Somsubhra Nath

Assistant Professor

Education and research experiences:

• 2013 – 2015: Post Doctoral Research Associate at University of Nebraska Medical Center, Omaha, USA
• 2013 (February-July): Visiting Scientist at University of Texas Medical Branch, Galveston, USA
• 2012: Ph.D. in Cancer Cell and Molecular Biology, CSIR-Indian Institute of Chemical Biology (Degree awarded from the Dept. of Biotechnology, University of Calcutta)
• 2005: M.Sc. in Biochemistry, University of Calcutta
• 2003: B.Sc. in Zoology (Hons.), Presidency College, University of Calcutta

Awards and Recognitions:

• Elected ‘Associate’ of the West Bengal Academy of Science & Technology (WAST), 2021
• Shri Ramnath Jaju Award for Best Oral Presentation for Mid-level Scientists, 39th Annual Conference of Indian Association of Cancer Research (IACR), 2020
• Science and Engineering Research Board (SERB), Govt. of India - Early Career Award (Reference No. ECR/2015/000206), 2016
• University of Nebraska Medical Center Spring Travel Fellowship Award, 2015
• A.S. Mukherjee best platform presentation award for oral presentation by a young cell biologist at the XXXIV All India Cell Biology Conference (AICBC), 2010
• Fellowship- Council of Scientific & Industrial Research (CSIR)-National Eligibility Test, India (2006-2011)
• 1st class 1st position in M.Sc (Biochemistry) in 2005 from the University of Calcutta
• 1st class 1st position in B.Sc (Zoology Hons.) in 2003 from the University of Calcutta
• National Scholarship awarded for Bachelors Degree, 2003

With an interest in pursuing my future studies in Biology, I completed B.Sc. in Zoology honors from Presidency College (University of Calcutta), followed by M.Sc. in Biochemistry from the University of Calcutta. I pursued PhD from CSIR-Indian Institute of Chemical Biology, under the guidance of Prof. Susanta Roychoudhury, who is instrumental in my inclination towards adopting a career on research in Cancer Biology. Following PhD, I completed post-doctoralship from the University of Texas Medical Branch at Galveston and the University of Nebraska Medical Center at Omaha. After completing my post-doctoral work, I returned to India and joined Saroj Gupta Cancer Centre and Research Institute (SGCCRI), Kolkata in August 2015 as a scientist in the Basic and Translational Research division. I received the Early Career Award from SERB, Govt of India and started my independent research under this scheme. Subsequently, I received a few more grants (from DSTBT-Govt of WB & Lady Tata Memorial Trust-Institutional Research Grant), working through which I have focused on three major areas, namely, a) ‘Targeted therapy responsiveness in breast cancer’, b) ‘Front-line resistance therapy resistance in chronic myeloid leukemia (CML)’, c) ‘Ploidy status of breast cancer stem cells’. By the same time, I was acting as the Technical Director of Molecular Diagnostics Laboratory at SGCCRI. Under my direction, a dedicated team of technicians started offering RT-PCR and FISH based tests for cancer diagnostics and RT-PCR based detection of COVID-19. Indeed, this was an immensely satisfying part of my job where my scientific expertise was directly involved in the patient service. In my next move, I got the position of Assistant Professor at the Institute of Health Sciences, Presidency University and joined there in July 2022 with the assignment of teaching post-graduate students, along with continuing my career as an independent researcher.

Administrative Experience:

Technical Director, Molecular Diagnostics Laboratory, Saroj Gupta Cancer Centre & Research Institute, Sept, 2020 – June, 2022

Research Experience:

I.  As Assistant Professor (Institute of Health Sciences, Presidency University, Kolkata, from July, 2022 – till date) and as a Scientist (at Saroj Gupta Cancer Centre & Research Institute, Kolkata, August, 2015 to June, 2022)

After completing my post-doctoral work, I returned to India and joined Saroj Gupta Cancer Centre and Research Institute, Kolkata in August 2015 as a scientist in the Basic and Translational Research division and worked there till June, 2022. Following this, I joined the Institute of Health Sciences, Presidency University, Kolkata, as an Assistant Professor. I am working on the following areas:

