Srividya Bhaskara, PhD

Research Interests

  • Genome Stability
  • Chromatin
  • Histone Deacetylases
  • Immunology
  • DNA Repair
  • DNA Replication
  • Cancer Biology
  • Mouse Models of Cancer


Lab Website


  • English

Academic Information

  • Departments: Oncological Sciences - Adjunct Assistant Professor, Radiation Oncology - Associate Professor
  • Cancer Center Programs: Nuclear Control of Cell Growth & Differentiation

Academic Office Information

  • 801-213-4219
  • Huntsman Cancer Hospital
    1950 Circle of Hope, Room: 4242
    Salt Lake City, UT 84112

Academic Bio

Dr. Bhaskara's research goal is to understand the functions for histone deacetylases (HDACs) in genome maintenance, with the ultimate objective of using the knowledge gained to improve the therapeutic benefits of HDAC inhibition as a treatment for cancer. In Dr. Bhaskara's post-doctoral research, she made the discovery that HDAC inhibitors induce cancer cell death by directly targeting genome stability programs independent of their effect on transcription opening up a new field of HDACs and genome stability. She showed HDAC inhibitors trigger genotoxic stress and death only in cycling cells, thereby providing a mechanistic explanation for how HDAC inhibitors selectively kill rapidly cycling cancer cells and not the quiescent normal cells. Using genetic deletion systems, she further found novel functions for HDAC3 in DNA repair, DNA replication, chromatin structure maintenance and B-cell development. Collectively, these findings provide a new paradigm for the mode-of-action of HDAC inhibitors, which are FDA-approved drugs for certain hematologic malignancies.

As an independent investigator, Dr. Bhaskara's lab goal is to investigate the fundamental functions of HDACs in genome maintenance, with the ultimate objective of using the knowledge gained to test the therapeutic benefits of HDAC inhibition as a treatment for cancers including B-cell malignancies. The lab projects are aimed at identifying new therapeutic regimens for a subset of leukemia and lymphoma with altered epigenetics or genome maintenance signals. For example, Dr. Bhaskara’s lab recently showed a new therapeutic strategy for Philadelphia chromosome-positive B-cell precursor acute lymphoblastic leukemia (Ph+B-ALL). This is highly significant as Ph+B-ALL is a major subclass of ALL with poor prognosis. Overall, Bhaskara's long-term goal is to effectively solve complex problems in cancer biology and rapidly move the field of cancer therapeutics forward to make a real difference in the lives of cancer patients. Dr. Bhaskara performed her post-doctoral training at Vanderbilt University, Nashville in Dr. Scott Hiebert's lab.

Education History

Type School Degree
Research Fellow Vanderbilt University Medical Center
Postdoctoral Research Fellow
Doctoral Training Department of Biochemistry, Cellular and Molecular Biology, University of Tennessee
Graduate Training Department of Biochemistry, Dr. A. L. M. Mudaliar Post-graduate Institute of Basic Medical Sciences,
Medical Biochemistry
Undergraduate Department of Biochemistry, Mohammad Sathak College of Arts and Science, University of Madras

Global Impact

Education History

Type School Degree Country
Graduate Training Department of Biochemistry, Dr. A. L. M. Mudaliar Post-graduate Institute of Basic Medical Sciences,
Medical Biochemistry
M.S. India
Undergraduate Department of Biochemistry, Mohammad Sathak College of Arts and Science, University of Madras
B.S. India

