國家衛生研究院 NHRI:Item 3990099045/12199
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    题名: Prognostic and clinicopathologic associations of Casein Kinase (CK) 1 alpha in acral lentiginous melanoma
    其它题名: Prognostic and clinicopathologic associations of Casein Kinase (CK) 1 α in acral lentiginous melanoma
    作者: Chang, C;Huang, S;Ito, T;Lo, Y;Shen, C;Tsai, K;Wu, T;Hsu, Y;Chang, K;Lin, T
    贡献者: National Institute of Cancer Research
    摘要: Acral lentiginous melanoma (ALM), presenting on the palms of the hands, the soles of the feet, and the subungual area, is the most common type melanoma in Asian. Casein kinase 1α (CK1α, encoded by the CSNK1A1 gene) is involved in multiple cellular processes including gene transcription, cell division, nuclear localization, DNA repair, and carcinogenesis. CK1α has been reported as tumor promoter or tumor suppressor in different tumor types and tumor sites. In this study, we aim to investigate the role of CK1α in ALM. A total of 158 cases of ALM registered in three medical centers, two in Taiwan and one in Japan, were enrolled. We analyzed the prognostic impact of CK1α on the survival of ALM patients using the clinicopathological data and immunohistochemistry in 158 formalin-fixed paraffin-embedded samples, and examined the CSNK1A1 gene copy number variation (CNV) using droplet digital PCR in 69 samples. Patients with CK1α-high expression had significantly shorter melanoma-specific survival compared to those with CK1α-low expression (5-year survival, 45.2 % vs. 91.6 %; P < 0.001). 92.8% (64/69) of ALM had increased CNV of CSNK1A1. Higher CSNK1A1 CNV was associated with more advanced Breslow thickness. In conclusion, overexpression of CK1α is an adverse prognostic factor in ALM. CK1α may function as a tumor promoter in ALM, and a potential therapeutic target of ALM.
    日期: 2019-09
    關聯: Journal of Investigative Dermatology. 2019 Sep;139(9):S299.
    Link to: http://dx.doi.org/10.1016/j.jid.2019.07.541
    JIF/Ranking 2023: http://gateway.webofknowledge.com/gateway/Gateway.cgi?GWVersion=2&SrcAuth=NHRI&SrcApp=NHRI_IR&KeyISSN=0022-202X&DestApp=IC2JCR
    Cited Times(WOS): https://www.webofscience.com/wos/woscc/full-record/WOS:000485661500486
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