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The effect of antineoplastic drugs in a male spontaneous mammary tumor model
Male breast cancer is a rare disease. The limited number of clinical cases has led to the primary treatments for men being derived from female breast cancer studies. Here the transgenic strain FVB/N-Tg(MMTV-PyVT)634Mul/J (also known as PyVT) was used as a model system for measuring tumor burden and...
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Published in: | PloS one 2013-06, Vol.8 (6), p.e64866-e64866 |
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description | Male breast cancer is a rare disease. The limited number of clinical cases has led to the primary treatments for men being derived from female breast cancer studies. Here the transgenic strain FVB/N-Tg(MMTV-PyVT)634Mul/J (also known as PyVT) was used as a model system for measuring tumor burden and drug sensitivity of the antineoplastic drugs tamoxifen, cisplatin, and paclitaxel on tumorigenesis at an early stage of mammary carcinoma development in a male mouse model. Cisplatin treatment significantly reduced tumor volume, while paclitaxel and tamoxifen did not attenuate tumor growth. Cisplatin treatment was shown to induce apoptosis, grossly observed by reduced tumor formation, through reduced Bcl-2 and survivin protein expression levels with an increase in caspase 3 expression compared to control tumors. Tamoxifen treatment significantly altered the hormone receptor expression levels of the tumor, while additionally upregulating Bcl-2 and Cyclin D1. This suggests an importance in hormonal signaling in male breast cancer pathogenesis. The results of this study provide valuable information toward the better understanding of male breast cancer and may help guide treatment decisions. |
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The limited number of clinical cases has led to the primary treatments for men being derived from female breast cancer studies. Here the transgenic strain FVB/N-Tg(MMTV-PyVT)634Mul/J (also known as PyVT) was used as a model system for measuring tumor burden and drug sensitivity of the antineoplastic drugs tamoxifen, cisplatin, and paclitaxel on tumorigenesis at an early stage of mammary carcinoma development in a male mouse model. Cisplatin treatment significantly reduced tumor volume, while paclitaxel and tamoxifen did not attenuate tumor growth. Cisplatin treatment was shown to induce apoptosis, grossly observed by reduced tumor formation, through reduced Bcl-2 and survivin protein expression levels with an increase in caspase 3 expression compared to control tumors. Tamoxifen treatment significantly altered the hormone receptor expression levels of the tumor, while additionally upregulating Bcl-2 and Cyclin D1. This suggests an importance in hormonal signaling in male breast cancer pathogenesis. The results of this study provide valuable information toward the better understanding of male breast cancer and may help guide treatment decisions.</description><identifier>ISSN: 1932-6203</identifier><identifier>EISSN: 1932-6203</identifier><identifier>DOI: 10.1371/journal.pone.0064866</identifier><identifier>PMID: 23755153</identifier><language>eng</language><publisher>United States: Public Library of Science</publisher><subject>Animals ; Antineoplastic agents ; Antineoplastic Agents - pharmacology ; Antineoplastic Agents - therapeutic use ; Antineoplastic drugs ; Apoptosis ; Bcl-2 protein ; Biology ; Biomarkers, Tumor - metabolism ; Breast cancer ; Cancer ; Carcinoma ; Caspase ; Caspase-3 ; Cell Proliferation - drug effects ; Cisplatin ; Cisplatin - pharmacology ; Cisplatin - therapeutic use ; Complications and side effects ; Cyclin D1 ; Disease control ; Disease Models, Animal ; Dosage and administration ; Drug therapy ; Drugs ; Estrogens ; Female ; Male ; Mammary gland ; Mammary Neoplasms, Experimental - drug therapy ; Mammary Neoplasms, Experimental - pathology ; Medicine ; Mens health ; Mice, Transgenic ; Mutation ; Neoplasm Proteins - metabolism ; Paclitaxel ; Paclitaxel - pharmacology ; Paclitaxel - therapeutic use ; Pathogenesis ; Phenotype ; Rare diseases ; Receptors, Estrogen - metabolism ; Receptors, Progesterone - metabolism ; Signaling ; Survivin ; Tamoxifen ; Tumorigenesis ; Tumors ; Veterinary colleges</subject><ispartof>PloS one, 2013-06, Vol.8 (6), p.e64866-e64866</ispartof><rights>COPYRIGHT 2013 Public Library of Science</rights><rights>2013 Shishido et al. 