Subhash Haldar

Subhash Haldar
Assistant Professor

Previous appointments:

1. Research Associate, Bose Institute, Kolkata (2009-2012).

2. Postdoctoral Scientist, Samuel Oschin Comprehensive Cancer Institute, Los Angeles, CA (2012-2016).

3. Project Scientist, Samuel Oschin Comprehensive Cancer Institute, Los Angeles, CA (2016-2017; 2018-2019).

4. Assistant Professor, University of Gour Banga, West Bengal (2021-2022). 

Research interests:

We  are interested to understand the role of the tumor microenvironment (TME) in cancer progression and different mediators involved in metastatic progression through the use of in vitro and in vivo model systems.


Address: Biological Sciences
Unified Academic Campus
Bose Institute
EN-80, Sector V
Bidhan Nagar
Kolkata - 700 091, India
E-Mail: subhash.haldar[at]
Phone: +91-33-25693279


1. Commonly used chemotherapeutic drugs  are known to induce inflammasome formation in the tumor microenvironment of certain cancers. Inflammasome components and pathways associated with  inflammation and cancer in TME could be novel targets to tackle cancer progression. In  TME,  many factors are being secreted as a result of chemotherapeutic treatment, including IL-1β, IL-18 etc. through the activation of the inflammasome complex. Since these cytokines are pro-inflammatory in nature, they have also pro-tumorigenic effects. We examine the signalling pathways involved  in cancer progression and therapy resistance in connection with inflammasome activation.

2. Secondly, chemotherapeutic drugs modulate epigenetic factors involved in tumorigenesis. It is established that tumor suppressor genes become switched off in a somatically heritable fashion through epigenetic changes, in addition to their classical mutations. Because of the dynamic nature and ready capacity for reversibility, epigenetic modifications are appealing therapeutic targets in cancer. Hence, we are exploring the epigenetic factors influencing inflammasome formation during tumor progression, metastasis, and in chemotherapy-resistant cancer.


1. Prognostic value of circulating mitochondrial DNA in prostate cancer and underlying mechanism. Borah S, Mishra R, Dey S, Suchanti S, Bhowmick NA, Giri B, Haldar S. Mitochondrion. 2023 May 19;71:40-49. doi: 10.1016/j.mito.2023.05.005.

2. Cancer epithelia-derived mitochondrial DNA is a targetable initiator of a paracrine signaling loop that confers taxane resistance. Haldar S, Mishra R, Billet S, Thiruvalluvan M, Placencio-Hickok VR, Madhav A, Duong F, Angara B, Agarwal P, Tighiouart M, Posadas EM, Bhowmick NA. Proc Natl Acad Sci U S A. 2020 Apr 14;117(15):8515-8523. doi: 10.1073/pnas.1910952117.

3. Stromal epigenetic alterations drive metabolic and neuroendocrine prostate cancer reprogramming. Mishra R, Haldar S, Placencio V, Madhav A, Rohena-Rivera K, Agarwal P, Duong F, Angara B, Tripathi M, Liu Z, Gottlieb RA, Wagner S, Posadas EM, Bhowmick NA. J Clin Invest. 2018 Oct 1;128(10):4472-4484. doi: 10.1172/JCI99397.

4. Inflammation and pyroptosis mediate muscle expansion in an interleukin-1β (IL-1β)-dependent manner. Haldar S, Dru C, Choudhury D, Mishra R, Fernandez A, Biondi S, Liu Z, Shimada K, Arditi M, Bhowmick NA. J Biol Chem. 2015 Mar 6;290(10):6574-83. doi: 10.1074/jbc.M114.617886.

5. Histone deacetylase inhibitors mediate DNA damage repair in ameliorating hemorrhagic cystitis. Haldar S, Dru C, Mishra R, Tripathi M, Duong F, Angara B, Fernandez A, Arditi M, Bhowmick NA. Sci Rep. 2016 Dec 20;6:39257. doi: 10.1038/srep39257.

6. Heterogeneous cancer-associated fibroblast population potentiates neuroendocrine differentiation and castrate resistance in a CD105-dependent manner.Kato M, Placencio-Hickok VR, Madhav A, Haldar S, Tripathi M, Billet S, Mishra R, Smith B, Rohena-Rivera K, Agarwal P, Duong F, Angara B, Hickok D, Liu Z, Bhowmick NA. Oncogene. 2019 Jan;38(5):716-730. doi: 10.1038/s41388-018-0461-3.