• Endocrine therapy responsiveness in breast cancer
• Front-line resistance therapy resistance in chronic myeloid leukemia (CML)
• Ploidy status of breast cancer stem cells

These research works were/are being carried by from the following grants:

Ongoing:

1.      Grant Title: To develop therapeutic leads to counter PD-L1 mediated suppression of immune system in cancer microenvironment

Reference Number: NCD/Ad-hoc/189/2022-23; Role as investigator: Co-Investigator; Funding agency: ICMR; Award period: 2023-2026

2.      Grant Title: Clinical role of a pair of novel mutations in BCR-ABL1 towards therapy switch in imatinib-resistant chronic myeloid leukemia

Application No: 3330; Role as investigator: Principal Investigator; Funding agency: Lady Tata Memorial Trust (Institutional Research Grant); Award period: 2021-2024

Completed:

1.      Grant title: Impact of BCR-ABL mutations on front-line tyrosine kinase inhibitor therapy: an East Indian cohort study

Grant number: ST/P/S&T/9G-21/2016; Role as investigator: Principal Investigator

Funding agency: Department of Science, Technology and Biotechnology (DSTBT), Govt. of West Bengal; Award period: 2018-2022

2.      Grant Title: Delineating a novel transcriptional regulatory role of APC/C-Cdc20 complex and its impact on chromosomal instability in oral cancer (EMR/2015/001835)

Role as investigator: Co-Investigator; Funding agency: Science & Engineering Research Board (SERB)-Dept. of Science and Technology (DST), Govt. of India; Award period: 2019-2022

3.      Grant title: Deciphering CUEDC2-mediated molecular crosstalk between aneuploidy and receptor status of breast tumors (ECR/2015/000206)

Role as investigator: Principal Investigator; Funding agency: Science & Engineering Research Board (SERB)-Dept. of Science and Technology (DST), Govt. of India; Award period: 2016-2019

II. Post-doctoral work (carried out in UTMB & UNMC, USA):

After completing my pre-doctoral work, I pursued his research work as a post-doctoral fellow from University of Texas Medical Branch at Galveston, Texas and University of Nebraska Medical Centre at Omaha, Nebraska, USA. During this tenure, I investigated two novel aspects of DNA damage repair enzyme APE1: the functional relevance of secretory APE1 and the role of APE1 acetylation in potentiating cell survival.

A) The secretion of DNA damage repair protein APE1 by monocytes induces IL-6 production: implication of extracellular role of APE1 in inflammation

Apurinic/apyrimidinic endonuclease 1 (APE1) is a pleiotropic nuclear protein with roles in DNA base excision repair (BER) pathway as well as in transcriptional regulation. The extracellular release of APE1 in plasma has also been reported. However, the physiological importance of this secretion remained elusive. We showed that monocytes secrete APE1 upon inflammatory challenges. This secretion follows a non-classical route of transportation through microvesicle shedding and requires ATP-binding cassette transporters. Furthermore, challenging the monocytes with APE1 (recAPE1) increased expression and secretion of pro-inflammatory cytokine IL6. Phosphorylation of transcription factor NF?B-p65 upon APE1 treatment preceded increased occupancy to IL6 promoter resulting in the induced expression of the cytokine. This pool of APE1-induced IL6 further served to elicit immunological responses in both autocrine and paracrine fashions. Moreover, the extracellular IL6 promoted the secretion of APE1, thus indicating a functional positive feedback loop in this pathway. Additionally, the release of APE1 by necrotic cells indicates stress responsive behavior of this secretion. Together, this study demonstrated a novel role of extracellular APE1 and identified secretory APE1 as a mediator of IL6 dependent inflammatory responses (published in Cell Signal, 2017).

B) The role of acetylated APE1 in mitotic bookmarking of genes, DNA damage repair, and cell proliferation

Lineage maintenance of cells following mitotic exit relies on re-establishing gene expression patterns in progeny cells. Here, we showed that mammalian APE1, when acetylated (AcAPE1), constitutively associates with thousands of gene promoters and enhancer regions, and persists throughout mitosis. Notably, mitotic retention of AcAPE1 contributes to rapid post-mitotic reactivation of target genes via preferential repair of the specific region of the active genes. Tumor cells exhibit higher level of AcAPE1 and maintain full length APE1, which otherwise undergoes limited proteolytic-cleavage by a serine protease when un-acetylated. The results demonstrated a critical requirement of AcAPE1 for sustained cell proliferation (published in Oncotarget, 2016a), DNA damage repair (published in Oncotarget, 2016b) and a novel role of AcAPE1 in bookmarking of active genes through mitosis, potentially facilitating the inheritance of gene expression patterns in progeny cells (published in Mol Cell Biol, 2017).

