• Researcher Profile

    Kwok-Kin Wong, MD, PhD

    Scientific Director, Belfer Institute for Applied Cancer Science

    Professor of Medicine, Harvard Medical School


    Thoracic Oncology

    Office phone: 617-632-6084
    Fax: 617-582-7683
    Email: kwok-kin_wong@dfci.harvard.edu
    Website: Wong Lab Website

    Preferred contact method: office phone

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    Lung cancer, Developmental therapeutics

    Area of Research

    Pathogenesis of Human Lung Cancer

    Dana-Farber Cancer Institute
    450 Brookline Avenue
    Boston, MA 02215

    Recent Awards

    • Sidney Kimmel Foundation Scholar, 2004
    • Tisch Foundation Solid Tumor Scholar Award, 2004


    Pathogenesis of Human Lung Cancer

    Our research focuses on understanding the pathogenesis and genetic alterations involved in lung cancer and on testing novel lung cancer therapeutics in vivo. Our laboratory integrates genomic studies of human lung cancer, new mouse models of lung cancers, and studies of novel drug treatment in these models.

    We have been using oligonucleotide array-based comparative genomic hybridization (CGH), coupled with expression profiling, to interrogate the oncogenome and transcriptome of primary human lung cancer samples. This series of experiments has revealed many novel genes that might play important roles in human lung cancer. We are now validating the roles of these genes in tumorigenesis in vitro and in vivo.

    To understand the genetic role of mutated B-RAF, HER2/NEU, EGFR, and PI3 kinases in lung cancer, our laboratory generated various inducible bitransgenic mice harboring these mutations. We demonstrated that activation of EGFR and B-RAF are oncogenic in vivo, because mice expressing these activated alleles develop lung tumors de novo. We are now characterizing these mice in detail and plan to use them as a unique platform for testing therapeutics that specifically target these pathways.

    In addition, we are constructing a realistic model of human lung cancer using the unique experimental attributes of the telomerase-deficient mouse model and tobacco smoke.

    Tobacco use accounts for 85 percent of all lung cancers, and one hypothesis explaining this relationship states that tobacco smoke induces genetic mutations and causes accelerated cell renewals; these events rapidly erode telomeres, causing chromosomes to become unstable and increasing the probability that lung cells will become cancerous.

    Thus, we are in the process of chronically exposing telomerase-mutant mice with dysfunctional telomeres to environmental tobacco smoke. We also constructed a mouse tobacco smoke exposure facility for these models at DFCI, which will aid in studying other cancers and diseases caused by tobacco smoke (e.g., emphysema and bladder cancer).

    These three areas of research give us a better understanding of the genetic alterations involved in the initiation and progression of cancer.

    Select Publications

    • Kobayashi S, Ji H, Yuza Y, Meyerson M, Wong KK, Tenen DG, Halmos B. An alternative inhibitor overcomes resistance caused by a mutation of the epidermal growth factor receptor. Cancer Res 2005;65:7096-101
    • Tonon G, Wong KK, Maulik G, Brennan C, Feng B, Zhang Y, Khatry DB, Protopopov A, You MJ, Aguirre AJ, Martin ES, Yang Z, Ji H, Chin L, DePinho RA. High-resolution genomic profiles of human lung cancer. Proc Natl Acad Sci U S A 2005;102:9625-30.
    • Wong KK, Maser RS, Bachoo R, Menon J, Carrasco D, Gu Y, Alt F, DePinho R. Telomere dysfunction and Atm deficiency compromises organ homeostasis and accelerates ageing. Nature 2003;421:643-8.


    • Liang, Chen, PhD
    • Hongbin, Ji, PhD
    • Perera, Samanthi, PhD
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