in the Western blot analyses of mammary carcinomas, mammary gland, liver, and skeletal muscle.

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  • (PMID = 18708381.001).
  • [ISSN] 1055-9965
  • [Journal-full-title] Cancer epidemiology, biomarkers & prevention : a publication of the American Association for Cancer Research, cosponsored by the American Society of Preventive Oncology
  • [ISO-abbreviation] Cancer Epidemiol. Biomarkers Prev.
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / CA100693-04; United States / NCI NIH HHS / CA / R01 CA100693; United States / NCI NIH HHS / CA / CA100693; United States / NCI NIH HHS / CA / R01 CA100693-04
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Biomarkers, Tumor; 0 / Hormones; 0 / Intercellular Signaling Peptides and Proteins
  • [Other-IDs] NLM/ NIHMS104967; NLM/ PMC2667869
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51. Yang X, Pursell B, Lu S, Chang TK, Mercurio AM: Regulation of beta 4-integrin expression by epigenetic modifications in the mammary gland and during the epithelial-to-mesenchymal transition. J Cell Sci; 2009 Jul 15;122(Pt 14):2473-80
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  • [Title] Regulation of beta 4-integrin expression by epigenetic modifications in the mammary gland and during the epithelial-to-mesenchymal transition.
  • The beta 4 integrin is expressed in epithelial cells, a few other cell types and in some carcinomas.
  • Despite this restricted expression pattern and the functional importance of beta 4 integrin in epithelial and carcinoma biology, little is known about how its expression is regulated.
  • We separated basal (beta 4+) and luminal (beta 4-) epithelial cells from the mammary glands of K14-eGFP mice and demonstrated that the beta 4-integrin promoter is unmethylated in basal cells and methylated in luminal cells.
  • We also observed that expression of beta 4 integrin and E-cadherin is lost during the epithelial-to-mesenchymal transition (EMT) of mammary gland cells induced by transforming growth factor beta (TGFbeta), which is coincident with de novo DNA methylation, a decrease in active histone modifications (H3K9Ac and H3K4me3) and an increase in the repressive histone modification H3K27me3.

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  • (PMID = 19549682.001).
  • [ISSN] 0021-9533
  • [Journal-full-title] Journal of cell science
  • [ISO-abbreviation] J. Cell. Sci.
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / R01 CA080789; United States / NCI NIH HHS / CA / CA1107548; United States / NCI NIH HHS / CA / CA80789; United States / PHS HHS / / T32130807
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Cadherins; 0 / Histones; 0 / Integrin beta4; 0 / Transforming Growth Factor beta
  • [Other-IDs] NLM/ PMC2704882
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52. Wang A, Arantes S, Yan L, Kiguchi K, McArthur MJ, Sahin A, Thames HD, Aldaz CM, Macleod MC: The transcription factor ATF3 acts as an oncogene in mouse mammary tumorigenesis. BMC Cancer; 2008 Sep 22;8:268
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  • [Title] The transcription factor ATF3 acts as an oncogene in mouse mammary tumorigenesis.
  • BACKGROUND: Overexpression of the bZip transcription factor, ATF3, in basal epithelial cells of transgenic mice under the control of the bovine cytokeratin-5 (CK5) promoter has previously been shown to induce epidermal hyperplasia, hair follicle anomalies and neoplastic lesions of the oral mucosa including squamous cell carcinomas.
  • CK5 is known to be expressed in myoepithelial cells of the mammary gland, suggesting the possibility that transgenic BK5.ATF3 mice may exhibit mammary gland phenotypes.
  • METHODS: Mammary glands from nulliparous mice in our BK5.ATF3 colony, both non-transgenic and transgenic, were examined for anomalies by histopathology and immunohistochemistry.
  • Nulliparous and biparous female mice were observed for possible mammary tumor development, and suspicious masses were analyzed by histopathology and immunohistochemistry.
  • RESULTS: Transgenic BK5.ATF3 mice expressed nuclear ATF3 in the basal layer of the mammary ductal epithelium, and often developed squamous metaplastic lesions in one or more mammary glands by 25 weeks of age.
  • However, biparous BK5.ATF3 mice developed mammary carcinomas with squamous metaplasia between 6 months and one year of age, reaching an incidence of 67%.
  • CONCLUSION: Overexpression of ATF3 in CK5-expressing cells of the murine mammary gland results in the development of squamous metaplastic lesions in nulliparous females, and in mammary tumors in biparous mice, suggesting that ATF3 acts as a mammary oncogene.

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  • (PMID = 18808719.001).
  • [ISSN] 1471-2407
  • [Journal-full-title] BMC cancer
  • [ISO-abbreviation] BMC Cancer
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / U19 CA084978; United States / NCI NIH HHS / CA / P30 CA016672; United States / NIEHS NIH HHS / ES / ES007784; United States / NCI NIH HHS / CA / R01 CA116620; United States / NCI NIH HHS / CA / CA016672; United States / NIEHS NIH HHS / ES / P30 ES007784; United States / NCI NIH HHS / CA / U19 CA84978
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Activating Transcription Factor 3; 0 / Atf3 protein, mouse; 0 / Biomarkers, Tumor; 0 / Keratin-5; 0 / Transcription Factors
  • [Other-IDs] NLM/ PMC2564979
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53. Jayasinghe MM, Golden JM, Nair P, O'Donnell CM, Werner MT, Kurt RA: Tumor-derived CCL5 does not contribute to breast cancer progression. Breast Cancer Res Treat; 2008 Oct;111(3):511-21
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Tumor-derived CCL5 does not contribute to breast cancer progression.
  • Besides functioning as a chemotactic factor, CCL5 has been associated with progression of disease in women with breast cancer, immune modulation and metastasis.
  • Here we asked whether CCL5 produced by tumor cells contributed to growth or metastasis of breast cancer.
  • For this purpose, we used two murine mammary carcinomas, the 4T1 tumor which is metastatic and constitutively expresses CCL5, and the 168 tumor which is not metastatic and does not constitutively express CCL5.
  • These results show that tumor-derived CCL5 expression alone does not make a significant contribution to breast cancer progression.
  • [MeSH-major] Chemokine CCL5 / metabolism. Mammary Neoplasms, Animal / immunology

