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.

Read less

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.

Read less

adaptation. In addition, my focus is to establish link between oral cancer genomic underpinning to the functional proteome by using mass-spectrometry based proteomic workflows that may serve as potential diagnostic/prognostic biomarkers. Read less

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.

Read less

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.

Read less

-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.

Read less

A et al., Journal of Pathology, 2022) identified signatures of tumour initiation and progression from oral precancerous lesions. Although the genomic underpinnings of post-treatment oral cancer recurrence are not heavily explored. Our data shows a subset of patients (~25%) come back with loco-regional-recurrence; sometimes within 1 year. The primary objective of my PhD-thesis is to understand the genomic and immunological underpinnings contributing to “early-recurrence” through comparative analysis of omics assays from – tumour and normal tissue samples - from oral cancer patients having (a) early and (b) late or no-recurrence; it will help in early patient stratification and informed clinical management. Read less

d histologic modifications that lead to malignant transformation which is yet to be delineated. Although much data on oral cancers have been generated by bulk genomic studies, the transcriptomic triggers of this progress from OSMF to OSCC is yet to be established. I am working on single cell RNA-sequencing to gain insights into the entire tumour ecology, including intratumoral and intertumoral heterogeneity, as well as cellular interactions that may play a critical role in in this process. Such information can facilitate early triaging of OSMF cases at risk of malignancy and hence reduce occurrences of OSCC. Read less

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.

Read less