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The limited number of clinical cases has led to the primary treatments for men being derived from female breast cancer studies. Here the transgenic strain FVB/N-Tg(MMTV-PyVT)634Mul/J (also known as PyVT) was used as a model system for measuring tumor burden and drug sensitivity of the antineoplastic drugs tamoxifen, cisplatin, and paclitaxel on tumorigenesis at an early stage of mammary carcinoma development in a male mouse model. Cisplatin treatment significantly reduced tumor volume, while paclitaxel and tamoxifen did not attenuate tumor growth. Cisplatin treatment was shown to induce apoptosis, grossly observed by reduced tumor formation, through reduced Bcl-2 and survivin protein expression levels with an increase in caspase 3 expression compared to control tumors. Tamoxifen treatment significantly altered the hormone receptor expression levels of the tumor, while additionally upregulating Bcl-2 and Cyclin D1. This suggests an importance in hormonal signaling in male breast cancer pathogenesis. The results of this study provide valuable information toward the better understanding of male breast cancer and may help guide treatment decisions.</description><subject>Animals</subject><subject>Antineoplastic agents</subject><subject>Antineoplastic Agents - pharmacology</subject><subject>Antineoplastic Agents - therapeutic use</subject><subject>Antineoplastic drugs</subject><subject>Apoptosis</subject><subject>Bcl-2 protein</subject><subject>Biology</subject><subject>Biomarkers, Tumor - metabolism</subject><subject>Breast cancer</subject><subject>Cancer</subject><subject>Carcinoma</subject><subject>Caspase</subject><subject>Caspase-3</subject><subject>Cell Proliferation - drug effects</subject><subject>Cisplatin</subject><subject>Cisplatin - pharmacology</subject><subject>Cisplatin - therapeutic use</subject><subject>Complications and side effects</subject><subject>Cyclin D1</subject><subject>Disease control</subject><subject>Disease Models, Animal</subject><subject>Dosage and administration</subject><subject>Drug therapy</subject><subject>Drugs</subject><subject>Estrogens</subject><subject>Female</subject><subject>Male</subject><subject>Mammary gland</subject><subject>Mammary Neoplasms, Experimental - 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The limited number of clinical cases has led to the primary treatments for men being derived from female breast cancer studies. Here the transgenic strain FVB/N-Tg(MMTV-PyVT)634Mul/J (also known as PyVT) was used as a model system for measuring tumor burden and drug sensitivity of the antineoplastic drugs tamoxifen, cisplatin, and paclitaxel on tumorigenesis at an early stage of mammary carcinoma development in a male mouse model. Cisplatin treatment significantly reduced tumor volume, while paclitaxel and tamoxifen did not attenuate tumor growth. Cisplatin treatment was shown to induce apoptosis, grossly observed by reduced tumor formation, through reduced Bcl-2 and survivin protein expression levels with an increase in caspase 3 expression compared to control tumors. Tamoxifen treatment significantly altered the hormone receptor expression levels of the tumor, while additionally upregulating Bcl-2 and Cyclin D1. This suggests an importance in hormonal signaling in male breast cancer pathogenesis. The results of this study provide valuable information toward the better understanding of male breast cancer and may help guide treatment decisions.</abstract><cop>United States</cop><pub>Public Library of Science</pub><pmid>23755153</pmid><doi>10.1371/journal.pone.0064866</doi><tpages>e64866</tpages><oa>free_for_read</oa></addata></record> |
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subjects | Animals Antineoplastic agents Antineoplastic Agents - pharmacology Antineoplastic Agents - therapeutic use Antineoplastic drugs Apoptosis Bcl-2 protein Biology Biomarkers, Tumor - metabolism Breast cancer Cancer Carcinoma Caspase Caspase-3 Cell Proliferation - drug effects Cisplatin Cisplatin - pharmacology Cisplatin - therapeutic use Complications and side effects Cyclin D1 Disease control Disease Models, Animal Dosage and administration Drug therapy Drugs Estrogens Female Male Mammary gland Mammary Neoplasms, Experimental - drug therapy Mammary Neoplasms, Experimental - pathology Medicine Mens health Mice, Transgenic Mutation Neoplasm Proteins - metabolism Paclitaxel Paclitaxel - pharmacology Paclitaxel - therapeutic use Pathogenesis Phenotype Rare diseases Receptors, Estrogen - metabolism Receptors, Progesterone - metabolism Signaling Survivin Tamoxifen Tumorigenesis Tumors Veterinary colleges |
title | The effect of antineoplastic drugs in a male spontaneous mammary tumor model |
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