ECM remodelling underlies fibrosis in chronic pancreatitis and desmoplasia in PDAC, shaping a pathological microenvironment that regulates tumour growth, immune infiltration, metastasis, and chemoresistance. Comprehensive profiling of ECM protein alterations is essential to understand disease progression and identify predictive biomarkers and novel therapeutic targets. My work aims to elucidate t he molecular basis of ECM protein changes and evaluate their functional consequences in CP and PDAC. Read less
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Pregnancy is a complex physiological process associated with successive changes in the uterine environment that facilitates childbirth. The period of gestation varies from 37-42 weeks in Term Birth and < 37 weeks in Preterm Birth (PTB). Globally, PTB is one of the leading cause of child mortality and morbidity. Many preterm survivors face a lifetime of disability, including respiratory, learn ing, visual disability and the number of premature babies is increasing exponentially with time. Identification of the complex aetiologies behind premature delivery is a big challenge worldwide. The vagina plays an important role in childbirth and is also home to a population of facultative and obligate anaerobic microorganisms that maintains the hygiene and pH of the vaginal milieu. This polymicrobial community is difficult to characterise through conventional microbiological culture based methods and are collectively termed as the Vaginal Microbiome. Recently, the role of oral as well as placental microbiome in preterm birth has also gained much interest. I am interested to investigate the change in composition and diversity of the Maternal Microbiome associated with Preterm birth in India. A multi-omics approach will be undertaken to dissect the host-microbiome interactions between host factors and differentially enriched microbial gene families as well as functional pathways that ultimately lead to Preterm Birth. Read less
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Maternal-fetal interactions play a major role during pregnancy. The optimal growth of the developing fetus and healthy birth depends on the nourishment it obtains during the gestational period. Placenta is the temporary feto-maternal organ that serves as a connective link between mother and fetus during pregnancy and is the hub of maternal-fetal dynamic interactions. This complex organ is made up of heterogeneous cell types which have diverse morphologies and dynamic functions at different time points during pregnancy. My aim is to study the variations in these cell type diversity and materno-fetal interactions at different periods of gestation at delivery using single cell transcriptomic approaches. Ultimately, I would like to identify single cell gene expression signatures which are associated with adverse outcomes. Such information can be used to triage women at risk of these birth outcomes so that appropriate clinical interventions can be used. Read less
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Oral cancer is a major health burden in India, with high incidence rates driven by tobacco use and betel quid chewing, leading to late-stage diagnoses and poor survival outcomes. My research focuses on understanding how genomic and epigenomic alterations, such as DNA methylation aberrations, mutations, and copy number variations, influence immune cell infiltration in head and neck squamous cell c arcinoma (HNSCC), particularly in oral cavity tumors. By analyzing these molecular changes, we aim to decipher their impact on tumor progression, immune response, and patient survival. This knowledge can help stratify patients into risk groups and enhance prognostic models, ultimately guiding personalized therapeutic strategies for better clinical outcomes. Read less
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Pancreatic cancer is the seventh leading cause of cancer related death globally. Late detection is one of the major obstacles for pancreatic cancer diagnosis. Metastasis is a very common phenomenon of pancreatic cancer with most people having advanced pancreatic cancer at the time of diagnosis. Metastatic pancreatic cancer is aggressive with poor prognosis. Epithelial mesenchymal transition (EMT) is a critical driver of metastasis that allow tumour cells to migrate, invade and colonize new sites. Recent studies show that TGF-beta can induce EMT. lncRNAs which were initially considered as junk element, in recent years they have been found to play important roles in different types of metastatic cancers, with their role to promote EMT and metastasis. Aim of my research project is to find out deregulated lncRNAs in TGF-beta induced cellular model of pancreatic cancer and also to explore functional involvement of selected lncRNA in pancreatic cancer metastasis. Read less
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I am Priyanshi Sisodia, integrated MSc-PhD student of NIBMG. Despite advancements in therapies, the major challenge in treating patients with oral cancer is loco-regional metastasis and recurrence. Tumor-stroma crosstalk is one of the non-cell autonomous factors that drives plasticity in cancer cells eventually leads to recurrence of more aggressive tumor. Among the diverse components of regulato rs, long non-coding RNAs (lncRNAs) have emerged critical for gene regulation and cellular plasticity. My study focuses on understanding how tumor microenvironment induced lncRNAs contribute to oral cancer progression. Read less
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In recent years, astroglial dysfunction has garnered considerable attention in Alzheimer’s disease (AD) research alongside neuro-centric approaches. Astrocytes are the predominant glial cells of the CNS and maintain panglial communication through gap junction (GJ) networks. Connexin 43 (Cx43) is the major astroglial GJ protein. Our overarching goal is to define how proteotoxic amyloid-beta (Aβ )-induced disruption of astroglial proteostasis triggers a cascade resulting in impaired Cx43 intracellular trafficking and Cx43-mediated astroglial communication. Identifying key triggers of Aβ-induced proteostatic deregulation that orchestrates Cx43 gap junctional intercellular communication (GJIC) deficit and molecular players involved in defective intracellular trafficking of Cx43 associated with overstimulated pathological hemichannel activity response are central to our present objectives. Furthermore, our research is directed towards unveiling ameliorative strategies to counteract the pathological effect of Aβ on Cx43 GJs for functional recovery of compromised GJIC in context of AD astrodegeneration. Read less
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In recent years, astrocytic dysfunction has garnered considerable attention in neurodegeneration in Alzheimer’s disease (AD) research. Connexin 43 (Cx43) is the major astroglial gap junction (GJ) protein. Cx43 hexamers constitute hemichannels and head-on docking of hemichannels of two apposed cells forms gap junctions (GJs). While GJs are of paramount importance for maintenance of panglial netw ork communication in central nervous system, providing trophic support to neurons and forming conduits for synaptic informational processing, increased Cx43 hemichannel activity leads to excitotoxicity. Interestingly, Aβ, the bonafide player of AD triggers Cx43 internalization in astrocytes with concomitant loss of gap junctional activity and increase in hemichannel activity. At this juncture, our study is directed towards understanding the Aβ-mediated astrocytic dysfunction process through gaining profound insights into the mechanistic underpinnings of Aβ mediated dysregulation of Cx43 gap junctional functions and how it contributes to AD neuropathology. Read less
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I am Rimpa Nandi, obtained my MSc from Vidyasagar University, Midnapore, West Bengal. Our lab is focused on studying oral cancer biology. Oral cancer ranks high among aggressive cancers. In India it is most frequent among male and fourth most common in female because of habit of chewing tobacco. One of the key players behind this aggressiveness is tumor-stroma crosstalk and cytokine receptor sign aling is important in this context. Therefore, I am investigating the possible targets against cytokine receptor signaling induced due to diversity in tumor stromal cells in oral tumor microenvironment. Read less
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Preterm birth is a major health burden as it is the leading cause of neonatal mortality. It is well established that there are genetic variations in the maternal genome that have the potential to regulate birth outcome. Structural variations like large deletions and insertions are likely to impact gene expression and contribute to higher variation in the genome than SNPs. Yet very few studies hav e been done to understand the role of SVs in the maternal genome how they might be leading to preterm birth. I am working on understanding the role of structural variations in the maternal genome of women delivering preterm using both long read and short read sequencing methods to identify SVs and to understand the biological mechanisms by which these SVs might be leading to preterm birth. Overall, I will be attempting to solve a strategically important public health problem using approaches of genome biology. Read less
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