Harshyne Research


Name: Larry Harshyne, PhD
  • Assistant Professor, Department of Microbiology & Immunology
  • Assistant Provost, Research Conduct & Compliance
  • Director, Sidney Kimmel Comprehensive Cancer Center Flow Cytometry & Human Immune Monitoring Core

1020 Locust Street
Philadelphia, PA 19107

Contact Number(s):

My research focuses on the interactions between cancer and the immune system.  Alcohol/tobacco use and human papilloma virus (HPV) infection are risk factors for developing Head and Neck Squamous Cell Carcinoma (HNSCC).  Patients with HPV-driven cancer often have better prognoses.  We use sequencing, spatial transcriptomics, flow cytometry, and multiplex Luminex assays to assess immune bias in the tumor, draining lymph nodes, and the circulation.  Immune fitness, exhaustion, B cell activation, and small extracellular vesicles are some of parameters we track in these patients

Research Projects

Discordant Clinical Responses Between the Primary Tumor & Lymph Nodes

All locations within the body are accessible and monitored by the immune system.  Yet some patients exhibit complete tumor destruction in certain areas while others areas are left untouched by the immune response.  We are interested in identifying biomarkers within the tumor microenvironment or peripheral blood that either aid or block immune activity as they relate to clinical response in the context of immunotherapy.

Small Extracellular Vesicles & Their Role in Modulating Immune Bias & Exhaustion

Extracellular vesicles (EV) are secreted by cells and serve as a means of local and distant communication.  EV contain distinct lipids, proteins, and nucleic acids that can serve to modulate the activity of tumor and immune cells.  We are interested in how these species change in the context of immune checkpoint therapy for the treatment of cancer

Intratumoral HPV Gene Expression & Clinical Responses to Immunotherapy in HNSCC Patients

The immune response comes in different ‘flavors’ that are fine-tuned to target specific pathogens.  For example, anti-viral immune responses are driven by IFN-g, also known as, a type I immune response.  In contrast, tumors thrive in the presence of IL4, IL10, and TGF-b, or a type II immune environment.  We are interested in mechanisms by which activation of potent HPV-specific T cells can drive tumor destruction as a bystander effect.