R
Ravesanker Ezhilarasan
Researcher at University of Texas MD Anderson Cancer Center
Publications - 35
Citations - 1959
Ravesanker Ezhilarasan is an academic researcher from University of Texas MD Anderson Cancer Center. The author has contributed to research in topics: Biology & Glioma. The author has an hindex of 15, co-authored 26 publications receiving 1538 citations. Previous affiliations of Ravesanker Ezhilarasan include New York University & University of Illinois at Urbana–Champaign.
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Journal ArticleDOI
Mesenchymal Differentiation Mediated by NF-κB Promotes Radiation Resistance in Glioblastoma
Krishna P.L. Bhat,Veerakumar Balasubramaniyan,Brian Vaillant,Ravesanker Ezhilarasan,Karlijn Hummelink,Faith Hollingsworth,Khalida Wani,Lindsey Heathcock,Johanna D. James,Lindsey D. Goodman,Siobhan Conroy,Lihong Long,Nina Lelic,Suzhen Wang,Joy Gumin,Divya Raj,Yoshinori Kodama,Aditya Raghunathan,Adriana Olar,Kaushal Joshi,Christopher E. Pelloski,Amy B. Heimberger,Se Hoon Kim,Daniel P. Cahill,Ganesh Rao,Wilfred F. A. den Dunnen,Hendrikus Boddeke,Heidi S. Phillips,Ichiro Nakano,Frederick F. Lang,Howard Colman,Erik P. Sulman,Kenneth Aldape +32 more
TL;DR: It is shown that patient-derived glioma sphere cultures that resemble either the proneural (PN) or mesenchymal (MES) transcriptomal subtypes differ significantly in their biological characteristics, and it is suggested that the tumor microenvironment cell types such as macrophages/microglia may play an integral role in this process.
Journal ArticleDOI
Glioblastoma-infiltrated innate immune cells resemble M0 macrophage phenotype.
Konrad Gabrusiewicz,Benjamin Rodriguez,Jun Wei,Yuuri Hashimoto,Luke M. Healy,Sourindra Maiti,Ginu Thomas,Shouhao Zhou,Qianghu Wang,Ahmed Elakkad,Brandon D. Liebelt,Nasser K. Yaghi,Ravesanker Ezhilarasan,Neal Huang,Jeffrey S. Weinberg,Sujit S. Prabhu,Ganesh Rao,Raymond Sawaya,Lauren A. Langford,Janet M. Bruner,Gregory N. Fuller,Amit Bar-Or,Wei Li,Rivka R. Colen,Michael A. Curran,Krishna P. Bhat,Jack P. Antel,Laurence J.N. Cooper,Erik P. Sulman,Amy B. Heimberger +29 more
TL;DR: G GAM profiling using flow cytometry studies revealed a continuum between the M1- and M2-like phenotype, and contrary to current dogma, GAMs exhibited distinct immunological functions, with the former aligned close to nonpolarized M0 macrophages.
Journal ArticleDOI
EZH2 protects glioma stem cells from radiation-induced cell death in a MELK/FOXM1-dependent manner.
Sung Hak Kim,Kaushal Joshi,Ravesanker Ezhilarasan,Toshia R. Myers,Jason J. Siu,Chunyu Gu,Mariko Nakano-Okuno,David Taylor,Mutsuko Minata,Erik P. Sulman,Jeongwu Lee,Krishna P.L. Bhat,Anna Elisabetta Salcini,Ichiro Nakano +13 more
TL;DR: It is demonstrated that the catalytic subunit of Polycomb repressive complex 2, EZH2, is targeted by the MELK-FOXM1 complex, which in turn promotes resistance to radiation in GSCs.
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Serine/Threonine Kinase MLK4 Determines Mesenchymal Identity in Glioma Stem Cells in an NF-κB-dependent Manner.
Sung Hak Kim,Ravesanker Ezhilarasan,Emma Phillips,Daniel Gallego-Perez,Amanda E Sparks,David Taylor,Katherine J. Ladner,Takuya Furuta,Hemragul Sabit,Rishi Raj Chhipa,Ju Hwan Cho,Ahmed Mohyeldin,Samuel Beck,Kazuhiko Kurozumi,Toshihiko Kuroiwa,Ryoichi Iwata,Akio Asai,Jonghwan Kim,Erik P. Sulman,Shi Yuan Cheng,L. James Lee,Mitsutoshi Nakada,Denis C. Guttridge,Biplab Dasgupta,Violaine Goidts,Krishna P. Bhat,Ichiro Nakano +26 more
TL;DR: This work reports that mixed lineage kinase 4 (MLK4) is overexpressed in MES but not proneural (PN) GSCs, and uncovers MLK4 as an upstream regulator of NF-κB signaling and a potential molecular target for the MES subtype of glioblastomas.
Journal ArticleDOI
A survey of intragenic breakpoints in glioblastoma identifies a distinct subset associated with poor survival
Siyuan Zheng,Jun Fu,Rahulsimham Vegesna,Yong Mao,Lindsey Heathcock,Wandaliz Torres-Garcia,Ravesanker Ezhilarasan,Shuzhen Wang,Aaron McKenna,Lynda Chin,Cameron Brennan,W. K. Alfred Yung,John N. Weinstein,Kenneth D. Aldape,Erik P. Sulman,Ken Chen,Dimpy Koul,Roeland Verhaak +17 more
TL;DR: A previously underappreciated genomic mechanism of gene deregulation that can confer growth advantages on tumor cells and may generate cancer-specific vulnerabilities in subsets of GBM is uncovered.