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Oncology Experts

Patrick Swift


Radiation Therapy
Stanford University
United States of America

Biography

Professor of Radiation Oncology, Associate Chair for Research & Director of the Division of Radiation & Cancer Biology in the Department of Radiation Oncology. He also is the Director of Basic Science at the Stanford Cancer Institute and heads the Radiation Biology Program in Stanford’s Cancer Center, and is Director of the Cancer Biology Interdisciplinary Graduate Program. He was awarded an American Cancer Society Junior Faculty Research Award and the Michael Fry Award from the Radiation Research Society for his outstanding contributions on understanding the molecular mechanisms of resistance promoted by the tumor microenvironment. Additionally, he was the recipient of the 2013 ASTRO Gold Medal. In 2015, he was awarded an NIH R35 Outstanding Investigator Award and was inducted into the National Academy of Medicine. He co-authored the sixth & seventh editions of the textbook, “Radiation Biology for the Radiologist,” with Professor Eric Hall from Columbia. In addition, he is currently the “Jack, Lulu and Sam Willson Professor in Cancer Biology” in the Stanford University School of Medicine.

Research Interest

During the last five years, we have identified several small molecules that acted to kill VHL deficient renal cancer cells through a synthetic lethal screening approach. We published on one of the molecules (Cancer Cell 14: 90, 2008) that killed VHL deficient tumor and are performing screens to identify new therapeutics against other targets. Another major interest of my laboratory is in identifying hypoxia-induced genes involved in invasion and metastases. We have identified and characterized several genes that are induced by hypoxia and promote metastases in breast, ovarian, renal and head and neck cancer (Nature 440:1222, 2006, Cancer Cell 15:35, 2009) and are developing therapeutics against them. My group is also investigating how hypoxia regulates gene expression epigenetically through the regulation of histone demethylases and microRNAs.

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