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  • (PMID = 17978871.001).
  • [ISSN] 0167-6806
  • [Journal-full-title] Breast cancer research and treatment
  • [ISO-abbreviation] Breast Cancer Res. Treat.
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / R15 CA111539-01
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural
  • [Publication-country] Netherlands
  • [Chemical-registry-number] 0 / Ccl5 protein, mouse; 0 / Chemokine CCL5; 0 / Histocompatibility Antigens; 0 / RNA, Small Interfering
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54. 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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55. Ramakrishnappa N, Rajamahendran R, Lin YM, Leung PC: GnRH in non-hypothalamic reproductive tissues. Anim Reprod Sci; 2005 Aug;88(1-2):95-113
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  • Although hypothalamus and pituitary are the principal source and target sites for GnRH, several reports have recently suggested extra-hypothalamic GnRH and GnRH receptors in various reproductive tissues such as ovaries, placenta, endometrium, oviducts, testes, prostrate, and mammary glands.
  • Recent studies have shown that GnRH is more abundantly present in ovarian, endometrial and prostrate carcinomas.
  • The presence of type-II GnRH receptors in reproductive tissues (e.g. gonads, prostrate, endometrium, oviduct, placenta, and mammary glands) suggests existence of distinct role(s) for type-II GnRH molecule in these tissues.

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  • (PMID = 15982835.001).
  • [ISSN] 0378-4320
  • [Journal-full-title] Animal reproduction science
  • [ISO-abbreviation] Anim. Reprod. Sci.
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] Netherlands
  • [Chemical-registry-number] 0 / Receptors, LHRH; 33515-09-2 / Gonadotropin-Releasing Hormone
  • [Number-of-references] 156
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56. Murai T, Mori S, Kang JS, Morimura K, Wanibuchi H, Totsuka Y, Fukushima S: Evidence of a threshold-effect for 2-amino-3,8-dimethylimidazo-[4,5-f]quinoxaline liver carcinogenicity in F344/DuCrj rats. Toxicol Pathol; 2008 Apr;36(3):472-7
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  • Histopathological examination revealed significant induction of hepatocellular carcinomas, adenomas, and development of glutathione S-transferase placental form-positive foci with MeIQx at 100 ppm.
  • Moreover, the incidences of Zymbal's glands carcinoma, mammary fibroadenoma, and subcutaneous fibroma were found significantly increased in a 100 ppm MeIQx group.
  • [MeSH-major] Adenoma, Liver Cell / chemically induced. Carcinogens / toxicity. Carcinoma, Hepatocellular / chemically induced. Liver Neoplasms / chemically induced. Precancerous Conditions / chemically induced. Quinoxalines / toxicity
  • [MeSH-minor] Administration, Oral. Animal Feed. Animals. DNA Adducts / biosynthesis. DNA Adducts / chemistry. Deoxyguanosine / analogs & derivatives. Deoxyguanosine / chemistry. Deoxyguanosine / metabolism. Dose-Response Relationship, Drug. Glutathione Transferase / metabolism. Liver / drug effects. Liver / enzymology. Liver / pathology. Longevity / drug effects. Male. No-Observed-Adverse-Effect Level. Rats. Rats, Inbred F344

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  • (PMID = 18413788.001).
  • [ISSN] 1533-1601
  • [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 / Carcinogens; 0 / DNA Adducts; 0 / Quinoxalines; 77500-04-0 / 2-amino-3,8-dimethylimidazo(4,5-f)quinoxaline; 88847-89-6 / 8-oxo-7-hydrodeoxyguanosine; EC 2.5.1.18 / Glutathione Transferase; G9481N71RO / Deoxyguanosine
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57. 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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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [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


58. Smith AP, Verrecchia A, Fagà G, Doni M, Perna D, Martinato F, Guccione E, Amati B: A positive role for Myc in TGFbeta-induced Snail transcription and epithelial-to-mesenchymal transition. Oncogene; 2009 Jan 22;28(3):422-30
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  • Our findings suggest that Myc and TGFbeta signaling may cooperate in promoting EMT and metastasis in carcinomas.
  • [MeSH-minor] Animals. Cells, Cultured. Chromatin Immunoprecipitation. Humans. Immunoblotting. Mammary Glands, Animal / cytology. Mammary Glands, Animal / metabolism. Mice. RNA, Small Interfering / pharmacology. Smad2 Protein / antagonists & inhibitors. Smad2 Protein / genetics. Smad2 Protein / metabolism. Smad3 Protein / antagonists & inhibitors. Smad3 Protein / genetics. Smad3 Protein / metabolism. Smad4 Protein / antagonists & inhibitors. Smad4 Protein / genetics. Smad4 Protein / metabolism. Transcription, Genetic

