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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Journal ArticleDOI
Limited Environmental Serine and Glycine Confer Brain Metastasis Sensitivity to PHGDH Inhibition.
Bryan Ngo,Eugenie Kim,Victoria Osorio-Vasquez,Sophia Doll,Sophia Bustraan,Roger Liang,Alba Luengo,Shawn M. Davidson,Ahmed Ali,Gino B. Ferraro,Grant M. Fischer,Roozbeh Eskandari,Diane Kang,Jing Ni,Ariana Plasger,Vinagolu K. Rajasekhar,Edward R. Kastenhuber,Sarah Bacha,Roshan K. Sriram,Benjamin D. Stein,Samuel F. Bakhoum,Matija Snuderl,Paolo Cotzia,John H. Healey,Nello Mainolfi,Vipin Suri,Adam Friedman,Mark Manfredi,David M. Sabatini,David M. Sabatini,Drew R. Jones,Min Yu,Jean J. Zhao,Jean J. Zhao,Rakesh K. Jain,Kayvan R. Keshari,Michael A. Davies,Matthew G. Vander Heiden,Eva Hernando,Matthias Mann,Matthias Mann,Lewis C. Cantley,Michael E. Pacold +42 more
TL;DR: It is demonstrated that 3-phosphoglycerate dehydrogenase (PHGDH), which catalyzes the rate-limiting step of glucose-derived serine synthesis, is a major determinant of brain metastasis in multiple human cancer types and preclinical models and suggests that PHGDH inhibitors may be useful in the treatment of head metastasis.
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Characterization of Sialyloligosaccharide Binding by Recombinant Soluble and Native Cell-associated CD22 EVIDENCE FOR A MINIMAL STRUCTURAL RECOGNITION MOTIF AND THE POTENTIAL IMPORTANCE OF MULTISITE BINDING
TL;DR: Data are presented indicating that full-length native CD22, expressed on the surface of Chinese hamster ovary cells, is structurally and functionally a multimeric protein, demonstrating a higher apparent affinity for multiply sialylated compounds over monosialylation compounds.
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Angiogenesis as a therapeutic target in malignant gliomas.
TL;DR: The rationale for antiangiogenic agents in GBM, their potential mechanisms of action, and their clinical development in G BM patients are reviewed.
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Pancreas microenvironment promotes VEGF expression and tumor growth: novel window models for pancreatic tumor angiogenesis and microcirculation.
Yoshikazu Tsuzuki,Carla Mouta Carreira,Maximilian Bockhorn,Lei Xu,Rakesh K. Jain,Dai Fukumura +5 more
TL;DR: It is concluded that the orthotopic pancreas microenvironment enhances VEGF expression, which stimulates growth of PANC-1 tumors (compared with ectopic tumors), and the mechanism is autocrine and/or paracrine and also is involved in the maintenance of blood vessels.
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PDGF-C Induces Maturation of Blood Vessels in a Model of Glioblastoma and Attenuates the Response to Anti-VEGF Treatment
Emmanuelle di Tomaso,Nyall London,Daniel Fuja,James J. Logie,James Alex Tyrrell,Walid S. Kamoun,Lance L. Munn,Rakesh K. Jain +7 more
TL;DR: It is suggested that PDGF-C plays an important role in glioma vessel maturation and stabilization, and that it can attenuate the response to anti-VEGF therapy, potentially contributing to escape from vascular normalization.