"Receiving The Sontag Foundation Distinguished Scientist Award will provide me with the preparation and resources to conduct innovative research and will be instrumental in enabling me to achieve my career objective of improving the outcome of patients with gliomas."

- Dr. Tim Chan

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Academic Appointments

  • Associate Member, Human Oncology and Pathogenesis Program, Memorial Sloan-Kettering Cancer Center, September 2012 – present
  • Associate Professor, Gerstner-Sloan Kettering Graduate School of Biomedical Sciences, MSKCC, September 2012 –
    present
  • Associate Professor, Department of Cell and Developmental Biology, Weill Cornell School of Medicine, September 2012 – present
  • Vice Chair, Department of Radiation Oncology; Director, Translational Oncology Division; PaineWebber Chair in Cancer Genetics, MSKCC

About DSA-Funded Research

Glioblastoma is a malignancy of the central nervous system that is fatal. Despite progress in understanding the disease and in improving treatments, little progress has been made in increasing the survival rates of patients with this cancer. Currently, despite treatment with surgery, radiation, and chemotherapy, the average survival of GBM patient remains 12-15 months. Understanding the alterations that ultimately drive GBM development and progression is required if we are to improve outcomes of GBM patients. Recently, we have identified the PTPRD tumor suppressor as very frequently altered tumor suppressor in GBM (>50%). PTPRD is mutated or lost in a large number of gliomas as well as in a number of other human tumor types. Loss or mutation of the gene results in enhanced tumor cell growth. Our work also showed that PTPRD normally inactivates STAT3, a protein that is a master regulator of GBM aggressiveness. The mechanistic details of how PTPRD exerts its tumor suppressive effects and its role in GBM tumorigenesis is currently unknown. Our proposal here seeks to achieve a detailed understanding of the molecular mechanisms underlying the PTPRD/STAT3 axis and determine the effects PTPRD inactivation (and hence STAT3 activation) on clinical outcomes and the STAT3 transcriptional network. Furthermore, we propose to evaluate the efficacy of targeting the PTPRD/STAT3 axis as a novel approach to treat GBMs. Should this work succeed, we envision great utility for understanding the biology of gliomas and for enhancing clinical management of brain tumor patients.

Accolades

"Tim is an absolute wizard at applying sophisticated molecular genetics techniques to the evaluation of cell biological problems."

Bert Vogelstein, M.D.
Ludwig Center, Johns Hopkins

"Tim is off to an impressive start with two significant discoveries that should form the basis for his lab focus over the coming years."

Charles L. Sawyers, M.D..
Memorial Sloan-Kettering Cancer Center
Howard Hughes Medical Institute

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