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  • (PMID = 18978814.001).
  • [ISSN] 1476-5594
  • [Journal-full-title] Oncogene
  • [ISO-abbreviation] Oncogene
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Myc protein, mouse; 0 / Proto-Oncogene Proteins c-myc; 0 / RNA, Small Interfering; 0 / Smad2 Protein; 0 / Smad3 Protein; 0 / Smad4 Protein; 0 / Transcription Factors; 0 / Transforming Growth Factor beta; 0 / snail family transcription factors
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59. Nowak M, Madej J, Dziegiel P, Lopuszynski W, Rodo A, Ugorski M: Tumor-associated carbohydrate antigens: Sialyl Lea and T/Tn antigens in canine mammary tumors. Vet Pathol; 2009 Mar;46(2):222-6
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  • [Title] Tumor-associated carbohydrate antigens: Sialyl Lea and T/Tn antigens in canine mammary tumors.
  • Twenty-eight canine mammary tubulopapillary carcinomas and 14 simple adenomas were studied by immunohistochemistry for the expressions of the tumor-associated carbohydrate antigens.
  • Staining with anti-T and anti-Tn monoclonal antibodies revealed that 85.70% of the tubulopapillary carcinomas expressed T and Tn antigens.
  • Comparison of average values of reaction intensity (IRS) scale for malignant versus benign tumors by the Mann-Whitney U-test revealed a significant relationship between T and Tn antigens expression and type (malignant vs. benign) mammary tumors.
  • Based on the results obtained, it is suggested that each of the studied antigens can be treated as a tumor-associated antigen of canine mammary tumors.
  • However, only the T and Tn antigens seem to be associated with malignant transformation of mammary gland cells and to be of potential value as diagnostic markers.
  • [MeSH-major] Antigens, Tumor-Associated, Carbohydrate / metabolism. Dog Diseases / metabolism. Gangliosides / metabolism. Mammary Neoplasms, Animal / metabolism
  • [MeSH-minor] Adenoma / metabolism. Adenoma / veterinary. Animals. Biomarkers, Tumor / metabolism. Carcinoma / classification. Carcinoma / metabolism. Carcinoma / veterinary. Dogs. Female. Mammary Glands, Animal / cytology. Mammary Glands, Animal / metabolism

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  • (PMID = 19261632.001).
  • [ISSN] 0300-9858
  • [Journal-full-title] Veterinary pathology
  • [ISO-abbreviation] Vet. Pathol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antigens, Tumor-Associated, Carbohydrate; 0 / Biomarkers, Tumor; 0 / Gangliosides; 0 / sialosyl-Tn antigen; 91847-18-6 / sialyl Le(a) ganglioside
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60. Sum EY, Shackleton M, Hahm K, Thomas RM, O'Reilly LA, Wagner KU, Lindeman GJ, Visvader JE: Loss of the LIM domain protein Lmo4 in the mammary gland during pregnancy impedes lobuloalveolar development. Oncogene; 2005 Jul 14;24(30):4820-8
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  • [Title] Loss of the LIM domain protein Lmo4 in the mammary gland during pregnancy impedes lobuloalveolar development.
  • LMO4, a member of the LIM-only family of zinc-finger proteins, is overexpressed in a significant proportion of breast carcinomas and acts as a negative regulator of mammary epithelial differentiation.
  • To delineate cell types within the developing mouse mammary gland that express Lmo4, we analysed different stages of mammopoiesis by immunohistochemistry.
  • Lmo4 was found to be highly expressed in the proliferating cap cells of the terminal end bud and in the ductal and alveolar luminal cells of the mature mammary gland but was negligible or low in myoepithelial cells.
  • To assess the physiological role of Lmo4 in the mammary gland, we generated conditionally targeted mice lacking Lmo4 in the mammary epithelium during pregnancy.
  • In contrast, germline loss of Lmo4 did not alter lobuloalveolar development arising from transplanted mammary anlagen, implying the existence of a compensatory mechanism in these knockout mice.
  • Thus, the use of a conditional targeting strategy has revealed that Lmo4 is required for proper development of the mammary gland during pregnancy and indicated that Lmo4 acts as a positive regulator of alveolar epithelial proliferation.
  • [MeSH-major] Homeodomain Proteins / metabolism. Mammary Glands, Animal / growth & development. Mammary Glands, Animal / metabolism. Transcription Factors / metabolism

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  • (PMID = 15856027.001).
  • [ISSN] 0950-9232
  • [Journal-full-title] Oncogene
  • [ISO-abbreviation] Oncogene
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Adaptor Proteins, Signal Transducing; 0 / Homeodomain Proteins; 0 / LIM Domain Proteins; 0 / Lmo4 protein, mouse; 0 / Transcription Factors
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61. Nielsen BS, Egeblad M, Rank F, Askautrud HA, Pennington CJ, Pedersen TX, Christensen IJ, Edwards DR, Werb Z, Lund LR: Matrix metalloproteinase 13 is induced in fibroblasts in polyomavirus middle T antigen-driven mammary carcinoma without influencing tumor progression. PLoS One; 2008 Aug 13;3(8):e2959
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  • [Title] Matrix metalloproteinase 13 is induced in fibroblasts in polyomavirus middle T antigen-driven mammary carcinoma without influencing tumor progression.
  • Matrix metalloproteinase (MMP) 13 (collagenase 3) is an extracellular matrix remodeling enzyme that is induced in myofibroblasts during the earliest invasive stages of human breast carcinoma, suggesting that it is involved in tumor progression.
  • During progression of mammary carcinomas in the polyoma virus middle T oncogene mouse model (MMTV-PyMT), Mmp13 mRNA was strongly upregulated concurrently with the transition to invasive and metastatic carcinomas.
  • As in human tumors, Mmp13 mRNA was found in myofibroblasts of invasive grade II and III carcinomas, but not in benign grade I and II mammary intraepithelial neoplasias.
  • We conclude that the expression pattern of Mmp13 mRNA in myofibroblasts of invasive carcinomas in the MMTV-PyMT breast cancer model recapitulates the expression pattern observed in human breast cancer.
  • Our results suggest that MMP13 is a marker of carcinoma-associated myofibroblasts of invasive carcinoma, even though it does not make a major contribution to tumor progression in the MMTV-PyMT breast cancer model.
  • [MeSH-major] Antigens, Polyomavirus Transforming / pharmacology. Fibroblasts / enzymology. Fibroblasts / virology. Mammary Neoplasms, Animal / enzymology. Mammary Neoplasms, Animal / pathology. Matrix Metalloproteinase 13 / biosynthesis

