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p53 and PTEN are two major tumor suppressors that keep cell growth in check (1). Loss of tumor suppressor activity through deletion or mutation contributes to many human tumors.Figure 1Lloyd TrotmanLloyd Trotman was lured from Zurich, Switzerland, to do his postdoctoral work with Pier Paolo Pandolfi at Sloan-Kettering in New York City. There, he and his colleagues found that loss of one allele of PTEN triggers cancer, whereas biallelic loss exposes cells to growth suppression by a senescence pathway mediated by p53, findings that contradict the classic two-hit model of tumor suppression (2, 3). He also showed that PTEN shuttles between the cytoplasm and nucleus (4)—odd behavior for a protein thought to act mainly at the plasma membrane.  Now directing his own research group at Cold Spring Harbor, Trotman is working to understand the relevance of PTEN nuclear localization to PTEN function and cancer and to grasp the importance of the p53 senescence pathway in human cancer. We called him to discuss how he tackles big questions and dogmatic concepts in biology.

Lloyd Trotman: Of mice and men, cancer, and PTEN