Abhishek Bharadwaj Sharma

About

Dr Abhishek Bharadwaj Sharma is a Senior Scientist and independent investigator in genome stability and molecular oncology at CSIR-Central Drug Research Institute & Assistant Professor at AcSIR. His lab investigates how DNA damage, replication stress, and non-canonical nucleic acid structures drive genome instability, tumour progression, and therapeutic resistance in cancers such as glioblastoma.

Prior to CSIR-CDRI, Dr. Sharma completed his PhD at Heidelberg University and postdoctoral training at the Luxembourg Institute of Health and the University of Oxford. His work has uncovered critical mechanisms of DNA repair, chemoresistance, and R-loop dynamics (Nucleic Acids Res. 2012, 2021; Nat. Commun. 2023). By combining mechanistic biology, functional genomics, and patient-derived models, his research aims to translate fundamental genome stability insights into targeted cancer therapies and stratification strategies.

Employment

• AcSIR Assistant Professor
  2026 - Present
• Central Drug Research Institute PI and Senior Scientist
  2026 - Present
• University of Oxford Postdoctoral Research Associate
  2021 - 2025
• Luxembourg Institute of Health Post Doctoral Fellow
  2017 - 2021
• Newcastle University Centre for Cancer Research Technician
  2012 - 2013
• University of Sussex Research Technician
  2011 - 2012
• University of Oxford

Education

• Ruprecht Karls Universität Heidelberg Ph.D./ Dr. rer. nat.
  2013 - 2017
• University of Sussex M.Sc. in Genetic Manipulation and Molecular Biology
  2010 - 2011
• Sam Higginbottom University of Agriculture Technology and Sciences BSc (Hons) Biotechnology
  2005 - 2009

Projects & Funding

Projects & funding information is unavailable.

Publications (14)

• G-quadruplex homeostasis is a determinant of PARP inhibitor toxicity in BRCA2-deficient cells
  Nature Communications 2026 DOI: 10.1038/s41467-026-75083-9
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• DAXX promotes centromeric stability independently of ATRX by preventing the accumulation of R-loop-induced DNA double-stranded breaks
  Nucleic Acids Research 2024 DOI: 10.1093/nar/gkad1141
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• The loss of DNA polymerase epsilon accessory subunits POLE3–POLE4 leads to BRCA1-independent PARP inhibitor sensitivity
  Nucleic Acids Research 2024 DOI: 10.1093/nar/gkae439
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• Author Correction: C16orf72/HAPSTR1/TAPR1 functions with BRCA1/Senataxin to modulate replication-associated R-loops and confer resistance to PARP disruption (Nature Communications, (2023), 14, 1, (5003), 10.1038/s41467-023-40779-9)
  Nature Communications 2023 DOI: 10.1038/s41467-023-43353-5
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• C16orf72/HAPSTR1/TAPR1 functions with BRCA1/Senataxin to modulate replication-associated R-loops and confer resistance to PARP disruption
  Nature Communications 2023 DOI: 10.1038/s41467-023-40779-9
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• Regulation of Rad52-dependent replication fork recovery through serine ADP-ribosylation of PolD3
  Nature Communications 2023 DOI: 10.1038/s41467-023-40071-w
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• XAB2 promotes Ku eviction from single-ended DNA double-strand breaks independently of the ATM kinase
  Nucleic Acids Research 2021 DOI: 10.1093/nar/gkab785
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• XAB2 prevents abortive recombinational repair of replication-associated DNA double-strand breaks and its loss is synthetic lethal with RAD52 inhibition
  BioRxiv 2020 DOI: 10.1101/2020.04.10.035410
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• SURVEY AND SUMMARY Centromeric and ectopic assembly of CENP-A chromatin in health and cancer: old marks and new tracks
  Nucleic Acids Research 2019 DOI: 10.1093/nar/gky1298
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• Sensitizing ewing sarcoma to chemo- and radiotherapy by inhibition of the DNA-repair enzymes DNA protein kinase (DNA-PK) and poly-ADP-ribose polymerase (PARP) 1/2
  Oncotarget 2017 DOI: https://doi.org/10.18632/oncotarget.21300
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