期刊
JOURNAL OF CLINICAL INVESTIGATION
卷 120, 期 8, 页码 2655-2658出版社
AMER SOC CLINICAL INVESTIGATION INC
DOI: 10.1172/JCI44026
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资金
- NCI NIH HHS [CA88843, R01 CA109274, P50 CA088843, CA109274, R55 CA109274] Funding Source: Medline
- NIGMS NIH HHS [T32 GM007814] Funding Source: Medline
Targeted cancer therapeutics can be effective when patients are preselected to maximize the chance of response. Increasingly, molecular markers such as oncogenic DNA mutations are being exploited to help guide patient pre-selection. These DNA lesions can predict for either a positive or negative response to a given drug. Finding such predictive biomarkers is an ongoing challenge. New work by Di Nicolantonio and colleagues in this issue of the JCI demonstrates that PI3K catalytic a subunit (PIK3CA) mutations can sensitize cancer cells to the mammalian target of rapamycin (mTOR) inhibitor everolimus. In addition, they show that the concurrent presence of PIK3CA mutations and mutations in either KRAS or BRAF predict for resistance to this drug. These data suggest that mTOR inhibitors currently in use will be ineffective against cancers that have a mutation in either KRAS or BRAF despite having PI3K/AKT/mTOR pathway activation.
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