Jump to Navigation

Name of the PhD Student

Name of the Supervisor

Brief Description of Project

Abhisikta Ghosh

Sharmila Sengupta

Cervical cancer is one of the leading causes of cancer related deaths among Indian women. Persistent infection with oncogenic Human Papillomavirus (HPV) is the major etiology of the disease. Expression of the viral oncoproteins E6 and E7 are critical for malignant transformation of the host cells and is mediated through the interaction with other host encoded molecules. E6 regulates the decay 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.

Anand Bhushan

Sreedhar Chinnaswamy One of the important events in a pathogen infection is the host-pathogen interaction that is critical to decide its outcome.  In this event there are two major players, host and the pathogen (virus, bacteria, parasite etc.).Host immune system plays a major role for the elimination of the pathogen and pathogen also tries different options to escape from the immune system of the host. In this episode if pathogen succeeds then the host will come down with the disease otherwise the pathogen is likely to be eliminated. I am is interested to learn how genetic variation in the immune response genes particularly those in innate immunity pathways decide on the outcome of an infection at the population level and also to learn the molecular mechanisms leading to these decisions. Currently, I am focusing on host-pathogen interactions in RNA viral diseases and intracellular parasitic diseases.

Ankit Patel

Sandeep Singh

My overall research goal is to contribute to the better understanding of cancer progression and metastasis. Tumor cells have the properties to convert its niche as a supportive environment for cancer progression.  I am interested in exploring how tumor micro-environment supports progression of solid cancers like oral squamous cell carcinoma.

Ankita Chatterjee

Priyadarshi Basu

Nonalcoholic Fatty Liver Disease (NAFLD) occurs when fat deposition takes place within the hepatocytes without intake of alcohol. NAFLD prevalence is highly variable across different ethnic populations worldwide. NAFLD is considered as the hepatic manifestation of metabolic syndrome and is highly associated with insulin resistance and obesity. Till now the genetic basis of the disease was mostly studied in obese/ overweight individuals. In a recent study on the rural populations of West Bengal showed that NAFLD also exists among lean individuals. My primary research focus is to understand and distinguish the genetic basis of NAFLD among these lean individuals. NAFLD has been conceptualized as a proggresive disease from simple steatosis (SS; characterized by the deposition of Triglyceride (TG) as lipid droplets in hepatocytes) to Nonalcoholic steatohepatitis (NASH; characterized by hepatocyte injury, inflammation, and/or fibrosis) to liver cirrhosis and eventually hepatocellular carcinoma. NAFLD is a complex disorder and environmental risk factors certainly play a significant role in disease pathogenesis along with genetic factors. Thus to understand the environmental impact on the disease etiology, I am also interested in studying the epigenetic signature of NAFLD.

Antara Biswas

Kartiki V Desai

JMJD6 is a putative histone arginine demethylase and lysyl hydroxylase, robustly associated with poor prognosis in breast cancer. It rapidly increases proliferation and motility of breast cancer cells, and our preliminary data suggests it interacts with long non-coding HOX Transcript Antisense RNA (HOTAIR). HOTAIR and its binding partner Enhancer of Zeste Homolog 2 (EZH2) correlate with poor survival in breast cancer patients. We therefore hypothesize that JMJD6, EZH2 and HOTAIR may together as a complex to play important role(s) in modulating gene expression towards enhanced oncogenesis. 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.

Arindam Palodhi

Arindam Maitra

Head and neck cancer, especially oral and oropharyngeal cancer, is one of the major threats to public health. Investigations of genomic, epigenomic and transcriptomic alterations that are associated with initiation and progress of tumerigenesis might lead to the complete understanding of the underlying molecular processes and result in improved prediction of risk and response to therapy. My goal is to harness the cutting edge genomic technologies to identify the major genomic alterations in head and neck cancer and use such information for development of biomarkers for improved diagnosis and patient care. Specifically, I am working on identification of the genomic drivers of Warburg Effect in gingivobuccal oral cancer by performing comprehensive analysis of exome and mitochondrial DNA mutations as well as alterations in mitochondrial biogenesis.

Barsha Saha

Srikanta Goswami

Chronic pancreatitis (CP) is an irreversible disease characterized by progressive inflammation, fibrosis of pancreas, and loss of pancreatic functions. Epidemiological studies have identified CP to be a major risk factor for pancreatic ductal adenocarcinoma (PDAC). PDAC is one of the most lethal diseases with an incidence rate almost equal to the rate of mortality. Elucidation of the molecular 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.

Bishnupriya Chhatriya

Srikanta Goswami

Chronic pancreatitis (CP) is a condition characterized by progressive and irreversible damage to both exocrine and endocrine components of the pancreas, eventually resulting in significant exocrine insufficiency and diabetes. In the recent years, several genetic risk factors for chronic pancreatitis have been identified in genes like PRSS1, PRSS2, SPINK1, CFTR, CTRC etc. In view of these findings, 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.