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  • (PMID = 18698413.001).
  • [ISSN] 1932-6203
  • [Journal-full-title] PloS one
  • [ISO-abbreviation] PLoS ONE
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / CA057621; United Kingdom / Medical Research Council / / G0100250; United States / NCI NIH HHS / CA / CA072006; United States / NCI NIH HHS / CA / R01 CA057621; United States / NCI NIH HHS / CA / P01 CA072006
  • [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 / Antigens, Polyomavirus Transforming; 0 / DNA Primers; EC 3.4.24.- / Matrix Metalloproteinase 13
  • [Other-IDs] NLM/ PMC2493034
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62. Rolla S, Marchini C, Malinarich S, Quaglino E, Lanzardo S, Montani M, Iezzi M, Angeletti M, Ramadori G, Forni G, Cavallo F, Amici A: Protective immunity against neu-positive carcinomas elicited by electroporation of plasmids encoding decreasing fragments of rat neu extracellular domain. Hum Gene Ther; 2008 Mar;19(3):229-40
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  • [Title] Protective immunity against neu-positive carcinomas elicited by electroporation of plasmids encoding decreasing fragments of rat neu extracellular domain.
  • We have shown that electroporation of plasmid carrying extracellular and transmembrane domains (EC-TM plasmid) encoded by the rat neu oncogene triggers a protective immune response toward rat p185(neu)-positive tumors in both wild-type BALB/c mice and cancer-prone rat neu-transgenic BALB-neuT mice.
  • [MeSH-major] Genes, erbB-2. Mammary Neoplasms, Animal / immunology. Receptor, ErbB-2 / immunology. T-Lymphocytes, Cytotoxic / immunology

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  • (PMID = 18269312.001).
  • [ISSN] 1043-0342
  • [Journal-full-title] Human gene therapy
  • [ISO-abbreviation] Hum. Gene Ther.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antibodies; EC 2.7.10.1 / Receptor, ErbB-2
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63. 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
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  • [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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64. van Rossum AG, van Bragt MP, Schuuring-Scholtes E, van der Ploeg JC, van Krieken JH, Kluin PM, Schuuring E: Transgenic mice with mammary gland targeted expression of human cortactin do not develop (pre-malignant) breast tumors: studies in MMTV-cortactin and MMTV-cortactin/-cyclin D1 bitransgenic mice. BMC Cancer; 2006;6:58
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  • [Title] Transgenic mice with mammary gland targeted expression of human cortactin do not develop (pre-malignant) breast tumors: studies in MMTV-cortactin and MMTV-cortactin/-cyclin D1 bitransgenic mice.
  • To study the role of cortactin in mammary gland tumorigenesis, we examined mouse mammary tumor virus (MMTV)-cortactin transgenic mice and MMTV-cortactin/-MMTV-cyclin D1 bitransgenic mice.
  • Immunohistochemical, Northern and Western blot analyses were performed to study the expression of human transgene cortactin during mammary gland development and in mammary tumors.
  • For tumor incidence studies, forced-bred, multiparous mice were used to enhance transgene expression in the mammary gland.
  • RESULTS: Mammary gland tumors arose stochastically (incidence 21%) with a mean age of onset at 100 weeks.
  • This incidence, however, did not exceed that of aged-matched control FVB/N mice (38%), which unexpectedly, also developed spontaneous mammary gland tumors.
  • We mimicked 11q13 amplification by generating MMTV-cortactin/-MMTV-cyclin D1 bitransgenic mice but did not observe any synergistic effect of cortactin on cyclin D1-induced mammary hyperplasias or carcinomas, nor development of distant metastasis.
  • CONCLUSION: From this study, we conclude that development of (pre-malignant) breast tumors in either wild type or MMTV-cyclin D1 mice was not augmented due to mammary gland targeted overexpression of human cortactin.
  • [MeSH-major] Cortactin / genetics. Mammary Neoplasms, Experimental / genetics
  • [MeSH-minor] Animals. Cyclin D1 / genetics. Female. Gene Expression. Gene Targeting. Humans. Mammary Glands, Animal / anatomy & histology. Mammary Glands, Animal / metabolism. Mammary Glands, Animal / pathology. Mammary Tumor Virus, Mouse / genetics. Mice. Mice, Transgenic. Precancerous Conditions / genetics. Precancerous Conditions / pathology


65. Utz AC, Hirner H, Blatz A, Hillenbrand A, Schmidt B, Deppert W, Henne-Bruns D, Fischer D, Thal DR, Leithäuser F, Knippschild U: Analysis of cell type-specific expression of CK1 epsilon in various tissues of young adult BALB/c Mice and in mammary tumors of SV40 T-Ag-transgenic mice. J Histochem Cytochem; 2010 Jan;58(1):1-15
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  • [Title] Analysis of cell type-specific expression of CK1 epsilon in various tissues of young adult BALB/c Mice and in mammary tumors of SV40 T-Ag-transgenic mice.
  • Deregulation of CK1epsilon has been linked to neurodegenerative diseases and cancer.
  • To better understand the cell type-specific functions of CK1epsilon, we determined its localization by immunhistochemistry in tissues of healthy, young adult BALB/c mice and in mammary tumors of SV40 T-antigen-transgenic mice.
  • CK1epsilon expression was found to be highly regulated in normal tissues of endodermal, mesodermal, and ectodermal origin and in neoplastic tissue of mammary cancer.
  • The data presented here give an overview of CK1epsilon reactivity in different organs under normal conditions and outline changes in its expression in mammary carcinomas.
  • Our data suggest a cell/organ type-specific function of CK1epsilon and indicate that tumorigenic conversion of mammary glands in SV40 T-antigen-transgenic mice leads to downregulation of CK1epsilon.
  • [MeSH-major] Antigens, Viral, Tumor / genetics. Casein Kinase Iepsilon / genetics. Mammary Neoplasms, Animal / virology. Mammary Neoplasms, Experimental / enzymology
  • [MeSH-minor] Animals. Antigens, Polyomavirus Transforming / genetics. Cell Transformation, Neoplastic / genetics. Ectoderm / enzymology. Endoderm / enzymology. Female. Male. Mammary Glands, Animal / enzymology. Mammary Glands, Animal / physiology. Mesoderm / enzymology. Mice. Mice, Inbred BALB C. Mice, Transgenic. Organ Specificity

