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Dr. Hlatky received her Ph.D. in Physics and Biophysics from the University of California, Berkeley in 1985. During her time at Berkeley, she was funded by the National Cancer Institute, and the cancer models she developed using physics became industry standards. She served as a faculty member in the Department of Radiation and Oncology at Harvard University for 16 years, where she conducted "wet lab" research combining mathematics and cancer biology to improve cancer treatment modeling. In 2004, she received a $10 million grant from the National Aeronautics and Space Administration (NASA) and became the principal investigator at the Center for Cancer Systems Biology at Tufts University School of Medicine. In addition, she has directed review and research programs for the U.S. Department of Energy on low-dose effects.
Focuses on research in cancer systems biology, integrating cancer treatment with radiobiology studies.
Dr. Hlatky has long been engaged in quantitative and empirical studies of the effects of radiation damage at the cellular and chromosomal levels, as well as the dynamics of tumor development. For radiation showing linear killing kinetics, she was the first to determine that any form of prolonged administration to asynchronous cell populations is asymptotically more suppressive than acute doses of the same magnitude [Hahnfeldt P and Hlatky L. Cellular resensitization during long-term dosing of heterogeneous cell populations. Radiation Research 150:681-687, 1998]. She subsequently demonstrated that uniform dosing is optimal in this regard [Hahnfeldt P, Folkman J, and Hlatky L. Minimizing long-term tumor burden: rationale for metronomic chemotherapy dosing and its anti-angiogenic basis. J Theor Biol 220:545-554, 2003].
Her laboratory has extensive expertise in angiogenesis and was the first to show expression of the major angiogenic factor VEGF (Vascular Endothelial Growth Factor) in irradiated cells [Hlatky L, Hahnfeldt P, Tsionou C, Coleman CN. Vascular endothelial growth factor: environmental control and effect on angiogenesis. Br J Cancer 74 (Suppl XXVII): S151-6, 1996]. These early studies highlighted the role of endothelial and stromal cells in tumor radiation response. In the following decade, Dr. Hlatky's lab discovered many new inferences regarding angiogenesis and radiation response in tumor populations. Her lab demonstrated new relationships in the diversity of tumor population radiation responses under cellular stress, showing that the variability in cellular radiation responses under environmental stress (using self-imposed gradient ischemia across the population) decreases after simulated reperfusion and then sharply increases when oxygen/nutrients are reintroduced into cultures to mimic reperfusion [Hlatky L, Van Buren T, Hahnfeldt P. Quantifying intercellular radiation response heterogeneity in sandwich cultures using micronucleus expression. Int J Radiat Biol 67:541-8, 1995].
Her recent collaboration with Professor Rainer K. Sachs refuted the long-standing paradigm of chronic myeloid leukemia (CML)—a well-known radiation-induced cancer—arising from a single cell. When CML was considered to originate from two cells, they demonstrated that it statistically better fit the incidence data [Sachs RK, Johnsson K, Hahnfeldt P, Luo J, Chen A, Hlatky L. Multicellular origin of the progenitor cell crisis in chronic myeloid leukemia. Cancer Res 71(8):2838-47, 2011]. This study has profound implications for the role of intercellular interactions in carcinogenesis.
Principal Investigator, U.S. Center for Cancer Systems Biology
Ph.D. in Physics and Biophysics, University of California, Berkeley
● Carcinogenesis and tumor growth dynamics
● Radiobiology
● Translational research on microenvironmental influences
● DNA damage and repair
● Tumor angiogenesis
● Tumor-cell fusion
