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Dr. Wu received her MD from Stanford University School of Medicine in 1994. She completed postgraduate training in internal medicine at Brigham and Women's Hospital, followed by a fellowship in medical oncology and hematology at Dana-Farber/Partners CancerCare. In 2000, she joined Dana-Farber, where she currently leads the Division of Stem Cell Transplantation and Cellular Therapies. Her research interests include the identification of targets of the immune response associated with therapies and dissecting the basis of effective human antitumor responses.
My ongoing research studies focus on how best to effectively mount human immune responses to recognize and eradicate cancer, with dedicated effort on the discovery and targeting of tumor antigens. A longstanding theme of my studies has been how best to launch immunotherapeutic efforts in a personalized fashion, initially through studies in the area of hematopoietic stem cell transplantation (HSCT) together with whole tumor cell vaccination and more recently through the implementation of personal neoantigen-targeting cancer vaccines (Ott & Hu Nature 2017; NCT 01970358). Key to our antigen discovery efforts has been our pioneering of approaches to leverage the recent availability of next-generation massively parallel sequencing technologies to perform comprehensive genomic dissection of leukemia cells. Our efforts have led to the discovery of key mutated genes and pathways involved in the pathogenesis of chronic lymphocytic leukemia (CLL) (N Engl J Med 2011), understanding of the vast clonal heterogeneity of leukemia samples and its impact on clonal evolution (Cell 2013), and the development of resistance to therapy (Nature 2015). We have further leveraged these sequencing technologies to pioneer computational tools for the comprehensive discovery of potential personal tumor-specific neoantigens. Neoantigens are a promising novel class of cancer targets created by the personal mutations found in each patient’s tumor which we have demonstrated in first-in-human trials for advanced melanoma and glioblastoma (Nature 2017, Nature 2019). Because these mutations generate peptides that are distinct from “self”-peptides, the resulting epitopes are expected to escape the immune dampening effects of central tolerance. As a physician-scientist with deep insight into how to bridge important basic discoveries with questions of high clinical relevance, I am committed to dedicating our efforts on the critical question of addressing the challenge of understanding the basis of disease progression and of therapeutic resistance in blood malignancies.
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