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  • (PMID = 19755715.001).
  • [ISSN] 1551-5044
  • [Journal-full-title] The journal of histochemistry and cytochemistry : official journal of the Histochemistry Society
  • [ISO-abbreviation] J. Histochem. Cytochem.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antigens, Polyomavirus Transforming; 0 / Antigens, Viral, Tumor; EC 2.7.11.1 / Casein Kinase Iepsilon
  • [Other-IDs] NLM/ PMC2796610
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66. Fahmi T, Esendagli G, Yilmaz G, Kansu E, Guc D: Immune compartmentalization of T cell subsets in chemically-induced breast cancer. Scand J Immunol; 2010 Oct;72(4):339-48
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  • [Title] Immune compartmentalization of T cell subsets in chemically-induced breast cancer.
  • In cancer, the phenotype and/or the function of T cells may differ according to their distribution through immune-associated tissues, namely immune compartments.
  • Here, in N-methyl-N-nitrosourea (MNU)-induced mammary carcinomas of rat as a relevant model for human breast tumors, the impact of tumor burden on the T cell subsets populating the tumor microenvironment, the tumor-adjacent and -opposite mammary lymph nodes, and the spleen was assessed.
  • The selective presence of Tregs in the mammary tumors but not in neighboring-mammary tissue was also confirmed by the expression of Treg-associated genes.
  • The percentage of CD161(+) NKT cells was also significantly increased especially in the tumors and mammary lymph nodes.
  • Hence, the differential distribution of T cell subsets through the spleen, the mammary lymph nodes and the tumor mass in MNU-induced mammary tumor-bearing animals may contribute to a tumor-associated immunosuppression.
  • [MeSH-major] Lymph Nodes / immunology. Mammary Neoplasms, Experimental / immunology. Spleen / immunology. T-Lymphocyte Subsets / immunology
  • [MeSH-minor] Animals. Antigens, CD3 / metabolism. Female. Flow Cytometry. Forkhead Transcription Factors / genetics. Forkhead Transcription Factors / metabolism. Gene Expression Regulation, Neoplastic. Interleukin-10 / genetics. Interleukin-10 / metabolism. Mammary Glands, Animal / immunology. Mammary Glands, Animal / metabolism. Mammary Glands, Animal / pathology. Methylnitrosourea. Natural Killer T-Cells / immunology. Natural Killer T-Cells / metabolism. Rats. Rats, Sprague-Dawley. T-Lymphocytes / immunology. T-Lymphocytes / metabolism. T-Lymphocytes, Cytotoxic / immunology. T-Lymphocytes, Cytotoxic / metabolism. T-Lymphocytes, Regulatory / immunology. T-Lymphocytes, Regulatory / metabolism. Transforming Growth Factor beta / genetics. Transforming Growth Factor beta / metabolism

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  • [Copyright] © 2010 The Authors. Scandinavian Journal of Immunology © 2010 Blackwell Publishing Ltd.
  • (PMID = 20883319.001).
  • [ISSN] 1365-3083
  • [Journal-full-title] Scandinavian journal of immunology
  • [ISO-abbreviation] Scand. J. Immunol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Antigens, CD3; 0 / FOXP3 protein, human; 0 / Forkhead Transcription Factors; 0 / Foxp3 protein, rat; 0 / Transforming Growth Factor beta; 130068-27-8 / Interleukin-10; 684-93-5 / Methylnitrosourea
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67. 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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68. 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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69. Zander SA, Kersbergen A, van der Burg E, de Water N, van Tellingen O, Gunnarsdottir S, Jaspers JE, Pajic M, Nygren AO, Jonkers J, Borst P, Rottenberg S: Sensitivity and acquired resistance of BRCA1;p53-deficient mouse mammary tumors to the topoisomerase I inhibitor topotecan. Cancer Res; 2010 Feb 15;70(4):1700-10
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  • [Title] Sensitivity and acquired resistance of BRCA1;p53-deficient mouse mammary tumors to the topoisomerase I inhibitor topotecan.
  • There is no tailored therapy yet for human basal-like mammary carcinomas.
  • We have evaluated this putative synthetic lethality in a genetically engineered mouse model for BRCA1-associated breast cancer, using the topoisomerase I (Top1) poison topotecan as monotherapy and in combination with poly(ADP-ribose) polymerase inhibition by olaparib.
  • [MeSH-major] Carcinoma / drug therapy. Drug Resistance, Neoplasm / genetics. Genes, BRCA1 / physiology. Genes, p53 / physiology. Mammary Neoplasms, Animal / drug therapy. Topotecan / therapeutic use


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. Dullin C, Zientkowska M, Napp J, Missbach-Guentner J, Krell HW, Müller F, Grabbe E, Tietze LF, Alves F: Semiautomatic landmark-based two-dimensional-three-dimensional image fusion in living mice: correlation of near-infrared fluorescence imaging of Cy5.5-labeled antibodies with flat-panel volume computed tomography. Mol Imaging; 2009 Jan-Feb;8(1):2-14
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  • We developed an algorithm to colocalize fluorescence signals of NIRF-labeled antibodies directed against matriptase and urokinase plasminogen activator receptor (uPAR) to orthotopic carcinomas in mice visualized by fpVCT.
  • For this purpose, mice were anesthetized and fixed on a multimodality animal bed containing fiducial markers filled with iodine-containing contrast agent and fluorescent dye.
  • Binding of Cy5.5-labeled matriptase-specific antibody to pancreatic tumors and Cy5.5-labeled uPAR-specific antibody to mammary carcinomas was assessed by time-domain NIRF imaging measuring the location of fluorescence intensity and its lifetime.
  • [MeSH-minor] Animals. Automation / methods. Carcinoma / diagnosis. Carcinoma / pathology. Feasibility Studies. Female. Fluorescent Antibody Technique / methods. Humans. Male. Mammary Neoplasms, Experimental / diagnosis. Mammary Neoplasms, Experimental / pathology. Mice. Mice, Nude. Mice, SCID. Spectrometry, Fluorescence / methods. Spectroscopy, Near-Infrared / methods. Tumor Cells, Cultured. Xenograft Model Antitumor Assays / instrumentation. Xenograft Model Antitumor Assays / methods