Chandrika Bhattacharyya

Bhaswati Pandit

Tuberculosis is a disease of antiquity and it remains a major health problem with two million deaths annually. One third of the total world population is infected with the aetiological agent, Mycobacterium tuberculosis. Of these, fewer than 10% ever develop disease, although the pathogen is not eradicated but rather contained. The underlying reasons for this variable outcome of pathogen infection is very ambiguous. This inconsistent pattern of outcome intrigued me a research problem, that how host immunological and genetic components play role in the tuberculosis infection. The main objective of my study is to identify the cytokines that are differentially expressed between tuberculosis patients and their immediate household contacts and to decipher the underlying associated genetic polymorphisms.

Debashree Tagore

Analabha Basu

Modern human originated in Africa nearly 150K YBP (Years Before Present) from where they spread to different parts of the world. This “out-of-Africa” migration took place nearly 60-75K YBP. The migrating population carried with them the genetic variants inherited from their parents but simultaneously, with the passage of time, accumulated mutations which gave rise to new variants. This migrating 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.

Jagyashila Das

Arindam Maitra

Birth outcome is an important determinant of an infant’s survival and health even during adulthood. Identifying the complex physiological and molecular pathways involved in modulation of pregnancy outcomes is thus of paramount importance for understanding and developing strategies to reduce adverse birth outcomes like preterm birth (PTB). Genetic markers alone may not provide sufficient insights 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.

Kavya Vipparthi

Sandeep Singh My research goal is to explore the role of tumor initiating or cancer stem cells in oral squamous cell carcinoma, one of the most aggressive cancers in Indians with high rates of metastasis. According to Cancer Stem Cell theory, targeting stem-like cells would be more helpful rather than the whole tumor because only these cells would have the potential to self-renew and maintain tumor growth and spreading while other cells do not. I am interested in learning the molecular mechanisms underlying the self- renewal and differentiation of stem-like cancer cells in oral cancer and how they contribute in tumor spread and metastasis. I am developing methods to identify and isolate these cells from oral-tumor tissue for its genomic and functional characterization. 

Krittika Bhattacharyya

Samsiddhi Bhattacharjee

Identification of causal variants together with the potential mechanism contributing to differential disease risk among individuals can offer most critical insights into the proper understanding of complex diseases. So far, Genome-Wide Association Studies have been remarkably successful in identifying genetic variants associated with various complex diseases. However, the interpretation of GWAS variants in terms of causality and the perception regarding the role played by these variants in the etiology of complex diseases have remained significantly ambiguous. Hence, we require robust statistical methods to efficiently integrate epigenomic and transcriptomic signatures and the intricate network of gene-regulation in relevant tissues along with functional annotations, pathways, and other evidence from publicly available databases. My primary interest lies in developing statistical methods for integrative analysis of multi-omics data to systematically identify causal variants within an associated region and to elucidate the causal mechanism through which they act. Methods developed will facilitate interpretation of complex disease associated loci not only to infer genetic causality through the epigenomic, transcriptomic and functional landscape in relevant tissues but also to highlight the upstream genes, pathways directly modulated by these genetic variants and consequent downstream changes.

Samanwoy Mukhopadhyay

Saroj K Mohapatra

Sepsis is one of the leading causes of morbidity and mortality in all age groups, despite improved care in the recent years. In the pediatric group, sepsis accounts for a large fraction of mortality under 5 years of age, and is one of the leading causes of death in neonates. There is no specific drug for treatment, owing to incomplete understanding of the biology of this disease. I believe that genomics of sepsis is an exciting area of research. For example, recent findings hint at reprogramming of the leukocyte transcriptome in the patients; and this change is coordinated, reproducible and linked to the progression of the disease. I am performing whole-genome gene expression profiling in patients of sepsis to detect strong and reliable signature of outcome (e.g., survival versus death). Additionally, I am interested in discovering the genetic and epigenetic underpinnings of the transcriptional signatures.

Shamita Sanga

Moulinath Acharya

There are more than seventy million patients in India, affected by rare diseases, many of which are related to vision. Rare eye diseases (REDs) are often congenital and more than 80% have a genetic basis. These diseases are associated with many genetic and allelic heterogeneity that lead to variable clinical phenotypes in patients.  Mutations in these genes, causal to REDs may cause alteration in regulatory pathways pertinent to eye development, there by leading to various disease conditions including developmental malformations. Mutations in the same genes lead to diverse clinical phenotypes, thereby making it difficult for genetic counsellors and clinicians to counsel the patients accurately. To delineate that,  I hypothesize that  the altered regulation of certain biochemical pathways is responsible for the pathogenesis of REDs and their varied clinical manifestations. Towards that goal, my aim rests on complete identification of the genomic risk factors and their underlying functions in the pathogenesis of REDs.

