Biological Sciences Research and Sponsored Projects

Active Research and Sponsored Projects

Current research and sponsored projects are listed below.


Head and Neck Cancer, Beta-Defensins, and Immune Responses

Sponsor: NIH – NIDCR
PI: Dr. Ge Jin
Period of Performance: 07/01/2015 – 06/30/2020
Summary: Head and neck cancer accounts for 3-5% of all malignancies in the US, corresponding to over 50,000 new cases and more than 10,000 deaths each year. Despite our improved understanding of the cancer and advances in therapeutics, the 5-year survival rate of oral cancer remains low at about 50-60%. The proposed research is expected to help us understand how head and neck cancer-released peptides promote cancer growth and progression through triggering a set of tumor-promoting immune responses, which will eventually lead to uncover new targets for immunotherapeutic interventions for this deadly disease.


Identification and Elimination of HIV Reservoirs in Oral Lymphoid Tissues by Engineered NK Cells

Sponsor: NIH – NIDCR
Co-Investigator: Dr. Pushpa Pandiyan (Lead PI: Dr. Jonathan Karn, School of Medicine)
Period of Performance: 08/01/2015 – 07/31/2020
Summary: In the United States at least 1 million people are living with AIDS and require life-long treatment with antiretroviral drugs because HIV can remain silent in some cells, referred to as latent infection. Here we will be developing a strategy to identify and eliminate those latent cells that reside in the oral cavity using immune cells derived from the infected patients known as Natural Killer (NK) cells. Eradication of the latent cells provides a functional cure for the patients and will allow them to discontinue costly drug therapy.


Mechanisms of Th17 and Treg Cells Dysregulation in Oral Mucosal Inflammation During HIV Disease

Sponsor: NIH – NIDCR
PI: Dr. Pushpa Pandiyan
Period of Performance: 04/01/2017 – 01/31/2022
Summary: Oral immunological complications in HIV+ patients are a major public health concern. Such complications persist in patients that are treated with anti-retroviral drugs. Our proposal will examine the possible cause for inflammation, by examining the interactions among inflammatory cytokines, oral microbial products and immune cells, with a specific focus on two important subsets of CD4+ T lymphocytes. Successful completion of this project will lead to novel ways of mitigating oral residual inflammation by a combined approach of replenishing protective CD4 T cells and reducing dysfunctional T cells.  


Oral Immune Plasticity, HIV-Infected T Cell Extracellular Vesicles, and Oral Cancer

Sponsor: NIH – NIDCR
PI: Dr. Ge Jin
Period of Performance: 05/01/2017 – 02/28/2022
Summary: HIV-infected individuals under combination antiretroviral therapy (cART) have more oral cancer cases than those in the general population. HIV-infected cells secrete nanoparticle-like extracellular vesicles (EVs), which contain proteins, lipids, and RNA to influence many diseases, including cancer. We found that HIV-infected T cells produce EVs that stimulate oral cancer cell proliferation and tumor progression. This proposed research will help us understand why and how HIV-infected T cell EVs promote oral cancer and find a new method to control oral cancer development in the chronically HIV-infected population.


Point-of-Care Device for Diagnosis and Monitoring of Oral Cancer

Sponsor: CWRU Technology Validation and Start-Up Fund via the Ohio Development Services Agency
PI: Dr. Aaron Weinberg
Period of Performance: 01/01/2018 – 12/31/2019
Summary: Validation of a microfluidic-based point-of-care device to determine the presence of cancer in suspicious oral lesions.


hBD-3: A novel Factor Orchestrating Microbial Persistence in Suspicious Oral Lesions

Sponsor: NIH – NIDCR
PI: Dr. Aaron Weinberg
Period of Performance: 08/01/2019 – 05/31/2021
Summary: It is becoming more evident, by studying bacterial communities (microbiome studies), that certain bacteria belonging to a group called Fusobacteria are playing a role in promoting oral cancer. We have identified that a specific protein that kills bacteria – human beta defensin 3 (hBD-3) – that is overexpressed in oral cancer cells can be used to distinguish cancerous lesions from non-cancerous ones. We hypothesize that overexpression of hBD-3 in oral cancer promotes selective persistence of Fusobacteria that are resistant to hBD-3. We intend to recruit subjects with suspicious oral lesions and (1) distinguish cancer from non-cancer by determining the level of hBD-3, (2) conduct microbiome analysis to correlate high hBD-3 levels with specific retentive bacteria which we suspect will belong to organisms belonging to Fusobacterium, and (3) isolate hBD-3 resistant fusobacterial organisms from the cancer sites and compare them to non-cancer sites.