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  • (PMID = 19344571.001).
  • [ISSN] 1535-3508
  • [Journal-full-title] Molecular imaging
  • [ISO-abbreviation] Mol Imaging
  • [Language] eng
  • [Publication-type] Evaluation Studies; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antibodies; 0 / CY5.5 cyanine dye; 0 / Carbocyanines
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72. Wakshlag JJ, McNeill CJ, Antonyak MA, Boehm JE, Fuji R, Balkman CE, Zgola M, Cerione RA, Page RL: Expression and activity of transglutaminase II in spontaneous tumours of dogs and cats. J Comp Pathol; 2006 Feb-Apr;134(2-3):202-10
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  • Bladder, liver and adrenal gland exhibited prominent expression of TGase II while other tissues, including mammary gland, displayed limited expression and activity.
  • Normal mammary tissue and that showing benign hyperplasia did not express TGase II.
  • However, 11/25 (44%) of canine mammary carcinomas and 10/12 (83%) of feline mammary carcinomas strongly expressed TGase II in either a stromal, cellular or combined pattern.
  • The pattern of expression was not related to the classification of mammary carcinoma (solid, tubulopapillary, complex or anaplastic), except that two anaplastic canine mammary carcinomas showed prominent TGase II expression.
  • Two canine mammary carcinoma cell lines showed prominent TGase expression, and when the TGase activity was inhibited, the cells became more sensitive to doxorubicin-induced cell death.
  • Thus, TGase II was significantly expressed in mammary cancers from dogs and cats and immunoreactivity of TGase II was similar to that reported in humans beings.
  • The pro-survival effect of TGase II in canine mammary carcinoma cell lines was similar to that previously reported in humans patients.
  • [MeSH-major] Carcinoma / veterinary. GTP-Binding Proteins / metabolism. Mammary Glands, Animal / enzymology. Mammary Neoplasms, Animal / enzymology. Transglutaminases / metabolism

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  • (PMID = 16615935.001).
  • [ISSN] 0021-9975
  • [Journal-full-title] Journal of comparative pathology
  • [ISO-abbreviation] J. Comp. Pathol.
  • [Language] eng
  • [Grant] United States / NIGMS NIH HHS / GM / GM61762
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 80168379AG / Doxorubicin; EC 2.3.2.- / transglutaminase 2; EC 2.3.2.13 / Transglutaminases; EC 3.6.1.- / GTP-Binding Proteins
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73. 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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74. Bergmann S, Royer-Pokora B, Fietze E, Jürchott K, Hildebrandt B, Trost D, Leenders F, Claude JC, Theuring F, Bargou R, Dietel M, Royer HD: YB-1 provokes breast cancer through the induction of chromosomal instability that emerges from mitotic failure and centrosome amplification. Cancer Res; 2005 May 15;65(10):4078-87
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  • [Title] YB-1 provokes breast cancer through the induction of chromosomal instability that emerges from mitotic failure and centrosome amplification.
  • In this study, we show in a novel transgenic mouse model that human hemagglutinin-tagged YB-1 provokes remarkably diverse breast carcinomas through the induction of genetic instability that emerges from mitotic failure and centrosome amplification.
  • The increase of centrosome numbers proceeds during breast cancer development and explanted tumor cell cultures show the phenotype of ongoing numerical chromosomal instability.
  • These data illustrate a mechanism that might contribute to human breast cancer development.
  • [MeSH-major] Breast Neoplasms / genetics. Cell Transformation, Neoplastic / genetics. Centrosome / physiology. DNA-Binding Proteins / genetics. Mammary Neoplasms, Experimental / genetics
  • [MeSH-minor] Animals. Chromosomal Instability. Disease Models, Animal. Female. Gene Amplification. Humans. Mice. Mice, Transgenic. Nuclear Proteins. Y-Box-Binding Protein 1


75. de Moura NA, Grassi TF, Rodrigues MA, Barbisan LF: Potential effects of the herbicide Diuron on mammary and urinary bladder two-stage carcinogenesis in a female Swiss mouse model. Arch Toxicol; 2010 Feb;84(2):165-73
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  • [Title] Potential effects of the herbicide Diuron on mammary and urinary bladder two-stage carcinogenesis in a female Swiss mouse model.
  • The potential promoting effect of Diuron was investigated in a mouse model of mammary and urinary bladder carcinogenesis induced by 7,12-dimethylbenz(a)anthracene (DMBA) and N-butyl-N-(4-hydroxybutyl)nitrosamine (BBN).
  • Mammary glands and urinary bladder were processed for histopathological analysis.
  • Two transitional cell carcinomas were observed in the group initiated and fed Diuron 2,500 ppm (G3).
  • In contrast, in the mammary gland, Diuron feeding for 13 weeks did not significantly alter cell proliferation and apoptosis indexes or the incidence of hyperplastic lesions or neoplasms in the DMBA/BBN-initiated groups.
  • These findings suggest that Diuron is a promoting agent to the urinary bladder but not to the mammary gland in female Swiss mice submitted to a medium-term two-stage carcinogenesis bioassay.
  • [MeSH-major] Diuron / pharmacology. Herbicides / pharmacology. Mammary Glands, Animal / metabolism. Urinary Bladder Neoplasms / chemically induced
  • [MeSH-minor] 9,10-Dimethyl-1,2-benzanthracene / toxicity. Animals. Butylhydroxybutylnitrosamine / toxicity. Carcinogens / toxicity. Disease Models, Animal. Dose-Response Relationship, Drug. Female. Immunohistochemistry. Mice. Random Allocation

