Elucidating Mycosis Fungoides Gene Expression in Skin of Color Patients from Howard University Dermatology

Nina C. Nwade, N. James, Akanksha D. Nagarkar, S. Desse, Ummugulsum Yildiz-Altay, G. Okoye, A. Byrd, J. Richmond
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Abstract

Mycosis fungoides (MF) is the most common type of cutaneous T cell lymphoma.There are notable differences in MF presentation in Skin of Color (SOC) versus White skin, such as asymptomatic hyperpigmented and hypopigmented lesions resulting from malignant T-cell interaction from keratinocytes and melanocytes. Therefore, this work aims at elucidating MF immunopathogenesis and gene expression in SOC patients and determining whether clinical presentation differences are dependent on the cytokine type produced by the tumor. We used both hypopigmented and hyperpigmented MF biopsy samples from SOC patients with MF from Howard University Dermatology and compared their gene expression to that of biopsy samples from SOC healthy patients. Preliminary data showed an upregulation of genes such as PRDX1, HLA-DRA, CTNNB1, CSTB, and S100A4 in MF samples versus their healthy counterparts. The MF samples also exhibited downregulation of CCL3, CCRL2, PDGFB and HOXD4 genes when compared to their healthy counterparts. Lastly, the pathways ‘cell cycle and apoptosis’, ‘antigen presentation’, and ‘interferon signaling’ were increased in MF and decreased in the healthy samples. Overall, these data will elucidate MF gene expression in SOC patients as well as the immunopathogenesis that results in varying presentations. This may facilitate the development of more concise diagnostic criteria and personalized targeted immunotherapies to better health outcomes within a minority population. Supported by grants from Dermatology Foundation DRSA (SD), the Skin of Color Society Research Grant (JMR), and the American Skin Association Milstein Research Scholar Award for Melanoma/Non-Melanoma Skin Cancer (ASB).
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霍华德大学皮肤病学研究揭示有色人种皮肤中蕈样真菌病基因表达
蕈样真菌病(MF)是最常见的皮肤T细胞淋巴瘤。在有色皮肤(SOC)和白色皮肤中,MF的表现有显著差异,例如由角化细胞和黑素细胞的恶性t细胞相互作用引起的无症状色素沉着和色素沉着病变。因此,本研究旨在阐明MF在SOC患者中的免疫发病机制和基因表达,并确定临床表现差异是否取决于肿瘤产生的细胞因子类型。我们使用来自霍华德大学皮肤科的患有MF的SOC患者的低色素和高色素MF活检样本,并将其基因表达与来自SOC健康患者的活检样本进行比较。初步数据显示,与健康样本相比,MF样本中的PRDX1、HLA-DRA、CTNNB1、CSTB和S100A4等基因上调。与健康样品相比,MF样品也表现出CCL3、CCRL2、PDGFB和HOXD4基因的下调。最后,“细胞周期和凋亡”、“抗原呈递”和“干扰素信号传导”通路在MF中增加,而在健康样本中减少。总的来说,这些数据将阐明MF基因在SOC患者中的表达以及导致不同表现的免疫发病机制。这可能有助于制定更简洁的诊断标准和个性化的靶向免疫疗法,以改善少数群体的健康状况。由皮肤科基金会DRSA (SD),肤色协会研究基金(JMR)和美国皮肤协会米尔斯坦黑色素瘤/非黑色素瘤皮肤癌研究学者奖(ASB)资助。
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