UAMS Department of Pathology

About the Department

Anatomic Pathology

Clinical Pathology

Outreach Referral and Consultative Services

Fellowships

Pathophysiology Course

Research

Experimental Pathology Core Lab

Mayumi Nakagawa, MD, PhD Associate Professor of Pathology
Residency Laboratory Medicine, University of California at San Francisco Post Doctoral Training Laboratory Medicine, University of California at San Francisco Board Certification(s) Clinical Pathology Clinical Interests Transfusion Medicine, Blood Banking, Cell Therapy and Apheresis Research Interests Human Papillomavirus (HPV) Immunology Papillomaviruses are small, non-enveloped, icosohedral DNA viruses that replicate in the nucleus of squamous epithelial cells. They can infect many different species of animals, but the mode of transmission is specie-specific. There are over 100 types of HPV described to date, and approximately a third is known to have genital tropism. The types that have genital tropism are grouped into high risk HPV types which are associated with development of anogenital cancer, and to low risk HPV types which are associated with genital warts. Among the high risk types, human papillomavirus type 16 (HPV 16) is the most common. Each year, approximately 13,000 new cases of cervical cancer (squamous cell cancer of the cervix) are reported in the United States, resulting in over 3,500 deaths per year. World-wide, cervical cancer is the second most common cancer among women with approximately 470,000 new cases per year. HPV infection is also associated with the precursor lesion of cervical cancer, known as squamous intraepithelial lesion (SIL). A majority of the cases of low-grade SILs (LSIL) is known to regress spontaneously, while a significant number of high-grade SILs (HSIL) is expected to persist/progress. Therefore, HSILs are typically treated with a loop electrical excision procedure (LEEP), while LSILs are closely observed. T cell immunity is thought to have an important role at various stages of HPV pathogenesis: in clearance of HPV infection, regression of LSIL, recurrence-free recovery from treated HSIL, and even in recovery from cervical cancer treated by conventional methods. However, HPV therapeutic vaccines that can enhance such immunity are currently not available. The overall goal of our research project is to develop new preventative strategies and treatments for cervical cancer by studying how natural immunity eliminates HPV in some individuals. HPV infection by some other HPV types (most commonly HPV types 2a, 27, and 57) can cause skin warts. While the condition is not life threatening, many people seek medical treatment because of cosmetic issues and/or pain. It is estimated that skin warts contribute to 7% of all visits to dermatologists. Injections of recall antigens such as mumps, Candida, and trichophyton to skin warts have been shown to induce their regression. Because not only the wart which is treated but also distant warts demonstrate regression, we hypothesize that the immunity induced is HPV-specific. Our goal is to identify portions of HPV that are playing a role in wart regression in order to develop more rapidly effective treatment. Email: mnakagawa@uams.edu

Selected Publications

Nakagawa, M., Kim, K. H., and Moscicki, A-B. Different Methods of Identifying New Antigenic Epitopes of Human Papillomavirus Type 16 E6 and E7 Proteins. Clinical & Diagnostic Laboratory Immunology, 11, 889-896, 2004.

Nakagawa, M., and Toy, P. Acute and Transient Decrease in Neutrophil Count in Transfusion-Related Acute Lung Injury: Cases at One Hospital. Transfusion, 44, 1689-1694, 2004.

Toy, P., Hollis-Perry, M., Jun, J., and Nakagawa, M. Recipients of Blood from a Donor with Multiple HLA Antibodies: A lookback study of TRALI, Transfusion, 44, 1683-1688, 2004.

Tugizov, S., Berline, J., Herrera, R., Penaranda, M.-E., Nakagawa, M. and Palefsky, J.M. Inhibition of HPV 16 E7 Phosphorylation by Cellular Protein Complex MRP-8/14. Journal of Virology, 79, 1099-1112, 2005.

Nakagawa, M., Kim, K. H., and Moscicki, A-B. Patterns of CD8 T Cell Epitopes within the Human Papillomavirus Type 16 (HPV 16) E6 Protein Among Young Women Whose HPV 16 Infection Has Become Undetectable. Clinical & Diagnostic Laboratory Immunology, 12, 1003-1005, 2005.

Kim, K.H., Dishongh, R., Santin, A.D., Cannon, M.J., Bellone, S., and Nakagawa, M. Recognition of a Cervical Cancer Derived Tumor Cell Line by a Human Papillomavirus Type 16 E6 52-61-Specific CD8 T Cell Clone. Cancer Immunity, 6, 9-15, 2006.

Nakagawa, M., Kim, K. H., and Moscicki, A.-B. HLA Class I Binding Promiscuity of the CD8 T Cell Epitopes of the Human Papillomavirus Type 16 E6 Protein. Journal of Virology, 81, 1412-1423, 2007.

Wang, X., Santin, A.D., Bellone, S., Gupta, S., and Nakagawa, M. A novel CD4 T-cell epitope described from one of the cervical cancer patients vaccinated with HPV 16 or 18 E7-pulsed dendritic cells. Cancer Immunology,Immunotherapy, 58, 301-308, 2008.

Wang, X., Moscicki, A.-B., Tsang, L., Brockman, A., and Nakagawa, M. Memory T-Cells Specific for Novel HPV 16 E6 Epitopes in Women Whose HPV 16 Infection Has Become Undetectable. Clinical & Vaccine Immunology, 15, 937-945, 2008.

Farhat,S.,Nakagawa, M.,and Moscicki, A.-B. Cell-mediated immune responses to humanpapillomavirus 16 E6 and E7 antigens as measured by interferon gamma enzyme-linked immunospot in women with cleared or persistent human papillomavirus infection.Int J Gynecol Cancer, 19, 508-12, 2009.

Nakagawa, M., Gupta, S., Coleman, H., Sellers, M., Banken, J., and Greenfield, W. A Favorable Clinical Trend is Associated with CD8 T-Cell Immune Responses to the Human Papillomavirus Type 16 E6 Antigens in Women Being Studied for Abnormal Papanicolous Smear Results. Journal of Lower Genital Tract Disease, In Press.

UAMS Department of Pathology
4301 West Markham #517
Little Rock AR 72205
501-686-5170
Bruce Smoller, M.D., Chair

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