报告地点：闵行生科院534报告厅

报告人简介：Dr. Peter K. Vogt于德国图宾根大学（University of Tübingen）获得博士学位，美国加州大学伯克利分校博士后（UC Berkeley）。先后任职于科罗拉多大学医学院University of Colorado School of Medicine（助理教授），华盛顿大学医学院University of Washington School of Medicine（副教授）， 南加州大学University of South California（教授，系主任）。现为美国The Scripps Research Institute教授，执行副所长。Dr. Vogt 对病毒致癌基因的研究为其赢获得了无数的奖励，为美国国立卫生研究院（NIH）多项Study Section的主席，美国微生物和癌症研究界多种协会的主席。并当选为美国科学院（1980）和美国艺术与科学学院（2004）双院院士，德国科学院院士（1998）。2013年被聘为中国科学院爱因斯坦讲席教授。

报告摘要：Current sequencing techniques have uncovered an abundance of genetic changes in cancer cells. Even after most of these changes are discounted as insignificant bystanders, there still remain numerous mutations of potential significance for the oncogenic phenotype. This multiplicity has given rise to the suggestion that the role of individual mutations must be marginal and hence that there are no real dominant driver mutations. The fact that the 1047 mutation in p110α, a single nucleotide substitution, can induce deep changes in RNA and protein profiles and can reproduce a large proportion of the expression signature of basal breast cancer challenges this conclusion. It is clear that there are mutations, even single point mutations, that can push the cell far into the oncogenic phenotype. This is encouraging news for the development of PI3K-based therapy. PI3K can be a potent and perhaps dominant cancer driver, and shutting this force down is bound to have significant beneficial effects in the clinic.