III. Pre-doctoral work (carried out at CSIR-IICB, Kolkata, India):

A) Study of the regulation of spindle assembly checkpoint gene, UBCH10 and its role in genomic instability in human cancer

I completed his thesis work on the topic of “Study of the regulation of spindle assembly checkpoint gene, UBCH10 and its role in genomic instability in human cancer” from CSIR-Indian Institute of Chemical Biology, Kolkata, India. To study the regulation of mitotic ubiquitin carrier protein UbcH10, we identified a novel role of spindle assembly checkpoint (SAC) protein Cdc20 in transcription regulation of UbcH10. Proper mitotic progression depends on orderly ubiquitination and degradation of various mitotic inhibitors. At molecular level, Cdc20 activates the ubiquitin ligase APC/C that along with ubiquitin conjugating enzyme, UbcH10, executes this function. This is monitored by SAC that ensures accurate chromosome segregation. Both Cdc20 and UbcH10 are overexpressed in many cancer types and associated with defective SAC and chromosomal instability. The precise mechanism of correlated over-expression of these proteins remained elusive. We dissected that Cdc20 is a novel transcription factor regulating UBCH10 expression in a cell cycle specific manner by acetylation dependent chromatin remodelling. The WD40 domain of Cdc20 is required for this activity. Physical interaction between Cdc20 and APC/C-CBP/p300 complex and its subsequent recruitment to UBCH10 promoter is involved in this transactivation. We identified that Cdc20, in combination with mitotic ubiquitin ligase APC/C and co-activator CBP/p300, transcriptionally regulates UbcH10 expression (published in J Biol Chem., 2011). However, this Cdc20 transcription complex does not have any DNA binding domain. Towards this, we found a novel role of Rb-E2F1 axis in Cdc20-mediated UBCH10 transcription regulation. E2F1 interacts with and modulates the activity of Cdc20-transcription complex. Physical recruitment of Cdc20-transcription complex on UBCH10 promoter occurs through E2F1 consensus element. Furthermore, we provided evidence for the occurrence of mitotic abnormalities upon E2F deregulation. We showed that upregulated E2F1 activity drives mitotic slippage in Cdc20 and UbcH10 dependent manner, and associates with increased mitotic abnormalities in cancer cells (published in Mol Cell Biol, 2015). It could be speculated that Cdc20 overexpression and thus UbcH10 up-regulation synergistically cause the onset of aneuploidy and tumorigenesis. Further, this study contributes to the enrichment of information on E2F1 mediated cell cycle regulation and open therapeutic avenues in tumorigenesis.

B) Germline transmission of MAD2 deletion is associated with human foetal abortions

During my Ph.D. tenure, I also worked on a parallel project investigating the involvement of a functional spindle assembly checkpoint (SAC) in the maintenance of foetal growth during pregnancy. Germline transmission of a mutation is likely to be a prominent cause of recurrent abortions and birth defects. Mad2 is one of the crucial SAC molecules. Deregulated Mad2 has been associated with defective SAC and abnormal meiotic progression. We reported the germline transmission of a MAD2 copy number deletion in three trisomic aborted fetuses (published in Mol Hum Reprod, 2012). To the best of knowledge, no such germline human mutations have been reported for any of the SAC genes in aborted foetal samples. This study implicates the possible involvement of the SAC genes in pregnancy loss.

C) Additional participation:

During my PhD tenure, I also participated in projects investigating the role of p53 in the regulation of Cdc20 (published in Nucleic Acids Res, 2009) and UbcH10 (published in J Biol Chem, 2016), and the role of microRNA-125b in the regulation of mitotic cell death (published in Cell Death Differ, 2013). These important findings have broader implications in understanding the regulation of cell cycle and the nature of origin of chromosomal instability in human cancer.

