(1) Molecular mechanisms linked to HIV-1 induced pathogenesis. Role of HIV-1 transactivator (Tat) protein in regulating viral latency and infectivity. Possible pharmacological interventions to enhance the efficacy and reduce the toxic side effects of anti-retroviral drugs.
(2) The role of drug-efflux transporters (ABC-transporters) in regulating chemoresistance development in Prostate and Breast cancer cells. Role of Cancer Stem Cells (CSCs). Identification of novel strategies to suppress the efflux of chemotherapeutic drugs and enhance their therapeutic efficacy.
PhD: Dept. of Microbiology, Immunology and Parasitology. LSU HSC, New Orleans, LA, 1995
Post-doctoral Research: Dept. of Pharmacology, TU HSC, New Orleans, LA, 1996-2001
Research Assistant Professor: Dept. of Pharmacology, TU HSC, New Orleans, LA, 2002-2003
Assistant Professor: Dept. of Pharmacology, TU HSC, New Orleans, LA, 2003-2010
Research Associate Professor: Dept. of Pharmacology, TU HSC, New Orleans, LA, 2010-present
Adjunct Assistant Professor: Neuroscience program, TU HSC, New Orleans, LA, 2008-present
Department of Pharmacology SL83, Tulane University School of Medicine, 1430 Tulane Avenue, New Orleans, LA 70112-2699. tel 504-988-4668; fax 504-988-5283; e-mail: firstname.lastname@example.org
Pubmed listing of Dr. Mondal's research publications
Despite the availability of potent anti-retroviral drugs against HIV-1 and potent chemotherapeutic agents against neoplasias, lack of efficacy at the site of action and increased toxicities linked to their long term use, has posed significant barriers to their utility in both AIDS and cancer. The focus of our research has been to develop novel strategies to increase the therapeutic concentrations of both anti-HIV drugs in HIV-infected microenvironments and of chemotherapeutic drugs in metastatic cancer foci. The following approaches are being employed to address these pharmacokinetic challenges: (i) We are currently working on a funded project to investigate the role of ABC family of membrane transporters (e.g. P-gp, MRP, and BCRP) in the efflux of anti-HIV drugs and of chemotherapeutic agents. (ii) Another avenue to increase drug concentrations at the site of action is being addressed via chemical conjugation of drugs with peptide-analogs which target cell surface receptors, on either HIV-infected cells or metastasized cancer cells, in order to increase their local concentrations and decrease their systemic toxicities. (iii). A third strategy being developed, in order to increase the therapeutic efficacy of both anti-HIV and anti-cancer gene therapy vectors. It has been recently shown that normal hematopoietic stem cells (HSCs) home to the sequestered reservoirs of HIV-infected cells and mesenchymal stem cells (MSCs) migrate towards the sequestered tumor foci. We plan to utilize a ‘trojan-horse’ approach to deliver gene therapy vectors which can abrogate the sanctuary sites of productive HIV-infection and of tumor growth. The persistence and propagation of these reservoirs select for drug resistant mutants of the virus and cancerous clones, and strategies towards their targeted elimination would be of significant importance to both of these fields
1430 Tulane Avenue, SL-83, New Orleans, LA 70112 504-988-5444 email@example.com