AG
ATANU GHORAI
Mazumdar Shaw Medical Foundation, Advanced Centre for Treatment, Research and Education in Cancer, Tata Memorial Centre, University of Kalyani, Vidyasagar University
About
Currently, I am fostering and leading a young team in the Neuro-Oncology Program at MSCTR to carry out clinically relevant projects in CNS tumors (mainly Glioblastoma). The aim is to understand its pathogenesis and treatment response/therapy resistance. Using multi-omics approaches and biochemical studies (at the cellular and molecular levels), I am trying to identify and develop novel therapeutics and diagnostics for better patient outcomes.
Employment
-
Mazumdar Shaw Medical Foundation Senior Research Scientist2023 - Present
-
Mazumdar Shaw Medical Foundation Research Scientist2021 - 2023
-
Advanced Centre for Treatment, Research and Education in Cancer, Tata Memorial Centre ACTREC Post-Doctoral Fellow2019 - 2021
-
Advanced Centre for Treatment, Research and Education in Cancer, Tata Memorial Centre National Post-Doctoral Fellow (NPDF), DST-SERB2017 - 2019
-
Tata Institute of Fundamental Research Post-Doctoral Visiting Fellow2015 - 2017
Education
-
University of Kalyani PhD? - 2015
-
University of Kalyani MSc? - 2007
-
Vidyasagar University BSc? - 2005
Projects & Funding
Projects & funding information is unavailable.
Publications (19)
- Hypoxia-Induced DNA Damage Response and Genomic Instability Dictate Cancer Treatment Response Save
- Biphasic DNA damage and non-canonical replication stress response govern radiation-induced senescence in glioblastoma Save
- First person – Atanu Ghorai Save
- PARP-1 negatively regulates nucleolar protein pool and mitochondrial activity: a cell protective mechanism Save
- 14-3-3ζ negatively regulates mitochondrial biogenesis in GBM residual cells. Save
- Inhibition of SETMAR-H3K36me2-NHEJ repair axis in residual disease cells prevents glioblastoma recurrence. Save
- Metabolic rewiring in drug resistant cells exhibit higher OXPHOS and fatty acids as preferred major source to cellular energetics. Save
- Sustained inhibition of PARP-1 activity delays glioblastoma recurrence by enhancing radiation-induced senescence. Save
- Molecular features unique to glioblastoma radiation resistant residual cells may affect patient outcome - a short report. Save
- PARP-1 depletion in combination with carbon ion exposure significantly reduces MMPs activity and overall increases TIMPs expression in cultured HeLa cells. Save