R
Rakesh K. Jain
Researcher at Harvard University
Publications - 1528
Citations - 198912
Rakesh K. Jain is an academic researcher from Harvard University. The author has contributed to research in topics: Angiogenesis & Cancer. The author has an hindex of 200, co-authored 1467 publications receiving 177727 citations. Previous affiliations of Rakesh K. Jain include Government Medical College, Thiruvananthapuram & University of Oslo.
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Antiangiogenesis Strategies Revisited: From Starving Tumors to Alleviating Hypoxia
TL;DR: In this paper, the authors summarize lessons learned from preclinical and clinical studies over the past decade and propose strategies for improving antiangiogenic therapy outcomes for malignant and nonmalignant diseases.
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Polycyclic aromatic hydrocarbons: environmental pollution and bioremediation
TL;DR: The problems of PAH pollution and PAH degradation, and relevant bioremediation efforts are discussed and chemotaxis could also have an important role in enhancing biodegradation of pollutants.
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Lessons from phase III clinical trials on anti-VEGF therapy for cancer
TL;DR: Adding bevacizumab to chemotherapy failed to increase survival in patients with previously treated and refractory metastatic breast cancer, and addition of vatalanib, a kinase inhibitor developed as a VEGF receptor-selective agent, to chemotherapy did not show a similar benefit in metastatic colorectal cancer patients.
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Enhancing cancer immunotherapy using antiangiogenics: opportunities and challenges.
TL;DR: The roles of VEGF and ANG2 are outlined, and ways that antiangiogenic agents can be combined with immune-checkpoint inhibitors to potentially improve patient outcomes are suggested, and avenues of future research are highlighted.
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Abnormalities in Pericytes on Blood Vessels and Endothelial Sprouts in Tumors
Shunichi Morikawa,Peter Baluk,Toshiyuki Kaidoh,Amy Haskell,Rakesh K. Jain,Donald M. McDonald +5 more
TL;DR: It is concluded that pericytes are present on most tumor vessels but have multiple abnormalities, including altered expression of marker proteins, which raises the possibility of an involvement in sprout growth or retraction in tumors.