GOUTAM DEY
Case Western Reserve University
Research areas: Medicine · Oncology · Pancreatic and Hepatic Oncology Research · Cancer Immunotherapy and Biomarkers · Immune cells in cancer
About
Professional Summary
Cancer biologist with 12+ years of experience across pancreatic, ovarian, and breast cancer research. Expertise in non-canonical oncogenic signaling, including nuclear KRAS and nuclear CD55, DNA repair pathways, and therapy resistance. Strong track record of high-impact publications (H-index 27; >2,200 citations), translational discoveries, and invention disclosures. Experienced in leading independent research projects, mentoring trainees, and contributing to competitive grant development, with a clear trajectory toward establishing an independent academic research program.
Education
PhD (2017) in Cancer Biology from the Indian Institute of Technology Kharagpur, India
Master of Pharmacy (M. Pharm) (2010) in Pharmaceutical Engineering/Pharmacology from Jadavpur University, Kolkata, India
Bachelor of Pharmacy (B. Pharm) (2008) in Pharmaceutical Science from Jadavpur University, Kolkata, India
Experience
Senior research associate (2024-current) in pancreatic cancer at Case Western Reserve University, USA
Postdoctoral fellow (2018-2024) in ovarian cancer research from the Cleveland Clinic Foundation, USA
Research fellow (2017-2018) in Cancer Biology from the Indian Institute of Technology Kharagpur, India
Quality control trainee (2010-2011) in Fresenius Kabi Oncology, Kalyani, India
Research
Senior research associate at Case Western Reserve University, USA
• Non-canonical function of KRAS in pancreatic cancer.
Postdoctoral research at the Cleveland Clinic, USA
• Role of nuclear CD55 in chemoresistance and stemness phenotype in ovarian cancer.
• Disruption of the DNA repair pathway by blocking LCK signalling and its implication in PARP targeted therapy in BRCA proficient ovarian cancer.
• Heating immune cells to induce cytotoxic effect in ovarian cancer cells.
Research fellow at the Indian Institute of Technology Kharagpur, India
• IL-6/IL-6R Targeted Therapy in Breast Cancer.
Doctoral Research at the Indian Institute of Technology Kharagpur, India
• Akt Targeted Therapy in Breast Cancer with Marine Bacterial Lipopeptide in Preclinical Model.
Fresenius Kabi Oncology Ltd
• Quality control analysis of anti-cancer molecules.
Undergraduate Research
• Development and validation of an LC-MS/MS method for analysis of Zolpidem in human plasma and its application to a pharmacokinetic study.
Research statements
A central goal has driven my research career: to understand the molecular mechanisms that govern cancer initiation, progression, therapeutic resistance, and metastasis, with the long-term objective of developing effective and clinically relevant strategies to overcome drug resistance. Over the past decade, my work has integrated molecular signaling, pharmacology, and translational models to reveal previously unrecognized oncogenic pathways in breast, ovarian, and pancreatic cancers.
My doctoral research at the Indian Institute of Technology Kharagpur focused on identifying bioactive anticancer molecules derived from marine microorganisms. I discovered the lipopeptide Iturin A from Bacillus megaterium and demonstrated its potent anticancer activity in breast cancer (Scientific Reports, 2015). Mechanistically, I established Iturin A as a selective inhibitor of Akt kinase, leading to the suppression of GSK3β and FoxO3a signaling and triggering apoptotic cell death. I expanded this work by showing that Iturin A inhibits tumor angiogenesis through blockade of the MD2/TLR4 signaling axis (Cellular Signalling, 2017). I also demonstrated that Iturin A can reverse docetaxel resistance in breast cancer by suppressing Akt and sensitizing resistant cells to chemotherapy. These findings laid the foundation for advancing Iturin A as a preclinical anticancer therapeutic, which I validated through biodistribution and toxicity studies (RSC Advances, 2016).