Teaching & other experience:

Teaching experience:

• Theory and practical classes of MSc in i) Molecular Microbiology, ii) Biotechnology, and, iii) Virology & Immunology, Institute of Health Sciences, Presidency University (2022, July - till date), and, BSc in Biotechnology
• Certificate course on "Molecular Diagnostics", Institute of Health Sciences, Presidency University (2023 - till date)
• Course Coordinator, PhD Course work, Saroj Gupta Cancer Center & Research Institute (2017-2022)

Other experience:

• Convener, Colloquium Committee, Institute of Health Sciences (IHS), Presidency Univ
• Member, Purchase Committee, IHS, Presidency Univ
• Member, Admission Committee, IHS, Presidency Univ
• Member, Post Graduate Research Advisory Committee, IHS, Presidency Univ
• Member, Project Implementation Group, DST-FIST IHS, Presidency Univ
• EC member, Calcutta Consortium of Human Genetics (CCHuGe)
• EC member, Society of Biological Chemists (SBC), Kolkata Chapter

Editorial Role:

• Editorial Board Member, Scientific Reports
• Review Editor, Frontiers in Oncology (Section “Hematological Malignancies”)
• Guest Associate Editor, Frontiers in Genetics (Section “Cancer Genetics and Oncogenomics”; Topic “Genetic Regulation of Mitosis and Ploidy in Cancer”)
• Guest Associate Editor, Frontiers in Oncology (Section “Breast Cancer”; Topic “Novel Approaches to Overcome Drug Resistance in Breast Cancer”)

Current PhD students:

• Mr. Samya Dey [Thesis submitted]
• Mr. Ratnadip Paul [Thesis submitted]
• Mr. Debanil Dhar (SRF, DSTBT-Upendra Nath Brahmachari Research Fellow) [2022 - ]
• Mr. Souvik Alam (SRF, CSIR) [2023 - ]
• Mr. Koushik Saha (JRF, UGC) [2025 - ]
• Ms. Devlina Ganguly (JRF, CSIR) [2026 - ]

Lab alumni:

Dr. Stuti Roy [PhD awarded in 2024] (currently Post-doctoral Associate at Ohio State University, USA)

Dr. Suryendu Saha [PhD awarded in 2024] (currently Project Research Scientist-I at KIIT, India)

Ms. Puja Chakraborty (Project Fellow, SERB-DST) [2018 – 2021]

Ms. Soumi Basu (Project Fellow, DSTBT) [2018 - 2020]

• European Society of Medical Oncology (ESMO) [Membership ID 448284]
• Indian Association of Cancer Research (IACR) [Life Membership ID: LM-1060]
• European Hematology Association (EHA) [Membership ID 079249]
• Society of Biological Chemists (SBC) [Life Membership ID: 4317]
• Calcutta Consortium of Human Genetics (CCHuGe) [Life Member]

Original Article:  (* corresponding author)

1. Paul R, Sinharay S, Dhar D, Sarkar P, Chakraborty P, Ghosh S, Roy A, Saha A, Roychoudhury S, Nath S*. A signature of correlated CDC20 and UBCH10 expression indicates poor prognosis in primary head and neck squamous cell carcinoma. BMC Cancer. 2025 Sep 30;25(1):1458. doi: 10.1186/s12885-025-14773-x.

2. Dutta S, Chakraborty S, Ghosh A, Halder P, Majumder S, Paul R, Nath S, Mukherjee P. Tubulin hyperacetylation drives HMGB1 nuclear exit via the ROS-PARP1 axis, leading to rotenone-induced G2/M arrest. J Biol Chem. 2025 Sep 8;301(10):110695. doi: 10.1016/j.jbc.2025.110695.

3. Saha A, Sinha M, Roy S, Sengupta D, Banerjee S, Mitra R, Sarkar A, Chaudhuri T, Bhatatcharjee G, Nath S, Roychoudhury S, Sengupta M. Genetic association of regulatory single nucleotide variants in GSTA1 and SULT1A1 with cigarette smoke-related lung cancer in an eastern Indian population. Gene Protein Dis. 2024;3(3):3928. doi: 10.36922/gpd.3928.

