3rd Edition of Euro-Global Conference on Biotechnology and Bioengineering

June 14-15 | Online Event

June 14-15, 2023 | Online Event
ECBB 2023

Koustav Sarkar

Koustav Sarkar, Speaker at Biotechnology Conference
SRM Institute of Science and Technology, India
Title: Chronic obstructive pulmonary disease (COPD) And its association with non-small cell lung cancer (Nsclc): Role of epigenetic modification in t helper cells


Chronic Obstructive Pulmonary Disease (COPD) and Lung cancer are the major reasons for lung disease related mortality worldwide. Chronic inflammation is a key attribute of COPD and a potential driver of lung carcinogenesis. Among various environmental risk factors, cigarette smoke plays a crucial role in the development and progression of COPD and lung cancer. Several epidemiological studies show that COPD patients are at a greater risk of developing lung cancer independently of cigarette smoking which suggests the role of genetic predisposition in the disease development. Uncovering the mechanistic link between these two diseases is hampered due to their heterogeneous nature: each is characterized by several sub-phenotypes of diseases. Our laboratory is mainly focused to study the specific epigenetic mechanism that occur in both COPD and lung cancer. The purpose of the current study is to uncover the link between alterations in inflammatory cytokine levels and disease progression in CD4+T cells of patients suffering from COPD and lung cancer. We also investigated the epigenetic regulation of mitochondrial Transcriptional Factor A (mtTFA) to delineate the role of oxidative stress-mediated inflammation in Lung cancer and COPD. The RT2 Profiler PCR array was used to examine the differential expression pattern of inflammatory genes in CD4+ T helper (Th) cells from COPD, NSCLC, and control subjects. Candidate inflammatory gene loci were selected and the enrichment of transcriptional factor and histone modifiers was analysed using ChIP-qPCR. In comparison to control subjects, a set of genes (e.g., BMP2, CCL2, IL5, VEGFA, etc.) are over-expressed whereas another set of genes (e.g., AIMP1, IFNG, LTA, LTB, TNF, etc.) are under-expressed in both COPD and NSCLC patients. The increased percentage enrichment of inflammation-associated transcription factors including NF-kB, CREB, HIF1?, and MYC at the loci of inflammatory genes was revealed by our chromatin immunoprecipitation (ChIP) data. H3K4me3, H3K9me3, H3K14Ac, HDAC1, 2, 3, 6 all showed dysregulated enrichment at the VEGFA gene locus. One of the epigenetic modifications, histone methylation, was found to be abnormal in the mtTFA complex in COPD and NSCLC patients in comparison to controls. Although there is mounting evidence of several links between these disorders, therapeutic options remain inadequate. Our findings contribute to the body of knowledge about therapeutic techniques that use inflammatory cytokines as a prognostic marker and highlight the need for epigenetic therapy for these debilitating lung diseases.

Audience take away notes:

  • Audience will learn that COPD patients are at a greater risk of developing lung cancer.
  • Mechanistic link between COPD and lung cancer will help the researcher to develop different types of immunotherapeutic strategies for lung disease.
  • Our research will help the other researchers to study the specific epigenetic mechanism(s) that occur in two interconnected diseases.
  • Our findings contribute to the body of knowledge about therapeutic techniques that use inflammatory cytokines as a prognostic marker and highlight the need for epigenetic therapy for the debilitating lung diseases.
  • Our study will definitely improve to find out several links between the lung disorders to develop different immunotherapeutic strategies to combat those diseases.


Koustav Sarkar completed his Ph.D. at the age of 28 years from Chittaranjan National Cancer Institute/Jadavpur University, Kolkata, India. Currently, he is the Research Assistant Professor in the Department of Biotechnology, SRM Institute of Science and Technology, Chennai, India. He presented papers in more than 50 national and international conferences. Dr. Sarkar has been involved in research over the last twenty years (including a Ph.D. and three Post-Docs) and made several important contributions to the development of advanced science and technology. He was involved in understanding the molecular mechanisms of the development of human immune responses in health & disease. Dr. Sarkar has already published 46 high-impact scientific publications in internationally reputed journals. He was also co-author of four book chapters. During my Ph.D., Dr. Sarkar developed a process for isolating glycoprotein(s) from neem leaf, which has immunomodulatory and cancer-preventive functions. One patent (Patent Number: 259434; Grant Date: 12-Mar-2014) has been granted for this invention. He found out that the neem leaf glycoprotein helped to generate carcinoembryonic antigen-specific anti-tumor immune responses utilizing macrophage & dendritic cell-mediated antigen presentation to T and B cells and the induction of type 1 protective immunity. To study the intricate molecular mechanisms involved in type 1 protective immunity, Dr. Sarkar moved to the USA. Research from his US laboratory was essential in revealing for the first time a novel nuclear function for a well-known cytoskeleton structure-associated protein, Wiskott Aldrich Syndrome Protein (WASp) in the transcriptional regulation of T helper cell 1 (Th1)-differentiation through its effect on epigenetic modifications at the T-BET gene-promoter locus. Since that time, Dr. Sarkar has been actively involved in further understanding how different types of epigenetic mechanisms are involved in T helper cells of lung cancer in association with Chronic Obstructive Pulmonary Disease (COPD).