Rajdeep Chowdhury
Birla Institute of Technology and Science, Pilani, Massachusetts Institute of Technology, Indian Institute of Chemical Biology, University of Calcutta
About
Dr. Rajdeep Chowdhury is currently working as Professor, Department of Biological Sciences, BITS Pilani, Pilani Campus, Rajasthan. He earned his Bachelors and Masters degrees from Calcutta University and his PhD degree (CSIR-NET) from Jadavpur University. He has made contributions in the field of Cancer Biology. He was awarded DBT Post Doctoral Research Fellowship in 2008. In 2009, he joined Massachusetts Institute of Technology (MIT), USA, Department of Bioengineering, as a post doctoral researcher. At MIT he studied the myriad set of genetic events following Nitric Oxide (NO) exposure. In Oct 2012 he joined BITS-Pilani as an Assistant Professor in Dept of Bio-Sciences. He is currently investigating the molecular causes leading to cancer drug tolerance and subsequent resistance, with special emphasis on the role of the cellular homeostatic process, autophagy. He is also interested in understanding the epigenetic marks of drug tolerant cells. He has received research grants from various government funding authorities like (i) Department of Science and Technology (DST) under fast track scheme of Young Scientist; (ii) Science and Engineering Research Board (SERB) under Extra-Mural Research Funding; (iii) University Grants Commission (UGC) under Minor Research Project; (iv) Life Sciences Research Board (LSRB, DRDO) and (v) Department of Biotechnology under Pilot Project and (vi) projects from SERB and ICMR as co-PI as well. The findings from his works have been published in more than 30 international scientific journals.
Our research team is involved in understanding the diverse molecular mechanisms or adaptations of tumor cells contributing to drug tolerance and resistance. In this regard, the following aspects are investigated:
1. Characterizing signaling and epigenetic adaptations of tumor cells upon drug stress. 2. Understanding the role of autophagy during drug stress. 3. Exploring the role of master transcription regulator- YAP in drug resistance. 4. Analyzing role of high glucose in tumor drug resistance in pancreatic cancer. In this project, we explore alteration in expression of long non-coding RNAs (lncRNAs) with high glucose and explore its role in drug resistance.
Employment
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Birla Institute of Technology and Science, Pilani Professor2012 - Present
Education
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Massachusetts Institute of Technology Post Doctoral Research Associate2009 - 2012
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Indian Institute of Chemical Biology PhD2004 - 2009
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University of Calcutta Master of Science (MSc)1999 - 2001
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University of Calcutta Bachelor of Science (BSc)1996 - 1999
Projects & Funding
Projects & funding information is unavailable.
Publications (62)
- Photodynamic Therapy Induced Mitochondrial Targeting Strategies for Cancer Treatment: Emerging Trends and Insights. Save
- Nontoxic Aggregation-Induced Emissive Luminogen for the Detection of Amyloid Fibrils and Cellular Protein Aggregates. Save
- Mechanical microscopy of cancer cells: TGF-β induced epithelial to mesenchymal transition corresponds to low intracellular viscosity in cancer cells. Save
- Rational Molecular Designing of Aggregation-Enhanced Emission (AEE) Active Red-Emitting Iridium(III) Complexes: Effect of Lipophilicity and Nanoparticle Encapsulation on Photodynamic Therapy Efficacy. Save
- Transforming growth factor- β mediated regulation of epigenome is required for epithelial to mesenchymal transition associated features in liver cancer cells. Save
- Transcriptomic analysis reveals differential adaptation of colorectal cancer cells to low and acute doses of cisplatin. Save
- Epigenetic adaptations in drug-tolerant tumor cells. Save
- Chloroquine induces transitory attenuation of proliferation of human lung cancer cells through regulation of mutant P53 and YAP. Save
- Silver nanoparticle-induced alteration of mitochondrial and ER homeostasis affects human breast cancer cell fate. Save
- Interleukin-6 Induced Proliferation Is Attenuated by Transforming Growth Factor-β-Induced Signaling in Human Hepatocellular Carcinoma Cells. Save