معرفی
Sandy Chang, MD, PhD, is a Professor of Laboratory Medicine, Pathology, and Molecular Biophysics & Biochemistry at Yale University, holding primary affiliation with the Yale School of Medicine. He serves as Associate Director of the Molecular Diagnostics Laboratory. Dr. Chang's research focuses on telomere biology, exploring how telomeres protect chromosome ends, prevent genomic instability, and their roles in aging and cancer development. His work includes groundbreaking studies on Werner Syndrome mouse models, revealing links between telomere dysfunction, premature aging, and cancer. He is also Associate Dean for Science Education and Quantitative Reasoning at Yale College, emphasizing interdisciplinary education.
Education: BS from Yale University (1988), MD from Cornell University Medical College (1997), PhD from Rockefeller University (1996). Residency in Clinical Pathology at Brigham & Women's Hospital (1998–2000). Postdoctoral training under Ronald DePinho at Dana-Farber Cancer Institute.
Research highlights include discovering telomere dysfunction mechanisms in cancer, identifying POT1's role in genomic stability, and elucidating how telomere damage activates cellular senescence. His lab uses mouse models to study aging, cancer, and telomere repair pathways. Key findings include WRN helicase's role in preventing telomere aberrations and the development of ALT (Alternative Lengthening of Telomeres) phenotypes.
Awards include the American Society of Clinical Investigation (2009), Ellis Benson Award (2007), and fellowships from the Ellison Medical Foundation and Sidney Kimmel Foundation. Collaborations span molecular biology, genetics, and clinical diagnostics. He contributes to translational research, bridging basic science and medical practice.
Administrative roles include leadership in molecular diagnostics, medical education, and undergraduate research initiatives. His lab actively investigates telomere repair mechanisms, nuclear envelope interactions, and synthetic lethality targets in cancers with genomic instability.
