Hailing Cheng

TL;DR: The potential of and challenges for the development of therapeutic agents that target this pathway in cancer are discussed and the potential and challenges in understanding of the PI3K pathway are highlighted.

TL;DR: Genomic analyses of recurrent tumors revealed multiple lesions, including focal amplification of Met or Myc, which suggest that c-MYC elevation represents a potential mechanism by which tumors develop resistance to current PI3K- targeting therapies.

TL;DR: It is reported that PIK3CA-knockout mouse embryonic fibroblasts are deficient in cellular signaling in response to various growth factors, unable to differentiate into adipocytes, and resistant to oncogenic transformation induced by a variety ofoncogenic receptor tyrosine kinases, indicating a fundamental role for p110α in these biological processes.

TL;DR: PIK3CAH1047R accelerates Her2-mediated breast epithelial transformation and metastatic progression, alters the intrinsic phenotype of HER2-overexpressing cancers, and generates resistance to approved combinations of anti-HER2 therapies.

TL;DR: It is shown that the serine-threonine kinase SIK1 (salt-inducible kinase 1) regulates p53-dependent anoikis, and the presence of functional Sik1 was required for the activity of the kinase LKB1 in promoting p 53- dependent ano Kikis and suppressing anchorage-independent growth, Matrigel invasion, and metastatic potential.