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Laboratory of Cancer Biology and Genetics
The Laboratory of Cancer Biology and Genetics (LCBG) self-assembled in 2006 through the merger of the Laboratory of Cellular Carcinogenesis and Tumor Promotion (LCCTP), the Laboratory of Cell Regulation and Carcinogenesis (LCRC) and the Laboratory of Genetics (LG). The LCBG currently encompasses the work of 12 principal investigators supervising independent research programs with highly overlapping experimental goals and approaches. These investigators conduct a well integrated research program consisting of basic and translational components that are designed to: elucidate the cellular and tissue changes associated with specific stages of carcinogenesis, detect and characterize genetic modifiers fundamental to cancer susceptibility and progression, define the molecular mechanisms involved in the pathogenesis of major human cancers, and develop rational approaches for cancer prevention and treatment. Studies are performed in vivo in animal models, in vitro in cell and organ culture, and on tissues and cells obtained from human volunteers and cancer patients. The LCBG also develops and correlates novel protocols in molecular diagnostics for human and animal tissues, and in noninvasive medical imaging for animal models. Emanating from our studies are new therapeutic combinations for targeted cancers now in clinical trials. The LCBG operates a novel University-NCI graduate partnership research training program in comparative molecular pathology, including both Ph.D. granting and non-degree fellowships.
The research focus of the LCBG principal investigators is as follows:
- Dr. Peter Blumberg has been instrumental in the identification, characterization and understanding of the biochemical pharmacology of two systems of great biological importance and therapeutic potential: protein kinase C and the related families of proteins containing regulatory C1 domains, and the capsaicin receptor TRPV1, which integrates nociceptive inputs to regulate C-fiber sensory neuron activity, making a major contribution to chronic pain.
- Dr. Jeff Green is a pioneer in using a cross-species genomic approach to dissect molecular pathways important in breast cancer and using a mouse model of basal-type breast cancer he developed for accelerating pre-clinical testing of novel therapies, and is also studying mechanisms associated with tumor dormancy, an understudied and critical component of cancer recurrence.
- Dr. Jing Huang, a tenure-track investigator who has focused his research program on the epigenetic mechanisms underlying cancer and stem cells, has used genomics to uncover a role for the tumor suppressor p53 in regulating the differentiation of embryonic stem cells during DNA damage.
- Dr. Kent Hunter is a pioneer in systems genetics, having demonstrated first in mouse models and confirming by association studies in cancer patients that an individual's genetic background has a significant effect on the propensity of their tumors to metastasize; his work has established a new paradigm of inherited susceptibility in metastasis research.
- Dr. Ji Luo focuses on understanding the biology of cancers with mutations in the KRAS oncogene. In particular, he applies functional genomics approaches to dissect genetic dependencies and delineate mechanisms of non-oncogene addictions in KRAS mutant cells in order to identify new therapeutic modalities.
- Dr. Glenn Merlino has made key contributions to several areas of basic research, including receptor tyrosine kinase signaling, oncogenic transformation, transcription regulation, cell cycle regulation, and genomic instability, and is now developing new preclinical tools and approaches to determine how metastatic cells survive therapy and recur at distant sites.
- Dr. Beverly Mock investigates genetic susceptibility to mouse plasma cell tumors as a model system for analyzing complex genetic traits associated with cancer, and has identified four separate loci on two chromosomes that are involved in tumor susceptibility, including genes encoding Mndal, p16INK4a and mTOR. Drug combinations targeting the mTOR and p16 pathways are showing synergy in intervention studies.
- Dr. Miriam Poirier is a pioneer in biochemical dosimetry and molecular epidemiology, having introduced to the field highly sensitive immunoassays to detect DNA damage caused by carcinogenic chemicals, and investigates the extent and consequences of DNA damage caused by exposure to environmental agents and pharmaceuticals, using experimental models and human subjects to elucidate mechanisms of cancer causation and prevention.
- Dr. Mark Simpson, a D.V.M., Ph.D. with specialty board certification by the American College of Veterinary Pathologists, has established and directs a unique University-NCI graduate partnership research training program in comparative molecular pathology. The Comparative Biomedical Scientist Training Program provides interdisciplinary training for veterinarians in both diagnostic pathology and human disease-oriented medical research in order to increase the synergy for comparative biomedical research interactions and animal model predictability.
- Dr. Lalage Wakefield uses mouse models and genomic approaches to address the critical, complex dual role played by transforming growth factor-beta (TGF-beta) in breast cancer progression, in regulating breast cancer stem cell dynamics, and to develop TGF-beta-based therapeutic strategies.
- Dr. Li Yang is a tenure-track investigator who has focused her research on dissecting the cellular and molecular mechanisms underlying the metastatic process, with a focus on inflammation and tumor microenvironment; she has demonstrated that the recruitment of immature myeloid cells to the tumor microenvironment is responsible for the switch of TGF-beta signaling from tumor suppressor to tumor promoter.
- Dr. Stuart Yuspa has a longstanding interest in mechanisms of carcinogenesis with particular emphasis on signaling pathway alterations in premalignant lesions; his laboratory uses the mouse skin carcinogenesis model to study molecular events that determine the phenotypic evolution of normal keratinocytes through a benign tumor stage and conversion to squamous cell carcinoma.
This page was last updated on 7/10/2014.