4. Barik GK, Sahay O, Mukhopadhyay A, Manne RK, Islam S, Roy A, Nath S, Santra MK. FBXW2 suppresses breast tumorigenesis by targeting AKT-Moesin-SKP2 axis. Cell Death Dis. 2023 Sep 22;14(9):623. doi: 10.1038/s41419-023-06127-x

5. Kar S, Maji N, Sen K, Roy S, Maity A, Ghosh Dastidar S, Nath S, Basu G, Basu M. Reprogramming of glucose metabolism via PFKFB4 is critical in FGF16-driven invasion of breast cancer cells. Biosci Rep. 2023 24:BSR20230677. doi: 10.1042/BSR20230677

6. Saha S, Mukherjee M, Basak D, Panja P, Mondal PK, Ghosh R, Halder A, Chowdhury A, Dhali GK, Chattopadhyay BK, Ghosh S, Nath S, Datta S. High expression of mesothelin in plasma and tissue is associated with poor prognosis and promotes invasion and metastasis in gastric cancer. Adv Cancer Biol Metastasis. 2023, doi: https://doi.org/10.1016/j.adcanc.2023.100098.

7. Sengupta D, Mukhopadhyay P, Banerjee S, Ganguly K, Mascharak P, Mukherjee N, Mitra S, Bhattacharjee S, Mitra R, Sarkar A, Chaudhuri T, Bhattacharjee G, Nath S, Roychoudhury S, Sengupta M. Identifying polymorphic cis-regulatory variants as risk markers for lung carcinogenesis and chemotherapy responses in tobacco smokers from eastern India. Sci Rep. 2023 Mar 10;13(1):4019. doi: 10.1038/s41598-023-30962-9.

8. Mukhopadhyay A, Roy S, Saha S, Majumder S, Dey S, Bhattacharyya S, Gupta A, Nath S*. A comparative analysis of features and outcome of breast cancer in younger versus older women: A single center experience from Eastern Indian subcontinent. J Can Res Ther 2023 Apr;19(Supplement):S59-S66. doi: 10.4103/jcrt.jcrt_664_22.

9. Chakraborty P, Paul R, Chowdhury A, Mukherjee N, Nath S*, Roychoudhury S. The anaphase promoting complex/cyclosome ubiquitylates histone H2B on the promoter during UbcH10 transactivation. FEBS Lett. 2022 Feb;597(3):437-447. doi: 10.1002/1873-3468.14563

10. Dey S, Basu S, Shah S, Bhattacharyya D, Gupta PP, Acharjee M, Roychoudhury S, Nath S*. Deep sequencing reveals the spectrum of BCR-ABL1 mutations upon front-line therapy resistance in chronic myeloid leukemia: an Eastern-Indian cohort study. Cancer Treat Res Commun. 2022 Sep 15;33:100635. doi: 10.1016/j.ctarc.2022.100635

11. Roy S, Saha S, Dhar D, Chakraborty P, Singha Roy K, Mukherjee C, Gupta A, Bhattacharyya S, Roy A, Sengupta S, Roychoudhury S, Nath S*. Molecular crosstalk between CUEDC2 and ERα influences the clinical outcome by regulating mitosis in breast cancer. Cancer Gene Ther. 2022 Nov;29(11):1697-1706. doi: 10.1038/s41417-022-00494-x

12. Saha T, Bhowmick B, Sengupta D, Banerjee S, Mitra R, Sarkar A, Chaudhuri T, Bhattacharjee G, Nath S, Roychoudhury S, Sengupta M. No association of the common Asian mitochondrial DNA haplogroups with lung cancer in East Indian population. J Basic Clin Physiol Pharmacol. 2022 Mar 28. doi: 10.1515/jbcpp-2021-0352

13.  Ghuwalewala S, Ghatak D, Das S, Roy S, Das P, Butti M, Gorain M, Nath S, Kundu GC, Roychoudhury S. MiRNA-146a/AKT/β-catenin activation regulates cancer stem cell phenotype in oral squamous cell carcinoma by targeting CD24. Front Oncol. 2021 Oct 12;11:651692. doi: 10.3389/fonc.2021.651692

