作者: Amaury G. Dumont , Sarah N. Dumont , Jonathan C. Trent
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摘要: The phosphatidylinositol-3 kinase (PI3K) pathway regulates a number of cellular processes, including cell survival, growth, and cycle progression. Consequently, this is commonly deregulated in cancer. In particular, mutations the gene PIK3CA that encodes p110α catalytic subunit PI3K enzymes result proliferation resistance to apoptosis vitro induce breast tumors transgenic mice. These data underscore role during oncogenesis. Thus, an ongoing, large-scale effort underway develop clinically active drugs target elements pathway. However, conflicting suggest gain-of-function may be associated with either favorable or poor clinical outcome, compared wild-type gene. current study, we performed systematic review cancer studies. Upon evaluation 2587 cases from 12 independent studies, showed patients harboring mutation have better outcome than those Importantly, improved prognosis pertain only domain postmenopausal women estrogen receptor-positive We propose three potential explanations for paradoxical observation. First, interfere metastasis process senescence, which results mutated tumors. Secondly, speculate increase early tumor diagnosis by modification actin cytoskeleton cells. Lastly, predictive factor response hormonal therapy, giving therapeutic advantage these patients. Ultimately, understanding impact critical development optimally personalized therapeutics against other solid This will important prevent explain failures select who are most likely respond new therapies inhibit