PhD Students

ar mechanism driving the development of the diseases will not only help us understanding the disease biology but also help us identifying key molecules which could be used as potential biomarkers for early detection of the malignant disease. Regulation of gene expression by epigenetic mechanisms has gained much importance due to their important role in disease pathophysiology and my work revolves around delineating the role of key epigenetic factors in the development of chronic pancreatitis and pancreatic ductal adenocarcinoma.

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tent antiviral effects, its presence is associated with poor viral clearance in HCV-infected patients. Further studies have shown that polymorphisms, especially on IFNL4 and IFNL3, are intricately associated with many infectious and inflammatory diseases, such as fibrosis, COPD, asthma, thyroid, SLE, and certain cancers. Only a subset of individuals in our population (~>50% of Indians) can express a functional IFN-λ4. Even though strong association can be seen with IFNL4 polymorphisms with disease phenotypes in genetic studies, functional evidence for its role in such conditions has not been forthcoming. This has led to questions on the significance of IFN-λ4 in such studies at the same time favouring a role for the well-studied and more active IFN-λ3 in deciding some of the phenotypes. Healthy individuals can be good models to study the genetic and the consequent functional effects of IFN-λ3 or IFN-λ4 that may help us to understand the associated disease phenotypes better. I am interested in addressing the fundamental question of whether IFN-λ3 or IFN-λ4 or both could have functions in deciding the antiviral states in healthy individuals. I use an epidemiological study design to address this question. My work has the potential to decisively solve IFNL locus functional variant conundrum. Read less

r carcinoma. The pathogenicity of the disease is poorly understood and therapeutic options are very limited. My work emphasizes on understanding the molecular mechanisms and the role of related pathways involved in disease progression from mild to advanced stages and validation of the role of some specific genes associated with NAFLD in the Indian population in in vitro and in vivo models.

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particulate matters play significant role in COPD progression. Environmental triggers like cigarette smoke, pollen grains, carbon black nanoparticles, dust particles, microbial infection etc. are responsible for COPD exacerbations. NLRP3 inflammasome, a cardinal component of the innate immune system plays significant role in regulating the lung pathophysiology during exacerbations. The aim of my research is to examine the molecular pathway of NLRP3 inflammasome activation, identify the genetic factors associated with the disease in an unexplored heterogenic prototype study of Indian population and design intervention strategies using stem cells and genetically modified T cells. Read less

tients admitted to intensive care unit (ICU). I am focusing on the phenomenon called Neutrophil extracellular trap (NET), that is produced by neutrophil in response to pathogen. NETs consist primarily of decondensed chromatin of neutrophils and can trigger immune-thrombosis. The study shall have three components: computational (integrated analysis of multi-cohort transcriptomic data), clinical (collection of blood samples from neonates admitted to ICU with sepsis) and experimental (investigation of the molecules that trigger NET formation). Read less

e globe. The constant interaction between genotype(G) and environment(E) resulted in the local adaptation of human populations with phenotypic trait differences across populations. Thus, spatially structured populations and spatially varying phenotypic traits provide an opportunity to study the environmental factors which might have acted as selective forces for human populations to adapt to their local environment. My research work focuses on the development of deep learning architecture for modeling genotype-environment interactions to detect genomic regions under natural selection in different human populations. Read less

her and the fetus results in the preterm birth outcome. To combat the global health burden, early detection of the women having higher risk for delivering preterm is highly crucial which will help to provide personalized medical care to them. Since genomic markers have the potential to identify the high-risk women even to prior to pregnancy, so I intend to study the maternal genetic influences on preterm birth.

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helps in proper diagnosis. It has been found that some specific genes accelerate cancer progression rate in multiple pathways. There are some specific genes which act as biomarkers, affecting cell cycle regulation, cell signalling mechanisms etc. My research goal is the functional characterization of specified genes which act as progression biomarker and their interaction with other molecules that help retaining cellular proliferation in pancreatic cancer.

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sights into these processes. Epidemiologic observations, mostly from neonatal genomes, suggest probable role of epigenetic disruptions in enhancement of risk of PTB. However, very limited information is available on the role of maternal epigenome in PTB till date. My goal is to study the temporal variations in maternal DNA methylation landscape that occur during pregnancy and identify those that are associated with adverse outcomes.

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may induce several epigenetic changes. The consequence of such epigenetic modification in pancreatic cancer is not known completely yet. Moreover, a reliable epigenetic feature of active enhancers is the production of enhancer-directed transcripts (eRNAs). eRNAs are tightly regulated and play important roles in gene regulation, which was previously considered as junk element inside the cell with no function. My interest is to explore the role of eRNA in PDAC and how does eRNA regulate the progression of Chronic Pancreatitis to Pancreatic Cancer. Read less