摘要

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.

  • 出版日期2013-6