Rakesh Jain
Tumor microenvironment


The overarching goal of my research is to dissect the pathophysiology of the vascular and extra-vascular components of tumors, to determine the role of tumor-host interactions in tumor biology and, ultimately, to translate this knowledge into improved cancer detection, prevention and treatment in humans. To unravel the complex biology of tumors, my laboratory has developed an array of imaging technologies, mathematical models and sophisticated animal preparations. Our work has provided unprecedented molecular, cellular, anatomical and functional insights into the vascular, interstitial and cellular barriers to cancer treatment. It has also led to more than 25 clinical trials for various cancers and the development of new approaches to cancer therapy.

These days, my lab is perhaps best known for a new hypothesis that antiangiogenic therapy can “normalize” the abnormal tumor vasculature and improve both the delivery and the efficacy of therapeutics. We have validated this concept in glioblastoma, lung and breast cancer patients receiving antiangiogenic therapy and, in the process, discovered potential biomarkers of tumor escape from these therapies. Now we are exploring novel strategies to improve immunotherapy of cancer by “normalizing” blood vessels and the extracellular matrix.

I received my Ph.D. in chemical engineering from the University of Delaware and am today A. W. Cook Professor of Radiation Oncology (Tumor Biology) at Harvard Medical School and Director of the Edwin L. Steele Laboratories for Tumor Biology at Massachusetts General Hospital. I have received numerous honors for my research, including the 2013 National Medal of Science, awarded in 2016. I am a fellow of the National Academy of Medicine, the National Academy of Engineering, the American Academy of Arts and Sciences and the National Academy of Sciences.



Normalizing the tumor microenvironment to improve immunotherapy of cancer

Ludwig Harvard investigator Rakesh Jain discusses how the abnormal tumor vessels and matrix create a hostile microenvironment that fuels tumor progression and confers resistance to conventional and emerging cancer treatments.

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