Kartick Pramanik, PhD

Associate Professor of Pharmacology

  • Office: Coal Building, 814
  • Telephone: (606) 218-5423
  • E-mail: kartickpramanik@upike.edu

Medical Pharmacology
Physiology

BS, Pharmacy, Jadavpur University
MS, Pharmacology, Jadavpur University
PhD, Pharmacology, Jadavpur University
Postdoctoral, Pharmacology, Texas Tech University and Penn State University

  1. Ji, Z.-L., Yao, L., Pramanik, K. C., Cai, Z. J., eds. Artificial Intelligence for Translational Pharmacology. Lausanne: Frontiers Media SA. Frontier in Pharmacology, doi: 10.3389/978-2-88963-888-8, 2020
  2. Vijay P Kale, Hasan Habib, Robert Chistren, Milan Patel, Kartick C. Pramanik, Subash Jonnalagadda, Kishore Challagundla, Manoj K Pandey*. Old drugs new bold purpose: Assessing drug repurposing in hematological and childhood malignancies. Semen Cancer Biol. 2020 Mar 6. pii: S1044-579X(20)30063-8. doi: 10.1016/j.semcancer.2020.03.005.
  3. Monish Ram Makena, Himavanth Gatla, Dattesh Verlekar, Sahithi Sukhavasi, Manoj K. Pandey, and Kartick C. Pramanik*. Wnt/β-catenin Signaling: The culprit in Pancreatic Carcinogenesis and Therapeutic Resistance. Int. J. Mol. Sci. 20, 4242, 2019
  4. Kartick C. Pramanik, Monish Ram Makena, Kuntal Bhowmick and Manoj K. Pandey, Advancement of NF-κB Signaling Pathway: A Novel Target in Pancreatic Cancer. Int. J. Mol. Sci. Nov 19, 3890; doi:10.3390/ijms19123890. 2018
  5. Wu W, Karelia D, Pramanik K, Amin SG, Sharma AK, Jiang C, Lu J, Phenylbutyl isoselenocyanate induces reactive oxygen species to inhibit androgen receptor and to initiate p53-mediated apoptosis in LNCaP prostate cancer cells. Mol Carcinog. Aug;57(8):1055-1066, 2018
  6. Yong Zhang, Yinhui Dong, Michael W. Melkus, Shutao Yin, Su-Ni Tang, Peixin Jiang, Kartick Pramanik, Wei Wu, Sangyub Kim, Min Ye, Hongbo Hu, Junxuan Lu and Cheng Jiang. Role of P53-Senescence Induction in Suppression of LNCaP Prostate Cancer Growth by Cardiotonic Compound Bufalin Mol Cancer Ther. Nov;17(11):2341-2352. doi: 10.1158/1535-7163.MCT-17-1296. 2018

Certified by WBPC as a Registered Pharmacist

The central goal of my research is to discover natural, or biologic compounds in the prevention of pancreatic cancer progression and chemo-resistance.  Currently, my laboratory is actively engaged to understand the underlying mechanism of induction of senescence and activation of chemo-sensitization by natural agents: (A) Senescence is the proliferative arrest of cells in the cell cycle. Cells remain metabolically and synthetically active but are not able to proliferate. Therefore, senescence has become a favorable tumor suppressor therapy in cancer. Like many other cancers, pancreatic cancer often involves the inactivation of, or a mutation p53 tumor suppressor gene. Experimental evidence has shown that p53 loss allows cells to escape cell cycle proliferative arrest and activation of p53 induces senescence. My laboratory is actively involved to investigate the underlying mechanism of activation of p53 by natural agents in the induction of senescence. (B) The major obstacle to successful treatment in patients with pancreatic cancer is due to multi-drug resistance (MDR) which is a decreased effectiveness of an anticancer drug. Extensive studies reported that both p53 and multidrug transporters play important roles in chemoresistance. My laboratory is also involved to understand the fundamental mechanism of natural agents in the induction of P53 leading to chemo-sensitization of gemcitabine in pancreatic cancer cells.