PhD Students

hosts. It is seen that non-coding RNAs (miRNA and lnc-RNAs) play differential roles in the normal cellular physiology and molecular pathogenesis of several diseases, including cancer. My aim is to explore the involvement of miRNAs in HPV16 driven cervical cancers specifically associated with viral oncoprotein E7, the interaction or the crosstalk of lncRNA with cellular miRNAs, under the influence of E7 expression and to investigate how they influence HPV16 related CaCx pathogenesis.

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y of tumor suppressor p53, while E7 interacts with pRb leading to cellular transformation and neoplastic progression of the cervical epithelial cells. My aim is to identify the intrinsic HPV 16 E7 mediated pathways relevant for cervical cancer pathogenesis, focusing majorly on the immune pathway molecules and correlate such intrinsic host molecular factors with some of the extrinsic phenomena of tumor immune microenvironment in cervical cancer pathogenesis.

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n composition and diversity of the infant gut microbiome within the first 1 year of life and identifying the dysbiotic taxa along with their differentially enriched biosynthetic pathways that are associated with impaired child growth and development. The host-microbiome crosstalk will be investigated by a multi-omics approach and the contribution of both infant and maternal factors will be evaluated for their role in child growth impairment. Read less

care system is further compounded by the emergence of drug resistance. Multi-drug resistant (MDR)-TB is the resistance against at least two first line drugs: Isoniazid (INH) and Rifampicin (RIF). Resistance to standard antibiotic therapy allows for the drug-resistant M.tb to linger longer in the host and induce immunopathological changes which may differ from those caused by its drug-susceptible counterparts. The common determinants for developing drug resistant TB have been identified to include non-adherence to therapy, inadequate drug regimens, drug metabolism and immunological state of the host. Host genetic factors have been known to modulate drug metabolism genes. This has been exemplified in the studies regarding the NAT2 genotypes which are associated with the rates of acetylation of isoniazid. This clearly indicates at the involvement of host genetic factors in susceptibility to MDR-TB. The primary objective of my research is to explore the host genomics and functional genomics to dissect TB susceptibility and to determine host genetic basis of emergence of drug resistance. In doing so, I am studying the involvement of host genetic variants in susceptibility to drug resistant and drug sensitive TB cases through genome wide genotyping followed by identification of associated variants including variants in drug metabolism genes and validating these via targeted re-sequencing. Simultaneously in the functional genomics aspect, I am looking into the whole transcriptome to identify a gene signature which discriminates drug resistant and drug sensitive TB cases.

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her insight into the peopling of India. I will also look at the ancient gene flow from East and Southeast Asia into South Asia and ideally connect that to the ‘Out-of-Africa’ migration of anatomically modern humans.  I want to create new statistical methods for this purpose, as required, to supplement the existing methodology.

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-pause release of RNA pol-II on poised sites. To determine its complete function in tumorigenesis, we have haveperformed mass spectrometric analysis of proteins immunoprecipitated using JMJD6 specific antibodies. Many transcription and DNA binding factors were found and one such protein was Y-box interacting protein 1 (Ybox-1), a transcription factor that has both DNA and RNA binding activities.  This protein is also associated with poor prognosis and metastasis in breast cancer. We hypothesize that JMJD6 and Ybox1 may physically interact and influence gene expression to promote breast cancer progression leading to poor patient survival. Exploring these molecular mechanisms forms the basis of my thesis. In the long run, this may steer us towards developing effective drugs against advance breast cancer.

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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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dings, my proposed work aim to find out the prevalence of these common genetic changes causative to CP in the population of North-Eastern Region (NER) of India where CP and CP related death are of high incidence. Such population specific variations have significant contribution towards the formulation of diagnostic and therapeutic strategies specific for those individuals. The outcome of the study is also believed to add substantial information to the existing knowledge of the molecular mechanism of the development of CP. Furthermore, chronic pancreatitis (CP) is a progressive benign fibro-inflammatory disease of the pancreas and is one of the risk factors of pancreatic cancer. The development of pancreatic cancer in CP is a classic example of chronic inflammation progressing to cancer that is also found in other organs of the body. Pancreatic Cancer (CAPan) is one of the most aggressive forms of cancers, with only 4-5% 5-year survival. Not much is known about the molecular changes that lead to the development of CAPan in CP patients. Therefore, another important aspect of my research objective is to delineate that process and to find out whether these changes can be used for development of biomarkers for early detection of pancreatic cancer in CP patients, as well.

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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

igrating population entered into India through different corridors and created a rich pool of variants. My research objective is to study these variants to unravel finer intricacies of population migration in the Indian sub-continent. The Indian population harbors common and unique variations which have serious implications on human health and diseases. I, therefore, intend to study the genomic variations in detail and use this knowledge in deciphering association of genomic variants with diseases.

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