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Mouse models of PIK3CA mutations: one mutation initiates heterogeneous mammary tumors

Journal

FEBS JOURNAL
Volume 280, Issue 12, Pages 2758-2765

Publisher

WILEY
DOI: 10.1111/febs.12175

Keywords

breast cancer; mammary tumors; mouse models; PI3K; PIK3CA

Funding

  1. Novartis Research Foundation
  2. European Research Council (ERC) [243211-PTPsBDC]
  3. Swiss Cancer League
  4. Krebsliga Beider Basel

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The phosphoinositide 3-kinase (PI3K) signaling pathway is crucial for cell growth, proliferation, metabolism, and survival, and is frequently deregulated in human cancer, including similar to 70% of breast tumors. PIK3CA, the gene encoding the catalytic subunit p110 of PI3K, is mutated in similar to 30% of breast cancers. However, the exact mechanism of PIK3CA-evoked breast tumorigenesis has not yet been defined. Genetically engineered mouse models are valuable for examining the initiation, development and progression of cancer. Transgenic mice harboring hotspot mutations in p110 have helped to elucidate breast cancer pathogenesis and increase our knowledge about molecular and cellular alterations invivo. They are also useful for the development of therapeutic strategies. Here, we describe current mouse models of mutant PIK3CA in the mammary gland, and discuss differences in tumor latency and pathogenesis.

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