J
Joydeep Mukherjee
Researcher at University of California, San Francisco
Publications - 88
Citations - 1994
Joydeep Mukherjee is an academic researcher from University of California, San Francisco. The author has contributed to research in topics: Glioma & Medicine. The author has an hindex of 21, co-authored 67 publications receiving 1679 citations. Previous affiliations of Joydeep Mukherjee include Jadavpur University & Medical College and Hospital, Kolkata.
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Hexokinase 2 is a key mediator of aerobic glycolysis and promotes tumor growth in human glioblastoma multiforme
Amparo Wolf,Sameer Agnihotri,Johann Micallef,Joydeep Mukherjee,Nesrin Sabha,Rob A. Cairns,Cynthia Hawkins,Abhijit Guha,Abhijit Guha +8 more
TL;DR: In glioblastoma multiforme, the most common adult primary brain tumor, the glycolytic enzyme hexokinase 2 facilitates growth and therapeutic resistance.
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Sensitivity of Glioblastomas to Clinically Available MEK Inhibitors Is Defined by Neurofibromin 1 Deficiency
TL;DR: Findings indicate that a subset of NF1-deficient glioblastoma multiforme GBMs may respond to MEK inhibitors currently being tested in clinical trials.
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Pyruvate Kinase M2 Expression, but Not Pyruvate Kinase Activity, Is Up-Regulated in a Grade-Specific Manner in Human Glioma
Joydeep Mukherjee,Joanna J. Phillips,Shichun Zheng,John K. Wiencke,Sabrina M. Ronen,Russell O. Pieper +5 more
TL;DR: It is shown that pyruvate kinase M expression, but not pyruVate Kinase activity, is regulated in a grade-specific manner in glioma, but that changes in both PK activity and PKM2 expression contribute to growth of GBM.
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Rapid Conversion of Mutant IDH1 from Driver to Passenger in a Model of Human Gliomagenesis
Tor-Christian Aase Johannessen,Joydeep Mukherjee,Pavithra Viswanath,Shigeo Ohba,Sabrina M. Ronen,Rolf Bjerkvig,Russell O. Pieper +6 more
TL;DR: Although mutant IDH1 expression is thought to drive the gliomagenesis process, the extent to which it remains a viable therapeutic target remains unknown and agents that target mutantIDH may be effective for a narrow time and may require further optimization or additional therapeutics in glioma.
Journal ArticleDOI
Epidermal growth factor receptor variant III-induced glioma invasion is mediated through myristoylated alanine-rich protein kinase C substrate overexpression.
Johann Micallef,Michael S. Taccone,Joydeep Mukherjee,Sidney Croul,Jennifer Busby,Michael F. Moran,Abhijit Guha +6 more
TL;DR: Elucidation of mechanisms that promote EGFRvIII-mediated tumorigenesis in GBM, such as MARCKS, provides additional understanding and potential biological targets against this currently terminal human cancer.