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
Vascular regulation of antitumor immunity.
Lance L. Munn,Rakesh K. Jain +1 more
TL;DR: Emerging data show that the function of blood vessels associated with tumors is critical in the response to these immunotherapies and improving vascular function provides opportunities to enhance immunotherapy.
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Micelle-Encapsulated Quantum Dot-Porphyrin Assemblies as in Vivo Two-Photon Oxygen Sensors.
Christopher M. Lemon,Elizabeth Karnas,Xiaoxing Han,Oliver T. Bruns,Thomas J. Kempa,Dai Fukumura,Moungi G. Bawendi,Rakesh K. Jain,Dan G. Duda,Daniel G. Nocera +9 more
TL;DR: The results establish the utility of the QD-micelle approach for in vivo biological sensing applications and provide a means for signal transduction under both one- and two-photon excitation.
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Solid stress in brain tumours causes neuronal loss and neurological dysfunction and can be reversed by lithium
Giorgio Seano,Giorgio Seano,Hadi Tavakoli Nia,Kyrre E. Emblem,Meenal Datta,Meenal Datta,Jun Ren,Shanmugarajan Krishnan,Jonas Kloepper,Marco Da Cunha Pinho,William Ho,William Ho,Mitrajit Ghosh,Vasileios Askoxylakis,Gino B. Ferraro,Lars Riedemann,Elizabeth R. Gerstner,Tracy T. Batchelor,Patrick Y. Wen,Nan Lin,Alan J. Grodzinsky,Dai Fukumura,Peigen Huang,James W. Baish,Timothy P. Padera,Lance L. Munn,Rakesh K. Jain +26 more
TL;DR: It is shown that a subgroup of primary and metastatic brain tumours, classified as nodular on the basis of their growth pattern, exert solid stress on the surrounding brain tissue, causing a decrease in local vascular perfusion as well as neuronal death and impaired function, and that lithium as a therapeutic intervention could counter these effects.
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Blockade of MMP14 Activity in Murine Breast Carcinomas: Implications for Macrophages, Vessels, and Radiotherapy
Eleanor I Ager,Sergey V. Kozin,Nathaniel D. Kirkpatrick,Giorgio Seano,David P. Kodack,Vasileios Askoxylakis,Yuhui Huang,Shom Goel,Matija Snuderl,Alona Muzikansky,Dianne M. Finkelstein,Daniel T. Dransfield,Laetitia Devy,Yves Boucher,Dai Fukumura,Rakesh K. Jain +15 more
TL;DR: MMP14 blockade decreased immunosuppressive TGFβ, polarized macrophages to an antitumor phenotype, increased iNOS, and improved tumor perfusion, resulting in reduced primary tumor growth and enhanced response to radiation therapy, especially in high MMP14-expressing tumors.
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Effects of Vascular-Endothelial Protein Tyrosine Phosphatase Inhibition on Breast Cancer Vasculature and Metastatic Progression
Shom Goel,Nisha Gupta,Brian P. Walcott,Matija Snuderl,Cristina T. Kesler,Nathaniel D. Kirkpatrick,Takahiro Heishi,Yuhui Huang,John D. Martin,Eleanor I Ager,Rekha Samuel,Shuhan Wang,John Yazbek,Benjamin J. Vakoc,Randall T. Peterson,Timothy P. Padera,Dan G. Duda,Dai Fukumura,Rakesh K. Jain +18 more
TL;DR: It is demonstrated that pharmacological VE-PTP inhibition can normalize the structure and function of tumor vessels through Tie-2 activation, which delays tumor growth, slows metastatic progression, and enhances response to concomitant cytotoxic treatments.