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  • (PMID = 19902181.001).
  • [ISSN] 1432-0738
  • [Journal-full-title] Archives of toxicology
  • [ISO-abbreviation] Arch. Toxicol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Germany
  • [Chemical-registry-number] 0 / Carcinogens; 0 / Herbicides; 3817-11-6 / Butylhydroxybutylnitrosamine; 57-97-6 / 9,10-Dimethyl-1,2-benzanthracene; 9I3SDS92WY / Diuron
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76. Vazquez-Martin A, Oliveras-Ferraros C, Menendez JA: The antidiabetic drug metformin suppresses HER2 (erbB-2) oncoprotein overexpression via inhibition of the mTOR effector p70S6K1 in human breast carcinoma cells. Cell Cycle; 2009 Jan 1;8(1):88-96
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  • [Title] The antidiabetic drug metformin suppresses HER2 (erbB-2) oncoprotein overexpression via inhibition of the mTOR effector p70S6K1 in human breast carcinoma cells.
  • Population studies have revealed that treatment with the antidiabetic drug metformin significantly associates with reduced breast cancer risk.
  • Animal studies have shown that metformin suppresses the development of mammary carcinomas in transgenic female mice carrying a HER2 oncogene, but not that of spontaneous tumors.
  • We herein demonstrate that HER2 oncoprotein itself may represent a key cellular target involved in the anti-breast cancer actions of metformin.
  • First, ectopical overexpression of HER2 oncogene significantly enhances metformin-induced breast cancer cell growth inhibition.
  • HER2-positive breast cancer cells transfected with p70S6K1 siRNA become completely refractory to metformin-induced HER2 suppression.
  • From the perspective of chemoprevention, these findings altogether suggest that metformin might exert a protective mostly confined to the HER2-positive breast cancer subtype.
  • From the perspective of intervention, the presence/absence of molecular hallmarks such as HER2 overexpression and/or p70S6K1 hyperactivation might dictate alternative responses in metformin-based treatment of early breast cancer.
  • The importance of mTOR/p70S6K1-sensed ROS status at mediating the anti-oncogenic effects of metformin might represent a previously unrecognized linkage molecularly connecting its anti-aging and anti-cancer actions.


77. 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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78. 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
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  • [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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79. Rokicki J, Das PM, Giltnane JM, Wansbury O, Rimm DL, Howard BA, Jones FE: The ERalpha coactivator, HER4/4ICD, regulates progesterone receptor expression in normal and malignant breast epithelium. Mol Cancer; 2010 Jun 15;9:150
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  • The HER4 intracellular domain (4ICD) is a potent estrogen receptor (ERalpha) coactivator with activities in breast cancer and the developing mammary gland that appear to overlap with progesterone receptor (PgR).
  • Here we investigated the possibility that the 4ICD coactivator regulates PgR expression thereby providing a mechanistic explanation for their partially overlapping activities in breast cancer.
  • In the mouse mammary gland estrogen regulates expression of PgR-A whereas expression of PgR-B is estrogen independent.
  • Consistent with a role for 4ICD in estrogen regulated PgR expression in vivo, PgR-A, but not PgR-B, expression was abolished in HER4-null mouse mammary glands during pregnancy.
  • Coexpression of PgR and 4ICD is also commonly observed in ERalpha positive breast carcinomas.
  • We propose that direct coupling of these signaling pathways may have important implications for mammary development, breast carcinogenesis, and patient response to endocrine therapy.

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  • (PMID = 20550710.001).
  • [ISSN] 1476-4598
  • [Journal-full-title] Molecular cancer
  • [ISO-abbreviation] Mol. Cancer
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / R01CA095783; United States / NCI NIH HHS / CA / R01CA096717
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Estrogen Receptor alpha; 0 / Receptors, Progesterone; EC 2.7.10.1 / ERBB4 protein, human; EC 2.7.10.1 / Erbb4 protein, mouse; EC 2.7.10.1 / Receptor, Epidermal Growth Factor; EC 2.7.10.1 / Receptor, ErbB-4
  • [Other-IDs] NLM/ PMC2894764
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80. Wechselberger C, Strizzi L, Kenney N, Hirota M, Sun Y, Ebert A, Orozco O, Bianco C, Khan NI, Wallace-Jones B, Normanno N, Adkins H, Sanicola M, Salomon DS: Human Cripto-1 overexpression in the mouse mammary gland results in the development of hyperplasia and adenocarcinoma. Oncogene; 2005 Jun 9;24(25):4094-105
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  • [Title] Human Cripto-1 overexpression in the mouse mammary gland results in the development of hyperplasia and adenocarcinoma.
  • Human Cripto-1 (CR-1) is overexpressed in approximately 80% of human breast, colon and lung carcinomas.
  • Mouse Cr-1 upregulation is also observed in a number of transgenic (Tg) mouse mammary tumors.
  • To determine whether CR-1 can alter mammary gland development and/or may contribute to tumorigenesis in vivo, we have generated Tg mouse lines that express human CR-1 under the transcriptional control of the mouse mammary tumor virus (MMTV).
  • Virgin female MMTV/CR-1 Tg mice exhibited enhanced ductal branching, dilated ducts, intraductal hyperplasia, hyperplastic alveolar nodules and condensation of the mammary stroma.
  • The long latency period suggests that additional genetic alterations are required to facilitate mammary tumor formation in conjunction with CR-1.
  • [MeSH-major] Adenocarcinoma / genetics. Epidermal Growth Factor / genetics. Mammary Glands, Animal / pathology. Mammary Neoplasms, Animal / genetics. Membrane Glycoproteins / genetics. Neoplasm Proteins / genetics