14.  Dey S, Bhattacharyya D, Gupta PP, Nath S*. Long-term Outcome of Philadelphia Chromosome Positive Leukemia from Eastern Indian Sub-continent: An Experience in the Era of Tyrosine Kinase Inhibitor (TKI) Therapy. Clin Lymphoma Myeloma Leuk. 2021 Nov; 21(11):e8 doi: https://doi.org/10.1016/j.clml.2021.06.026

15.  Sengupta D, Banerjee S, Mukhopadhyay P, Mitra R, Chaudhuri T, Sarkar A, Bhattacharjee G, Nath S, Roychoudhury S, Bhatatcharjee S, Sengupta M. A comprehensive meta-analysis and a case-control study give insights into genetic susceptibility of lung cancer and subgroups. Sci Rep. 2021 Jul 16;11(1):14572. doi: 10.1038/s41598-021-92275-z

16.  Nath S, Roychoudhury S, Kling MJ, Song H, Biswas P, Shukla A, Band H, Joshi S, Bhakat KK. The extracellular role of DNA damage repair protein APE1 in regulation of IL-6 expression. Cell Signal. 2017 Nov; 39:18-31. doi: 10.1016/j.cellsig.2017.07.019.

17.  Roychoudhury S, Nath S, Song H, Hegde ML, Bellot LJ, Mantha AK, Sengupta S, Ray S, Natarajan A, Bhakat KK. Human AP-endonuclease (APE1) is acetylated at DNA damage sites in chromatin and acetylation modulates its DNA repair activity. Mol Cell Biol. 2017 Mar 1;37(6):e00401-16. doi: 10.1128/MCB.00401-16.

18.  Sengupta S, Mantha AK, Song H, Roychoudhury S, Nath S, Ray S, Bhak­­­at KK. Elevated level of acetylation of APE1 in tumor cells modulates DNA damage repair. Oncotarget. 2016 Nov 15;7(46):75197-75209. doi: 10.18632/oncotarget.12113

19.  Bajaj S, Alam SK, Singha Roy K, Datta A, Nath S, Roychoudhury S. E2-ubiquitin conjugating enzyme, UBE2C, is reciprocally regulated by wild-type and gain-of-function mutant p53. J Biol Chem. 2016 Jul 1;291(27):14231-47. doi: 10.1074/jbc.M116.731398

20.  Bhakat KK, Sengupta S, Adeniyi V, Roychoudhury S, Nath S, Bellot LJ, Feng D, Mantha AK, Sinha M, Luxon B. Regulation of limited N-terminal proteolysis of APE1 in tumor via acetylation and its role in cell proliferation. Oncotarget. 2016 Apr 19;7(16):22590-604. doi: 10.18632/oncotarget.8026

21. Nath S, Chowdhury A, Dey S, Roychoudhury A, Ganguly A, Bhattacharyya D, Roychoudhury S. Deregulation of Rb-E2F1 axis causes chromosomal instability by engaging the transactivation function of Cdc20-APC/C complex. Mol Cell Biol. 2015 Jan 15; 35(2):356-69. doi: 10.1128/MCB.00868-14

22. Bhattacharjya S, Nath S, Ghose J, Maiti G, Biswas N, Bhattacharyya NP, Bandopadhyay S, Panda CK, Roychoudhury S. miR-125b promotes cell death  by targeting Spindle Assembly Checkpoint gene MAD1 and modulating mitotic progression. Cell Death Differ. 2013 Mar;20(3):430-42. doi: 10.1038/cdd.2012.135

23.  Nath S, Moghe M, Chowdhury A, Godbole K, Godbole G, Doipodhe M, Roychoudhury S. Is Germline transmission of MAD2 gene deletion associated with human foetal loss? Mol Hum Reprod. 2012 November;18(11):554–562. doi: 10.1093/molehr/gas031

24.  Nath S, Banerjee T, Sen D, Das T, Roychoudhury S. Spindle assembly checkpoint protein Cdc20 transcriptionally activates expression of ubiquitin carrier protein UbcH10. J Biol Chem. 2011 May 6;286(18):15666-77. doi: 10.1074/jbc.M110.160671

25. Banerjee T, Nath S, Roychoudhury S. DNA damage induced p53 downregulates Cdc20 by direct binding to its promoter causing chromatin remodeling. Nucleic Acids Res. 2009 May;37(8):2688-98. doi: 10.1093/nar/gkp110   