Selected Publications

Journal Article

  1. Johnson DP, Chandrasekharan MB, Dutreix M, Bhaskara S (2021). Targeting DNA Repair and Chromatin Crosstalk in Cancer Therapy. Cancers (Basel), 13(3).
  2. Tiburcio PDB, Locke MC, Bhaskara S, Chandrasekharan MB, Huang LE (2020). The neural stem-cell marker CD24 is specifically upregulated in IDH-mutant glioma. Translational Oncology, 13(10), 100819.
  3. Johnson DP, Spitz-Becker GS, Chakraborti K, Bhaskara S (2019). Assessment of epigenetic mechanisms and DNA double-strand break repair using laser micro-irradiation technique developed for hematological cells. EBioMedicine, 43, 138-149.
  4. Bhaskara S (2018). Histone deacetylase 11 as a key regulator of metabolism and obesity. EBioMedicine, 35, 27-28.
  5. Tharkar-Promod S, Johnson DP, Bennett SE, Dennis EM, Banowsky BG, Jones SS, Shearstone JR, Quayle SN, Min C, Jarpe M, Mosbruger T, Pomicter AD, Miles RR, Chen WY, Bhalla KN, Zweidler-McKay PA, Shrieve DC, Deininger MW, Chandrasekharan MB, Bhaskara S (2017). HDAC1,2 inhibition and doxorubicin impair Mre11-dependent DNA repair and DISC to override BCR-ABL1-driven DSB repair in Philadelphia chromosome-positive B-cell precursor acute lymphoblastic leukemia. Leukemia, 32(1), 49-60.
  6. Stengel KR, Barnett KR, Wang J, Liu Q, Hodges E, Hiebert SW, Bhaskara S (2017). Deacetylase activity of histone deacetylase 3 is required for productive VDJ recombination and B-cell development. Proc Natl Acad Sci U S A, 114(32), 8608-8613.
  7. Ramakrishnan S, Pokhrel S, Palani S, Pflueger C, Parnell TJ, Cairns BR, Bhaskara S, Chandrasekharan MB (2016). Counteracting H3K4 methylation modulators Set1 and Jhd2 co-regulate chromatin dynamics and gene transcription. Nat Commun, 7, 11949.
  8. Chan E, Arlinghaus LR, Cardin DB, Goff L, Berlin JD, Parikh A, Abramson RG, Yankeelov TE, Hiebert S, Merchant N, Bhaskara S, Chakravarthy AB (2016). Phase I trial of vorinostat added to chemoradiation with capecitabine in pancreatic cancer. Radiother Oncol, 119(2), 312-8.
  9. Bhaskara S (2016). Examination of Proteins Bound to Nascent DNA in Mammalian Cells Using BrdU-ChIP-Slot-Western Technique. J Vis Exp, (107), e53647.
  10. Abegglen LM, Caulin AF, Chan A, Lee K, Robinson R, Campbell MS, Kiso WK, Schmitt DL, Waddell PJ, Bhaskara S, Jensen ST, Maley CC, Schiffman JD (2015). Potential Mechanisms for Cancer Resistance in Elephants and Comparative Cellular Response to DNA Damage in Humans. JAMA, 314(17), 1850-60.
  11. Johnson DP, Spitz GS, Tharkar S, Quayle SN, Shearstone JR, Jones S, McDowell ME, Wellman H, Tyler JK, Cairns BR, Chandrasekharan MB, Bhaskara S (2015). HDAC1,2 inhibition impairs EZH2- and BBAP-mediated DNA repair to overcome chemoresistance in EZH2 gain-of-function mutant diffuse large B-cell lymphoma. Oncotarget, 6(7), 4863-87.
  12. Bhaskara S (2015). Histone deacetylases 1 and 2 regulate DNA replication and DNA repair: potential targets for genome stability-mechanism-based therapeutics for a subset of cancers. Cell Cycle, 14(12), 1779-85.
  13. Ha K, Fiskus W, Choi DS, Bhaskara S, Cerchietti L, Devaraj SG, Shah B, Sharma S, Chang JC, Melnick AM, Hiebert S, Bhalla KN (2014). Histone deacetylase inhibitor treatment induces 'BRCAness' and synergistic lethality with PARP inhibitor and cisplatin against human triple negative breast cancer cells. Oncotarget, 5(14), 5637-50.
