Young cancer researchers rewarded.

generate truncated ETS proteins — rather than chimeric proteins — that are believed to drive prostate cancer development. Given the prevalence of prostate cancer (it accounts for approximately one-third of all cancer diagnoses in American men), researchers are seeking to determine whether TMPRSS2:ETS fusion genes provide an early detection diagnostic marker or a marker of aggressive disease. Others, including Chinnaiyan, are seeking to develop small-molecule inhibitors of the protein products of the TMPRSS2:ETS fusion genes in the hope that these will provide targeted prostate cancer therapeutics in the same way that imatinib, which inhibits the protein product of the BCR:ABL oncogenic fusion gene responsible for chronic myeloid leukemia (CML), is a targeted therapy for CML. Meyerson is being rewarded mainly for his work defining both the role of EGFR mutations in driving lung cancer and how these mutations determine a patient’s responsiveness to treatment with smallmolecule EGFR tyrosine kinase inhibitors such as erlotinib and gefitinib (4, 5). In 2003, the FDA approved gefitinib as a therapy for non–small cell lung cancer, despite the fact that only a small proportion of patients with the disease responded well to treatment and no one knew why. Two independent research groups, one headed by Meyerson, provided an answer to this conundrum in 2004: response to treatment with gefitinib correlated with the presence in the tumor tissue of somatic mutations in the EGFR gene (4, 6). These observations provided the underlying rationale for screening patients diagnosed with lung cancer for the presence of EGFR mutations, which is now standard in many clinics, in order to determine the most appropriate therapeutic intervention. Meyerson is now working on identifying and understanding other genetic alterations that drive lung cancer with the hope that additional personalized therapies can be developed for this disease, the most common cause of cancer-related death in both men and women. As a graduate student, Sabatini identified mammalian target of rapamycin (mTOR; ref. 7), inhibitors of which are now approved for the treatment of advanced renal cell carcinoma. Sabatini told the JCI that he “was drawn to studying the mechanism of action of rapamycin because it was clear back then that, whatever its target was, it would be interesting.” Ever since, he has worked on dissecting the molecular