7. Antagonizing CD105 enhances radiation sensitivity in prostate cancer. Madhav A, Andres A, Duong F, Mishra R, Haldar S, Liu Z, Angara B, Gottlieb R, Zumsteg ZS, Bhowmick NA. Oncogene. 2018 Aug;37(32):4385-4397. doi: 10.1038/s41388-018-0278-0.

8. Periodontal inflammation recruits distant metastatic breast cancer cells by increasing myeloid-derived suppressor cells. Cheng R, Billet S, Liu C, Haldar S, Choudhury D, Tripathi M, Hav M, Merchant A, Hu T, Huang H, Zhou H, Bhowmick NA. Oncogene. 2020 Feb;39(7):1543-1556. doi: 10.1038/s41388-019-1084-z.

9. Epigenetic changes in fibroblasts drive cancer metabolism and differentiation. Mishra R, Haldar S, Suchanti S, Bhowmick NA. Endocr Relat Cancer. 2019 Dec;26(12):R673-R688. doi: 10.1530/ERC-19-0347.

10. High copies of SUM1 enhance the stability of wild-type microtubules against adverse conditions in Saccharomyces cerevisiae. Haldar S, Sarkar S, Singh V, Sinha P. Biochem Biophys Res Commun. 2012 Feb 17;418(3):525-30. doi: 10.1016/j.bbrc.2012.01.059.

11. The budding yeast protein Sum1 functions independently of its binding partners Hst1 and Sir2 histone deacetylases to regulate microtubule assembly. Sarkar S, Haldar S, Hajra S, Sinha P. FEMS Yeast Res. 2010 Sep;10(6):660-73. doi: 10.1111/j.1567-1364.2010.00655.x.

12. TGF-β controls stromal telomere length through epigenetic modifications. Mishra R, Haldar S, Biondi S, Bhari VK, Singh G, Bhowmick NA. 3 Biotech. 2022 Nov;12(11):290. doi: 10.1007/s13205-022-03346-5.

13. Multifaceted entrancing role of glucose and its analogue, 2-deoxy-D-glucose in cancer cell proliferation, inflammation, and virus infection. Dey S, Murmu N, Mondal T, Saha I, Chatterjee S, Manna R, Haldar S, Dash SK, Sarkar TR, Giri B. Biomed Pharmacother. 2022 Oct 10;156:113801. doi: 10.1016/j.biopha.2022.113801.

14. Bone marrow mesenchymal stem cells interact with head and neck squamous cell carcinoma cells to promote cancer progression and drug resistance. Liu C, Billet S, Choudhury D, Cheng R, Haldar S, Fernandez A, Biondi S, Liu Z, Zhou H, Bhowmick NA. Neoplasia. 2021 Jan;23(1):118-128. doi: 10.1016/j.neo.2020.11.012.

15. Secondary Structure-Dependent Physicochemical Interaction of Oligonucleotides with Gold Nanorod and Photothermal Effect for Future Applications: A New Insight. Das U, Sahoo A, Haldar S, Bhattacharya S, Mandal SS, Gmeiner WH, Ghosh S. ACS Omega. 2018 Oct 31;3(10):14349-14360. doi: 10.1021/acsomega.8b00969.

16. Mechanisms of hemorrhagic cystitis. Haldar S, Dru C, Bhowmick NA. Am J Clin Exp Urol. 2014 Oct 2;2(3):199-208. 2014.

17. A high molecular weight protein Bengalin from the Indian black scorpion (Heterometrus bengalensis C.L. Koch) venom having antiosteoporosis activity in female albino rats. Haldar S, Das Gupta S, Gomes A, Giri B, Dasgupta SC, Biswas A, Mishra R, Gomes A. Toxicon. 2010 Feb-Mar;55(2-3):455-61. doi: 10.1016/j.toxicon.2009.09.013.

18. Experimental osteoporosis induced in female albino rats and its antagonism by Indian black scorpion (Heterometrus bengalensis C.L.Koch) venom. Gomes A, Haldar S, Giri B, Mishra R, Saha A, Dasgupta S, Gomes A. Toxicon. 2009 Jan;53(1):60-8. doi: 10.1016/j.toxicon.2008.10.011.

19. Compositions and methods for treating diseases and conditions by depletion of mitochondrial or genomic dna from circulation. S Borah, N Bhowmick, S Haldar. US Patent App. 17/779,716. Publication date: 2023/4/20


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