Abstract

Abstract Mycosis fungoides (MF) is the most prevalent Primary Cutaneous T Cell Lymphoma, comprising up to 60% of known cases. It is primarily a disease of resident memory T-lymphocytes that undergo phenotypic changes as a result of several gene alterations including ones coding for T-cell receptor (TCR) expression. The upregulation and downregulation of TCRs may give insight into the complex etiology of MF. There is a clear discrepancy in the morbidity and mortality of MF in the skin of color (SOC) population due to a myriad of factors including delayed diagnoses, biological differences, and limited research. Differences in the physiology of skin of color can cause atypical presentations, often mimicking other pigmentary and inflammatory dermatoses, causing delays in diagnosis and higher mortality. Therefore, further investigation into the molecular physiology of MF is warranted to better understand the disease presentation, progression, and appropriate therapies for SOC patients. Previous studies have identified the most common TCRs present in predominantly White cohorts including TCRVb3, TCRVb5, TCRVb6, TCRVb7, TCRVb20 and TCRVb21. Using MF biopsies from SOC patients at Howard University Dermatology, we analyzed lesional TCR gene expression and compared it to healthy SOC patients with the goal of considering novel therapeutic targets and analyzing how these molecular findings impact the diagnosis and treatment. Preliminary data shows that TRBC1 and TRBC2 are enriched in MF SOC patients whereas TRBV7–8 was enriched in the healthy margins. Because TCRs can be used as a biomarker to identify MF, this knowledge also has the potential to aid in the early diagnosis of MF, thus improving the disparity in outcomes seen in patients of color. Sachi Desse - recipient of the Dermatology Foundation DRSA Jillian M. Richmond - recipient of the Skin of Color Society Research Grant Angel S. Byrd - recipient of the American Skin Association Milstein Research Scholar Award for Melanoma/Non-Melanoma Skin Cancer

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