Physiological Levels of Pik3caH1047R Mutation in the Mouse Mammary Gland Results in Ductal Hyperplasia and Formation of ERα-Positive Tumors
PIK3CA, the gene coding for the p110α subunit of phosphoinositide 3-kinase, is frequently mutated in a variety of human tumors including breast cancers. To better understand the role of mutant PIK3CA in the initiation and/or progression of breast cancer, we have generated mice with a conditional kno...
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| Veröffentlicht in: | PloS one 2012-05, Vol.7 (5), p.e36924 |
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| description | PIK3CA, the gene coding for the p110α subunit of phosphoinositide 3-kinase, is frequently mutated in a variety of human tumors including breast cancers. To better understand the role of mutant PIK3CA in the initiation and/or progression of breast cancer, we have generated mice with a conditional knock-in of the common activating mutation, Pik3caH1047R, into one allele of the endogenous gene in the mammary gland. These mice developed a ductal anaplasia and hyperplasia by 6 weeks of age characterized by multi-layering of the epithelial lining of the mammary ducts and expansion of the luminal progenitor (Lin−; CD29lo; CD24+; CD61+) cell population. The Pik3caH1047R expressing mice eventually develop mammary tumors with 100% penetrance but with a long latency (>12 months). This is significantly longer than has been reported for transgenic models where expression of the mutant Pik3ca is driven by an exogenous promoter. Histological analysis of the tumors formed revealed predominantly ERα-positive fibroadenomas, carcinosarcomas and sarcomas. In vitro induction of Pik3caH1047R in immortalized mammary epithelial cells also resulted in tumor formation when injected into the mammary fat pad of immunodeficient recipient mice. This novel model, which reproduces the scenario of a heterozygous somatic mutation occurring in the endogenous PIK3CA gene, will thus be a valuable tool for investigating the role of Pik3caH1047R mutation in mammary tumorigenesis both in vivo and in vitro. |
| doi_str_mv | 10.1371/journal.pone.0036924 |
| format | Article |
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To better understand the role of mutant PIK3CA in the initiation and/or progression of breast cancer, we have generated mice with a conditional knock-in of the common activating mutation, Pik3caH1047R, into one allele of the endogenous gene in the mammary gland. These mice developed a ductal anaplasia and hyperplasia by 6 weeks of age characterized by multi-layering of the epithelial lining of the mammary ducts and expansion of the luminal progenitor (Lin−; CD29lo; CD24+; CD61+) cell population. The Pik3caH1047R expressing mice eventually develop mammary tumors with 100% penetrance but with a long latency (>12 months). This is significantly longer than has been reported for transgenic models where expression of the mutant Pik3ca is driven by an exogenous promoter. Histological analysis of the tumors formed revealed predominantly ERα-positive fibroadenomas, carcinosarcomas and sarcomas. In vitro induction of Pik3caH1047R in immortalized mammary epithelial cells also resulted in tumor formation when injected into the mammary fat pad of immunodeficient recipient mice. This novel model, which reproduces the scenario of a heterozygous somatic mutation occurring in the endogenous PIK3CA gene, will thus be a valuable tool for investigating the role of Pik3caH1047R mutation in mammary tumorigenesis both in vivo and in vitro.</description><identifier>ISSN: 1932-6203</identifier><identifier>EISSN: 1932-6203</identifier><identifier>DOI: 10.1371/journal.pone.0036924</identifier><language>eng</language><publisher>San Francisco: Public Library of Science</publisher><subject>Animal models ; Animals ; Biochemistry ; Breast cancer ; Breasts ; Cancer ; Cell cycle ; Cell growth ; Ducts ; Epidermal growth factor ; Epithelial cells ; Hyperplasia ; Immunodeficiency ; In vivo methods and tests ; Kinases ; Laboratories ; Latency ; Localization ; Mammary gland ; Medical prognosis ; Mice ; Molecular biology ; Morphogenesis ; Mutation ; Oncology ; Pathology ; Physiology ; Proteins ; Rodents ; Transgenic ; Tumorigenesis ; Tumors</subject><ispartof>PloS one, 2012-05, Vol.7 (5), p.e36924</ispartof><rights>2012 Tikoo et al. This is an open-access article distributed under the terms of the Creative Commons Attribution License: https://creativecommons.org/licenses/by/4.0/ (the “License”), which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited. 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To better understand the role of mutant PIK3CA in the initiation and/or progression of breast cancer, we have generated mice with a conditional knock-in of the common activating mutation, Pik3caH1047R, into one allele of the endogenous gene in the mammary gland. These mice developed a ductal anaplasia and hyperplasia by 6 weeks of age characterized by multi-layering of the epithelial lining of the mammary ducts and expansion of the luminal progenitor (Lin−; CD29lo; CD24+; CD61+) cell population. The Pik3caH1047R expressing mice eventually develop mammary tumors with 100% penetrance but with a long latency (>12 months). This is significantly longer than has been reported for transgenic models where expression of the mutant Pik3ca is driven by an exogenous promoter. Histological analysis of the tumors formed revealed predominantly ERα-positive fibroadenomas, carcinosarcomas and sarcomas. In vitro induction of Pik3caH1047R in immortalized mammary epithelial cells also resulted in tumor formation when injected into the mammary fat pad of immunodeficient recipient mice. This novel model, which reproduces the scenario of a heterozygous somatic mutation occurring in the endogenous PIK3CA gene, will thus be a valuable tool for investigating the role of Pik3caH1047R mutation in mammary tumorigenesis both in vivo and in vitro.</description><subject>Animal models</subject><subject>Animals</subject><subject>Biochemistry</subject><subject>Breast cancer</subject><subject>Breasts</subject><subject>Cancer</subject><subject>Cell cycle</subject><subject>Cell growth</subject><subject>Ducts</subject><subject>Epidermal growth factor</subject><subject>Epithelial cells</subject><subject>Hyperplasia</subject><subject>Immunodeficiency</subject><subject>In vivo methods and tests</subject><subject>Kinases</subject><subject>Laboratories</subject><subject>Latency</subject><subject>Localization</subject><subject>Mammary gland</subject><subject>Medical prognosis</subject><subject>Mice</subject><subject>Molecular 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In vitro induction of Pik3caH1047R in immortalized mammary epithelial cells also resulted in tumor formation when injected into the mammary fat pad of immunodeficient recipient mice. This novel model, which reproduces the scenario of a heterozygous somatic mutation occurring in the endogenous PIK3CA gene, will thus be a valuable tool for investigating the role of Pik3caH1047R mutation in mammary tumorigenesis both in vivo and in vitro.</abstract><cop>San Francisco</cop><pub>Public Library of Science</pub><doi>10.1371/journal.pone.0036924</doi><oa>free_for_read</oa></addata></record> |
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| subjects | Animal models Animals Biochemistry Breast cancer Breasts Cancer Cell cycle Cell growth Ducts Epidermal growth factor Epithelial cells Hyperplasia Immunodeficiency In vivo methods and tests Kinases Laboratories Latency Localization Mammary gland Medical prognosis Mice Molecular biology Morphogenesis Mutation Oncology Pathology Physiology Proteins Rodents Transgenic Tumorigenesis Tumors |
| title | Physiological Levels of Pik3caH1047R Mutation in the Mouse Mammary Gland Results in Ductal Hyperplasia and Formation of ERα-Positive Tumors |
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