Review Article: (* corresponding author)

1.      Saha S, Dey S, Nath S*. Steroid hormone receptors: links with cell cycle machinery and breast cancer progression. Front Oncol. 2021. Mar 12;11:620214. doi: 10.3389/fonc.2021.620214

2.      Nath S, Ghatak D, Das P, Roychoudhury S. Transcriptional control of mitosis: deregulation and cancer. Front Endocrinol (Lausanne). 2015 May 5;6:60. doi: 10.3389/fendo.2015.00060

Book Chapter: (* corresponding author)

1. Nath S*, Roy S. (2021) Genomic Instability in Carcinogenesis: the role of oxidative stress. In: Chakraborti S., Ray B.K., Roychowdhury S. (eds) Handbook of Oxidative Stress in Cancer: Mechanistic Aspects. Springer, Singapore. https://doi.org/10.1007/978-981-15-4501-6_155-1

2. Roychoudhury S, Banerjee T, Nath S. CDC20 (cell division cycle 20 homolog (S. cerevisiae)). Atlas Genet Cytogenet Oncol Haematol. 2009; 13(2):104-105. doi: 10.4267/2042/44399

Editorial: (* corresponding author)

1. Nath S and Agarwal P (2023), Editorial: Genetic regulation of mitosis and ploidy in cancer. Front Genet. 14:1264772. doi: 10.3389/fgene.2023.1264772

Web Resource:

1. Roychoudhury S, Banerjee T, Nath S. CDC20 (cell division cycle 20 homolog (S. cerevisiae)). Atlas Genet Cytogenet Oncol Haematol. 2009; 13(2):104-105. doi: 10.4267/2042/44399.

Conference publication:

1. D. Bhattacharyya, S. Dey, R. N. Ghosh, P. P. Gupta, A. Gupta, S. Roychoudhury, S. Nath. PB2498 Diagnosis of acute leukemia and its impact in a resource poor centre of Eastern India: A retrospective overview. Hemasphere. 2020; 4:S1, 1106
2. D. Bhattacharyya, R. N. Ghosh, P. P. Gupta, A. Gupta, S. Roy, S. Roychoudhury, S. Nath. PB1972 Prevalence of imatinib resistance in chronic myeloid leukemia (CML): experience from a tertiary care centre in Eastern India. Hemasphere. 2020; 4:S1, 897
3. S. Nath. 65P Investigating the molecular connection between hormone receptor status and ploidy management in breast cancer. Annals Oncol. Volume 31, Supplement 2, S37, May 01, 2020. https://doi.org/10.1016/j.annonc.2020.03.199
4. D. Bhattacharyya, R. Ghosh, P. Gupta, A. Gupta, S. Roychoudhury, S. Nath. 1098P - Incidence of imatinib resistance in chronic myeloid leukemia (CML) patients: Experience from resource poor center of eastern India. Annals Oncol. Volume 30, Supplement 5, October 2019, Page v445, doi:10.1093/annonc/mdz251
5. S Nath, A Shukla, S Joshi, K K Bhakat. DNA damage repair enzyme APE1 is a non-classical secretory protein and acts as a mediator of IL6 dependent inflammatory responses (IRM11P.626). J Immunol. May 1, 2015, 194 (1 Supplement) 132.
6. Sengupta, S., Bellot, L., Nath, S., Bhakat, K. K. Mitotic bookmarking of genes- a novel dimension of epigenetic memory in cancer. Anticancer Res. October, 2014 34(10); 5835
7. S Nath, T Banerjee, D Sen, T Das, S Roychoudhury. Abstract 3075: A novel transcriptional role of spindle assembly checkpoint protein Cdc20 regulating the expression of mitotic ubiquitin carrier protein UbcH10, Cancer Res. April 15, 2011 71; 3075
8. S Bajaj, S Nath, S Roychoudhury. Abstract # 4269 - Novel TP53 gain-of-function mutations that activate the cell cycle regulatory gene, UBE2C, Cancer Res. May 1, 2009 69; 4269
9. T Banerjee, S Nath, S Roychoudhury. Repression of the spindle assembly checkpoint gene CDC20 by p53 upon DNA damage, Cancer Res. May 1, 2008 68; 2597