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Lynda Chin, M.D.

Genomic Medicine
University of Texas MD Anderson Cancer Center
1515 Holcombe Blvd. Unit 0091, 4SCR6.1042
Houston, TX 77030
(713) 792-6232

Dr. Lynda Chin is Chair of the first-ever Department of Genomic Medicine, and is Scientific Director of the Institute for Applied Cancer Science at UT MD Anderson Cancer Center.  She continues to serve at the Broad Institute of MIT and Harvard as PI of the TCGA Genome Data Analysis Center.  For the 13 years prior to Sept 2011, she was a member of the Dana-Farber Cancer Institute and Harvard Medical School community where she was Professor of Dermatology at the Harvard Medical School, member of the Department of Medical Oncology at Dana-Farber Cancer Institute, and a Senior Associate Member of the Broad Institute.  Dr. Chin was also the Scientific Director of the Belfer Institute for Applied Cancer Science at the Dana-Farber Cancer Institute, and co-led the Dana-Farber / Harvard Cancer Center’s Melanoma Program and Harvard Skin SPORE.  

Dr. Chin’s research program focuses on the molecular biology and genetics/genomics of cancer genesis, maintenance and progression in multiple tumor types, with an emphasis on glioblastoma and melanoma. Major efforts to characterize the oncogenome in humans and mice are complemented by the development of refined mouse models of human cancers for use in genetic screens and functional genomics studies.  Some areas of research include:

1.  Oncogenomics
Development of array-based comparative genomic hybridization (CGH) technology and bioinformatics tools was an early focus of our research program. These are also core components of the NIH TCGA (The Cancer Genes Atlas) project, which has the primary goal of completely characterizing cancer genomes at multiple levels. In addition to developing systematic approaches to integrate data across species (e.g. comparison of mouse and human tumors) and across platforms (e.g. DNA copy number, mutations, methylation and RNA expression) to identify candidates, we continue to stay at the forefront of technology development in order to further expand our view of the oncogenome with increasing accuracy and sensitivity. We are now also assessing methods of integrating alterations at the proteomic level as well. Many novel candidate genes identified through such approaches are currently being studied in the lab at the clinicopathological, functional and biological levels to validate their relevance to cancer. In the current expanded phase of TCGA, we continue to remain actively engaged as a funded characterization center as well as PI of a Genome Data Analysis Center. We are also involved in the International Cancer Genome Consortium (ICGC) effort.

2. Functional genomics
Beyond generation and gathering of genomic data, our goal is to rapidly functionalize such data for translation into the clinic. Here, leveraging our cancer biology expertise and genetically engineered model systems, we are developing approaches to accelerate validation through high-content genetic screens. Based on the integration of genomic data with developmental or cancer biological insights, we are performing genome-wide RNAi screens and focused gain-of-function genetic screens using in vitro and in vivo model systems. These studies are allowing us to quickly and efficiently apply a functional filter to genomic datasets and thus identify the most promising cancer-relevant genes for detailed mechanistic studies.

3. Genetics and biology of metastasis
One of the major areas of emphasis in our functional genomics program is metastasis. Utilizing mouse and human systems, our efforts are directed at (1) elucidating early genetic lesions in primary tumors that can drive the very processes of metastatic progression thus can be prognostic of future metastasis risks; (2) identifying progression drivers that are keys to enabling dissemination to distal organ sites and investigating the molecular mechanisms mediating melanoma metastasis.

4. Mouse models of human cancers
Conditional transgenic and knockout technologies are used to engineer cancer relevant mutations in the mouse with the goal of generating cancer-prone conditions that recapitulate aspects of the human disease, particularly melanoma. Inducible tumor models where a dominant acting oncogene is regulated in a time- and tissue-specific manner are used to characterize the roles of such oncogenic lesions in tumor genesis and maintenance, as well as to explore the complexity of host-tumor interactions. Introduction of genome instability through telomerase deficiency humanizes the mouse cancer genome for comparative oncogenomics. Importantly, these systems are leveraged to establish and optimize preclinical therapeutics.

© 2014 The University of Texas MD Anderson Cancer Center