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  • (PMID = 15897912.001).
  • [ISSN] 0950-9232
  • [Journal-full-title] Oncogene
  • [ISO-abbreviation] Oncogene
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / DNA Primers; 0 / DNA, Complementary; 0 / GPI-Linked Proteins; 0 / Growth Substances; 0 / Intercellular Signaling Peptides and Proteins; 0 / Membrane Glycoproteins; 0 / Neoplasm Proteins; 0 / TDGF1 protein, human; 62229-50-9 / Epidermal Growth Factor
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81. 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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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [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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82. 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
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  • [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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83. Toxicology and carcinogenesis studies of androstenedione (CAS No. 63-05-8) in F344/N rats and B6C3F1 mice (gavage studies). Natl Toxicol Program Tech Rep Ser; 2010 Sep;(560):1, 7-31,33-171 passim
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  • Incidences of alveolar/bronchiolar adenoma and alveolar/bronchiolar adenoma or carcinoma (combined) were significantly increased in 20 mg/kg males.
  • In females, the incidences of mammary gland fibroadenoma were significantly decreased in the 20 and 50 mg/kg groups, the incidences of mammary gland hyperplasia were significantly decreased in all dosed groups, and the incidences of mammary gland cyst were significantly decreased in the 10 and 50 mg/kg groups.
  • In females, the incidences of hepatocellular carcinoma were significantly increased in all dosed groups.
  • Incidences of hepatocellular adenoma or carcinoma (combined) in males and females were significantly increased in the 50 mg/kg groups.
  • Incidences of multiple hepatocellular adenomas and carcinomas were significantly increased in 10 and 50 mg/kg males, and there was an increased incidence of multiple hepatocellular adenomas in 50 mg/kg females.
  • CONCLUSIONS: under the conditions of these 2-year gavage studies, there was equivocal evidence of carcinogenic activity of androstenedione in male F344/N rats based on increased incidences of alveolar/bronchiolar adenoma and alveolar/bronchiolar adenoma or carcinoma (combined).
  • There was clear evidence of carcinogenic activity of androstenedione in male B6C3F1 mice based on increased incidences of multiple hepatocellular adenoma and hepatocellular carcinoma and increased incidence of hepatoblastoma.
  • There was clear evidence of carcinogenic activity of androstenedione in female B6C3F1 mice based on increased incidences of hepatocellular adenoma and hepatocellular carcinoma.
  • Decreases in the incidences of testicular interstitial cell adenoma in male rats, mammary gland fibroadenoma, cysts, and hyperplasia in female rats, and malignant lymphoma in female mice were considered related to androstenedione administration.
  • [MeSH-minor] Animal Feed. Animals. Biomarkers. Body Weight / drug effects. Carcinogenicity Tests. Chemistry, Pharmaceutical. Dose-Response Relationship, Drug. Drug-Induced Liver Injury / metabolism. Drug-Induced Liver Injury / pathology. Estrous Cycle. Female. Genitalia / drug effects. Intubation, Gastrointestinal. Male. Mice. Mice, Inbred Strains. Micronucleus Tests. Mutagens / toxicity. Organ Size / drug effects. Rats. Rats, Inbred F344

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  • (PMID = 21037592.001).
  • [ISSN] 0888-8051
  • [Journal-full-title] National Toxicology Program technical report series
  • [ISO-abbreviation] Natl Toxicol Program Tech Rep Ser
  • [Language] eng
  • [Publication-type] Journal Article; Review; Technical Report
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Biomarkers; 0 / Mutagens; 409J2J96VR / Androstenedione
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84. 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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85. 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
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  • [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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86. 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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87. McNeill CJ, Sorenmo KU, Shofer FS, Gibeon L, Durham AC, Barber LG, Baez JL, Overley B: Evaluation of adjuvant doxorubicin-based chemotherapy for the treatment of feline mammary carcinoma. J Vet Intern Med; 2009 Jan-Feb;23(1):123-9
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  • [Title] Evaluation of adjuvant doxorubicin-based chemotherapy for the treatment of feline mammary carcinoma.
  • BACKGROUND: Feline mammary carcinomas (FMC) are locally invasive and highly metastatic tumors.

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  • (PMID = 19175730.001).
  • [ISSN] 0891-6640
  • [Journal-full-title] Journal of veterinary internal medicine
  • [ISO-abbreviation] J. Vet. Intern. Med.
  • [Language] ENG
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 80168379AG / Doxorubicin; 8N3DW7272P / Cyclophosphamide
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88. Pedersen TX, Pennington CJ, Almholt K, Christensen IJ, Nielsen BS, Edwards DR, Rømer J, Danø K, Johnsen M: Extracellular protease mRNAs are predominantly expressed in the stromal areas of microdissected mouse breast carcinomas. Carcinogenesis; 2005 Jul;26(7):1233-40
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  • [Title] Extracellular protease mRNAs are predominantly expressed in the stromal areas of microdissected mouse breast carcinomas.
  • Based on qualitative in situ hybridization studies in human cancer tissue, a range of components involved in proteolysis appear to be expressed by stromal cells rather than cancer cells.
  • We have now used laser capture microdissection and real-time PCR to quantify the mRNA expression of components of matrix-degrading proteolytic systems in cancer and stromal areas of mouse mammary tumors genetically induced by the polyoma virus middle T (PyMT) antigen.
  • Statistical analyses indicated that the quantitative expression patterns observed in cancer and stromal cells isolated from individual tumors from different PyMT mice are quite reproducible.
  • The methodology described in this study provides excellent tools to study the possible interactions between cancer and stromal cells during the development of breast cancer, and the results suggest that stromal cells are involved in carcinogenesis and tumor progression, which may have important implications for the biology and therapy of cancer.
  • [MeSH-major] Carcinoma / genetics. Mammary Neoplasms, Animal / genetics. Peptide Hydrolases / biosynthesis

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  • (PMID = 15760918.001).
  • [ISSN] 0143-3334
  • [Journal-full-title] Carcinogenesis
  • [ISO-abbreviation] Carcinogenesis
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / RNA, Messenger; EC 3.4.- / Peptide Hydrolases
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89.