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Subramanya Pandruvada PhD

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Rank
  • Assistant Professor
College
  • College of Dental Medicine
Department
  • Department of Biomedical & Community Health Sciences
Academic Focus
  • Osteoimmunology
  • Cancer cell signaling
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Locations

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Biography

 

Education

PhD Zoology/Endocrinology, Central Drug Research Institute, Lucknow/Dr BR Ambedkar University, Agra, India

Postdoctoral training, Osteoimmunology, Ecole Normale Supérieure de Lyon, Lyon, France

Postdoctoral training, Cellular interactions and development, Institut de Recherches Cliniques de Montreal, Montreal, Canada

 

Positions

Research Associate Sr, College of Dentistry, University of Kentucky

Assistant Professor, College of Dental Medicine, MUSC

Associate member of Graduate Faculty, College of Graduate Studies, MUSC

 

Honors

Research Scholarship, Central Drug Research Institute, Lucknow, India (2002-2004)

Senior Research Fellow, Council for Scientific and Industrial Research (CSIR), Government of India (2004-2007)

Postdoctoral Fellowship, PRES-Universite de Lyon, Universite Lyon1, Lyon, France (2010)

Travel award, 3rd International Conference on Osteoimmunology, Santorini, Greece (2010)

CSR Early Career Reviewer (2018-2021)

Travel award, 2020 ASBMB and Experimental Biology meeting, San Diego, CA (2020)

Travel award, 2022 ASBMB and Experimental Biology meeting, Philadelphia, PA (2022)

 

Research Interests

We are a basic science laboratory working on interactions between tumors and their microenvironment that regulate critical cellular functions dictating the therapeutic outcome. In addition, our lab is also interested in understanding the osteoimmunological connections in periodontal diseases.

 

Tumor microenvironment

Tumors are heterogeneous organs of diverse stromal components, not just bystanders in the tumorigenic process. The tumor microenvironment (TME) of head and neck squamous cell carcinoma (HNSCC) is comprised of cancer-associated fibroblasts (CAFs), immune cells, and other supporting cells. Mutations in the HNSCC cells, such as alterations to TP53, PI3K, and specific gene expression profiles, contributed to derangements in cancer and microenvironment cells, such as overproduction of chemokines and increased ROS and epithelial to mesenchymal transition (EMT). Furthermore, the overexpression of critical cytokines, such as transforming growth factor-β (TGF-β), and alterations in antigen processing machinery contribute to EMT and immune suppression; the adaptive immune response remains suppressed in HNSCC. We are investigating how immune and tumor cells interact and how productive and non-productive anti-tumor immune responses affect cancer development in humanized and syngeneic rodent models. In addition, our lab is interested in understanding the role of other innate immune cell types, such as macrophages, in recognizing tumor lesions and adaptive anti-tumor immunity. Gaining a better understanding of the molecular pathways involved in the bi-directional communication between tumor and stroma will help us develop novel and better cancer therapies targeting the tumor microenvironment's critical components.

 

Osteoimmunological aspects of periodontal diseases

Periodontal disease (PD) is a chronic inflammatory disorder characterized by the destruction of connective tissue, tooth loss, and systemic infections. Individuals with PD present a complex array of inflammatory mediators and cellular infiltration by neutrophils, lymphocytes, and monocytes/macrophages. Although macrophages comprise 5–30% of cells identified in the cellular infiltrate of human periodontal disease lesions, how macrophage skewing contributes to periodontal disease, specifically in the downstream development of a macrophage immune response to PD-associated bacteria, is relatively unknown. Macrophages can be recruited from the bone marrow into tissues in a steady state or response to inflammation at any point during development. As macrophages play an essential role in tissue damage, depending on their origins and activation status, their migration within the gingival tissues may be critical in the outcome of periodontal inflammation. We are investigating the role of the macrophage maturation stage during recruitment, which may be vital in determining its ultimate function.