After completing my PhD, I continued as a research fellow at IIT Kharagpur, where I uncovered a previously unknown role for IL-6/IL-6R/MAO-A signaling in promoting invasion and angiogenesis in breast cancer (British Journal of Cancer, 2018). This work deepened my interest in cytokine-driven resistance mechanisms and tumor microenvironment dynamics.
During my postdoctoral training at the Cleveland Clinic, I transitioned into translational ovarian cancer research. I discovered that the non-receptor tyrosine kinase LCK plays a central and unexpected role in regulating homologous recombination (HR) repair. I demonstrated that DNA damage induces nuclear activation of LCK, which stabilizes RAD51, BRCA1, and BRCA2, thereby promoting HR-mediated repair. Genetic or pharmacologic inhibition of LCK destabilized these repair proteins, blocked RAD51 foci formation, and sensitized HR-proficient ovarian cancer cells to PARP inhibitors both in vitro and in vivo (Journal of Ovarian Research, 2023). These results identify LCK as a novel and druggable regulator of DNA repair with strong therapeutic implications for expa
Employment
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Case Western Reserve University Senior Research Associate2024 - Present
Education
Education history is unavailable.
Projects & Funding
Projects & funding information is unavailable.
Publications (59)
- Data from Increased Glucose Availability Sensitizes Pancreatic Cancer to Macrophage-Targeting Immunotherapies Save
- Figure 1 from Increased Glucose Availability Sensitizes Pancreatic Cancer to Macrophage-Targeting Immunotherapies Save
- Figure 2 from Increased Glucose Availability Sensitizes Pancreatic Cancer to Macrophage-Targeting Immunotherapies Save
- Figure 3 from Increased Glucose Availability Sensitizes Pancreatic Cancer to Macrophage-Targeting Immunotherapies Save
- Figure 4 from Increased Glucose Availability Sensitizes Pancreatic Cancer to Macrophage-Targeting Immunotherapies Save
- Figure 5 from Increased Glucose Availability Sensitizes Pancreatic Cancer to Macrophage-Targeting Immunotherapies Save
- Figure 6 from Increased Glucose Availability Sensitizes Pancreatic Cancer to Macrophage-Targeting Immunotherapies Save
- Supplemental Figure 1 from Increased Glucose Availability Sensitizes Pancreatic Cancer to Macrophage-Targeting Immunotherapies Save
- Supplemental Figure 10 from Increased Glucose Availability Sensitizes Pancreatic Cancer to Macrophage-Targeting Immunotherapies Save
- Supplemental Figure 11 from Increased Glucose Availability Sensitizes Pancreatic Cancer to Macrophage-Targeting Immunotherapies Save
- Supplemental Figure 12 from Increased Glucose Availability Sensitizes Pancreatic Cancer to Macrophage-Targeting Immunotherapies Save
- Supplemental Figure 2 from Increased Glucose Availability Sensitizes Pancreatic Cancer to Macrophage-Targeting Immunotherapies Save
- Supplemental Figure 3 from Increased Glucose Availability Sensitizes Pancreatic Cancer to Macrophage-Targeting Immunotherapies Save
- Supplemental Figure 4 from Increased Glucose Availability Sensitizes Pancreatic Cancer to Macrophage-Targeting Immunotherapies Save
- Supplemental Figure 5 from Increased Glucose Availability Sensitizes Pancreatic Cancer to Macrophage-Targeting Immunotherapies Save
- Supplemental Figure 6 from Increased Glucose Availability Sensitizes Pancreatic Cancer to Macrophage-Targeting Immunotherapies Save
- Supplemental Figure 7 from Increased Glucose Availability Sensitizes Pancreatic Cancer to Macrophage-Targeting Immunotherapies Save
- Supplemental Figure 8 from Increased Glucose Availability Sensitizes Pancreatic Cancer to Macrophage-Targeting Immunotherapies Save
- Supplemental Figure 9 from Increased Glucose Availability Sensitizes Pancreatic Cancer to Macrophage-Targeting Immunotherapies Save
- Increased Glucose Availability Sensitizes Pancreatic Cancer to Macrophage-Targeting Immunotherapies Save