My research interest is in deciphering genotype-environmental interactions in common diseases. Currently, my laboratory is studying the genomic and transcriptomic causes of Non-alcoholic fatty liver disease (NAFLD) in Indian populations.
Chatterjee A, Basu A, Das K, Singh P, Mondal D, Bhattacharya B,Roychoudhury S, Majumder PP, Chowdhury A, BASU P. (2020) Hepatic transcriptome signature correlated with HOMA-IR explains early Nonalcoholic Fatty Liver Disease pathogenesis, Annals of Hepatology, doi:https://doi.org/10.1016/j.aohep.2020.06.009
BASU P, Lung T, Lemsaddek W, Giang Sargent T, Williams DC Jr, Basu M, Redmond LC, Lingrel JB, Haar JL, Lloyd JA. (2007) EKLF and KLF2 have compensatory roles in embryonic e-globin gene expression and primitive erythropoiesis, Blood. 110:3417-3425.
BASU P, Morris PE, Haar J, Wani MA, Lingrel JB, Gaensler KML and Lloyd JA. (2005) KLF2 is essential for primitive erythropoiesis and regulates the human and murine embryonic β–like globin gene in vivo, Blood. 106:2566-71.
BASU P, Majumder PP, Roychoudhury S and Bhattacharyya NP. (2001) Haplotype analysis of genomic polymorphisms in and around the myotonic dystrophy locus in diverse populations of India, Human Genetics. 108, 310-317.
Bhattacharyya NP, BASU P, Das M, Pramanik S, Banerjee R, Roychoudhury S and Majumder PP. (1999) Negligible male gene flow across ethnic boundaries in India, revealed by analysis of Y-chromosomal DNA polymorphisms, Genome Research. 9, 711-719.
NAFLD is emerging as an important cause of liver disease in India, with a prevalence of 9% in rural India to 32% in the general population. NAFLD is an umbrella term which describes a range of related and progressive disorders, characterized by insulin resistance. The earliest stage of NAFLD is hepatic steatosis, which is characterized by the deposition of TG as lipid droplets in more than 5% of hepatocytes. Hepatic steatosis can progress to nonalcoholic steatohepatitis (NASH), characterized by hepatocyte injury, inflammation, and/or collagen deposition (fibrosis). NASH, in turn, can progress to cirrhosis, where hepatocytes are replaced by scar tissue composed primarily of type 1 collagen. Between 10 to 29% of individuals with NASH develop cirrhosis within 10 years. Cirrhosis can ultimately progress to hepatocellular carcinoma (4 to 27% of individuals). NAFLD is a complex genomic disorder which is considered as the hepatic manifestation of the metabolic syndrome.
The factors that promote TG deposition in the liver and the transition from steatosis to steatohepatitis and cirrhosis in humans have not been clearly defined. We have identified 6 SNPs in 6 genes in Indians that are associated with the disease, as well as a 28 gene transcriptomic “signature” that changes during progression from mild to advanced stages of the disease. Insulin resistance and increased body weight are other risk factors. Now we want to functionally understand and validate the role of these genes in NAFLD initiation and progression in vivo and in vitro, with an aim to identify possible therapeutic targets.
Projects: Genomic and Epigenomic analyses of Non Alcoholic Fatty Liver Disease (NAFLD) in the Indian population (funded by Dept. of Biotechnology)
|1995-2000||Ph.D||Jadavpur University (Mentor: Prof. Nitai P. Bhattacharyya)|
|1994-1995||Post M.Sc.||Saha Institute of Nuclear Physics, Calcutta.|
|1992-1994||M.Sc||Biophysics and Molecular Biology, University of Calcutta.|
Life member SBC, Life member ISHG, Life member CCHuge
Dr. Ankita Chatterjee
Dr. Vikas Chandra