Shatakshee Chatterjee

Priyanka Pandey

My doctoral research is focused on “Assessment of Genomic Alterations Associated with Cancer Development, Progression and Therapy” with breast cancer as the disease model. I am currently working on the project entiltled “Unraveling the effect of pre-operative progesterone in operable breast cancer using RNA-sequencing” which is in collaboration with Tata Memorial Hospital, Mumbai. This project aims to find the molecular mechanisms that led to a beneficial effect of a single dose of progesterone to operable breast cancer patients through whole transcriptome profiling using RNA sequencing, an application of Next Generation Sequencing technology. I am associated with both the generation and analysis of RNA sequencing data. Development of workflow for analysis, management of data, pathway analysis and functional annotation of genes of interest are some of the interesting avenues of my work. My interests also lie in studying the impact of various levels hypoxia and its association on breast cancer patients. I am also interested in exploring the role of microRNAs in complex diseases like polycystic kidney disease.

Shrayashi Biswas

Samsiddhi Bhattacharjee

Genome wide association studies (GWAS) are used to discover association of genetic variants with various complex diseases and traits. However, testing markers across the genome in an unbiased manner leads to loss of power for such studies. My research project deals with increasing the power of such genome wide studies by incorporating information from other sources. Knowledge from pathways, gene expression/eQTL studies and transcriptional regulation can be integrated with the information from GWAS to help in identifying variants that could be otherwise missed in an unbiased genome-wise search. My work emphasizes on building a pipeline for integrative statistical analysis of such multi-omics data. The pipeline will enable investigators to discover novel genetic variants and understand their mode of action, thus helping to elucidate the underlying genetic makeup of complex diseases.

Subhashis Ghosh

Sandeep Singh

Human oral squamous cell carcinoma (OSCC) is the eighth most common cancer worldwide; and, the most prevalent cancer among men and fourth most common among women in India. Owing to the highly heterogeneous nature of oral carcinoma at both cellular and molecular levels, it is important to investigate the functions of altered pathways with respect to distinct cancer cell-types present within the tumor as well as in its microenvironment. In the context of cell-cell interactions, NOTCH related signaling is intriguing because of its juxtacrine mode of action. Therefore, I am interested in studying the functional consequences of altered NOTCH related genes and its regulation within oral tumors. My focus is to examine the mechanisms of reciprocal interactions between diverse cell-types and its significance in oral cancer initiation and progression.

Vijay Laxmi Roy

Partha Pratim Majumder

An individual is provided medication, whether vaccine or drug, without taking into account the genomic background of the individual; i.e., a one-size-fits-all approach is used.  However, it is known that genetic differences strongly account for inter-individual variability in treatment response, leading to huge wastage of funds and resources. This economic burden can be drastically minimized by genomic technologies. Very little is known in India about drug-response in relation to the genomic background of medication-recipient. The investigation of genetic backgrounds of recipients of medication can unfold key mechanisms associated with medication efficacy, which could be harnessed to design better medications for overcoming failure and poor response of current therapies.

Aim of the current study is to identify the genomic correlates of medication response to design a well represented panel of pharmacogenetic markers which will enable screening of individuals. These will help clinicians in selection of appropriate drug and genotype-specific dose. With plummeting cost of DNA sequencing technologies, genetic testing using such a panel will augment clinical decision making to meet personalized needs of each patient providing quality health care, while preventing adverse events and improve many lives.

Vikas Chandra

Priyadarshi Basu

I am doing my Ph. D. thesis under the supervision of Dr. Surajit Dhara at the NIBMG. Interest of our laboratory is to understand the genetic basis of chemotherapy resistance in cancer. I am pursuing my thesis to understand the therapy response in glioblastoma multiforme (GBM) as a disease model.  GBM is a devastating central nervous system malignancy with dismal prognosis. It shows a median survival of 14.6 months with standard care of surgery, radiotherapy and temozolomide (TMZ) chemotherapy. Both ionizing radiation (radiotherapy) and chemotherapy cause DNA damage by generating double and single strand breaks respectively followed by induction of a complex cascade of pathways called DNA damage response (DDR) pathways. Eventually the treatment determines the fate of the neoplastic cells, either to show a terminal phenotype like apoptosis/cellular senescence or a reversible phenotype like quiescence.  Apoptosis/senescence results better prognosis while quiescence results worse. I am trying to understand these treatment response phenotypes of GBM neoplastic cells at the cellular and molecular levels.