  14. Bhaskara S, Jacques V, Rusche JR, Olson EN, Cairns BR, Chandrasekharan MB (2013). Histone deacetylases 1 and 2 maintain S-phase chromatin and DNA replication fork progression. Epigenetics Chromatin, 6(1), 27.
  15. Hatzi K, Jiang Y, Huang C, Garrett-Bakelman F, Gearhart MD, Giannopoulou EG, Zumbo P, Kirouac K, Bhaskara S, Polo JM, Kormaksson M, MacKerell AD Jr, Xue F, Mason CE, Hiebert SW, Prive GG, Cerchietti L, Bardwell VJ, Elemento O, Melnick A (2013). A hybrid mechanism of action for BCL6 in B cells defined by formation of functionally distinct complexes at enhancers and promoters. Cell Rep, 4(3), 578-88.
  16. Summers AR, Fischer MA, Stengel KR, Zhao Y, Kaiser JF, Wells CE, Hunt A, Bhaskara S, Luzwick JW, Sampathi S, Chen X, Thompson MA, Cortez D, Hiebert SW (2013). HDAC3 is essential for DNA replication in hematopoietic progenitor cells. J Clin Invest, 123(7), 3112-23.
  17. Ziesche E, Kettner-Buhrow D, Weber A, Wittwer T, Jurida L, Soelch J, Muller H, Newel D, Kronich P, Schneider H, Dittrich-Breiholz O, Bhaskara S, Hiebert SW, Hottiger MO, Li H, Burstein E, Schmitz ML, Kracht M (2013). The coactivator role of histone deacetylase 3 in IL-1-signaling involves deacetylation of p65 NF-kappaB. Nucleic Acids Res, 41(1), 90-109.
  18. Wells CE, Bhaskara S, Stengel KR, Zhao Y, Sirbu B, Chagot B, Cortez D, Khabele D, Chazin WJ, Cooper A, Jacques V, Rusche J, Eischen CM, McGirt LY, Hiebert SW (2013). Inhibition of histone deacetylase 3 causes replication stress in cutaneous T cell lymphoma. PLoS ONE, 8(7), e68915.
  19. Wilson AJ, Holson E, Wagner F, Zhang YL, Fass DM, Haggarty SJ, Bhaskara S, Hiebert SW, Schreiber SL, Khabele D (2011). The DNA damage mark pH2AX differentiates the cytotoxic effects of small molecule HDAC inhibitors in ovarian cancer cells. Cancer Biol Ther, 12(6), 484-93.
  20. Sirbu BM, Couch FB, Feigerle JT, Bhaskara S, Hiebert SW, Cortez D (2011). Analysis of protein dynamics at active, stalled, and collapsed replication forks. Genes Dev, 25(12), 1320-7.
  21. Bhaskara S, Hiebert SW (2011). Role for histone deacetylase 3 in maintenance of genome stability. Cell Cycle, 10(5), 727-8.
  22. Bhaskara S, Knutson SK, Jiang G, Chandrasekharan MB, Wilson AJ, Zheng S, Yenamandra A, Locke K, Yuan JL, Bonine-Summers AR, Wells CE, Kaiser JF, Washington MK, Zhao Z, Wagner FF, Sun ZW, Xia F, Holson EB, Khabele D, Hiebert SW (2010). Hdac3 is essential for the maintenance of chromatin structure and genome stability. Cancer Cell, 18(5), 436-47.
  23. Chyla BJ, Moreno-Miralles I, Steapleton MA, Thompson MA, Bhaskara S, Engel M, Hiebert SW (2008). Deletion of Mtg16, a target of t(16;21), alters hematopoietic progenitor cell proliferation and lineage allocation. Mol Cell Biol, 28(20), 6234-47.
  24. Bhaskara S, Chyla BJ, Amann JM, Knutson SK, Cortez D, Sun ZW, Hiebert SW (2008). Deletion of histone deacetylase 3 reveals critical roles in S phase progression and DNA damage control. Mol Cell, 30(1), 61-72.
  25. Knutson SK, Chyla BJ, Amann JM, Bhaskara S, Huppert SS, Hiebert SW (2008). Liver-specific deletion of histone deacetylase 3 disrupts metabolic transcriptional networks. EMBO J, 27(7), 1017-28.


  1. Bhaskara S (2016). HDAC1,2 Inhibitors and Methods of Using the Same. U.S. Patent No. WO2016109549 A1. Washington, D.C.:U.S. Patent and Trademark Office.