Dr. Pramod K. Srivastava, an accomplished leader in basic and translational research, is the director of the Carole and Ray Neag Comprehensive Cancer Center.
Srivastava is a professor and interim chairman of the Department of Immunology, director of the Center for Immunotherapy of Cancer and Infectious Diseases, and part of the leadership team of the Connecticut Institute for Clinical and Translational Science (CICATS). He holds the Eversource Energy Chair in Experimental Oncology.
He has earned international acclaim for his groundbreaking work in the immunological function of heat shock proteins and in cancer immunology, is widely published in scholarly journals and serves on editorial boards for several major journals in immunology.
Areas of Expertise (2)
University of Connecticut School of Medicine: M.D.
Centre for Cellular and Molecular Biology: Ph.D., Biochemistry
University of Allahabad: M.S., Botany
- Scientific Advisory Council, CRI: Advisory Committee
- American Association of Immunologists
- American Association of Cancer Research
John Hans and Edna Alice Old Postdoctoral Fellowship (professional)
Awarded by the Cancer Research Institute
Media Appearances (2)
Hot peppers and weed work on the gut to tamp down inflammation
“This allows you to imagine ways the immune system and the brain might talk to each other. They share a common language,” said study author Pramod Srivastava, M.D., Ph.D., professor of immunology and medicine at UConn School of Medicine. Anadamide is that link and the researchers also found that it, when created, works to make more anandamide and spurs another receptor to make macrophages, which are immune cells that tamp down inflammation...
Algorithms compete to predict recipe for cancer vaccine
The trick that vaccine researchers must master is using a tumour’s DNA to predict which mutations to home in on. “We can do the sequencing and find out the mutations, but it’s very hard to know which of these tens or hundreds or thousands of mutations are actually going to protect people from the growth of their cancers,” says Pramod Srivastava, an immunologist at the University of Connecticut School of Medicine in Farmington...
Measurement of tumor diameters, tumor volumes, or area under the curve has been traditionally used to quantitate and compare tumor growth curves in immune competent as well as immune-compromised mice and rats. Here, using tumor growth data from a large number of mice challenged with live tumor cells, we describe the use of a new composite parameter, Tumor Control Index (TCI) as an alternative method to do the same. This index, comprised of three distinct values, the Tumor Inhibition Score, Tumor Rejection Score, and Tumor Stability Score, provides a complete picture of nearly every aspect of tumor growth in large numbers of animals, can be deduced automatically from tumor diameter or volume data, and can be used to compare several groups of animals in different experiments. This automatically derivable index also corresponds neatly to the use of complete and partial responses and tumor stability data generated in human tumors, and can be used to assess the efficacy of interventions to be used in clinical studies.
We propose here that cigarette smoke (CS), in addition to its established genotoxic effects, elicits chronic albeit sub-clinical immune suppression, which is a major contributor to cancer progression. This hypothesis, presented here primarily in the context of bladder cancers (BCs), is applicable to other cancers, including those without a confirmed link to smoking.
During the past decades, anticancer immunotherapy has evolved from a promising therapeutic option to a robust clinical reality. Many immunotherapeutic regimens are now approved by the US Food and Drug Administration and the European Medicines Agency for use in cancer patients, and many others are being investigated as standalone therapeutic interventions or combined with conventional treatments in clinical studies. Immunotherapies may be subdivided into "passive" and "active" based on their ability to engage the host immune system against cancer. Since the anticancer activity of most passive immunotherapeutics (including tumor-targeting monoclonal antibodies) also relies on the host immune system, this classification does not properly reflect the complexity of the drug-host-tumor interaction. Alternatively, anticancer immunotherapeutics can be classified according to their antigen specificity. While some immunotherapies specifically target one (or a few) defined tumor-associated antigen(s), others operate in a relatively non-specific manner and boost natural or therapy-elicited anticancer immune responses of unknown and often broad specificity. Here, we propose a critical, integrated classification of anticancer immunotherapies and discuss the clinical relevance of these approaches.