Pigment Cell & Melanoma Research最新文献_第8页

Low-Dose Baricitinib Plus Narrow-Band Ultraviolet B for the Treatment of Progressive Non-Segmental Vitiligo: A Prospective, Controlled, Open-Label Study 低剂量巴利替尼加窄带紫外线 B 治疗进展期非节段性白癜风：一项前瞻性、对照、开放标签研究。

IF 3.9 3区医学

Pigment Cell & Melanoma Research Pub Date : 2024-10-23 DOI: 10.1111/pcmr.13209

Zhonghui Hu, Lu Lu, Jindi Feng, Hongbin Song, Shiyu Zhang, Lu Yang, Yuehua Liu, Tao Wang

{"title":"Low-Dose Baricitinib Plus Narrow-Band Ultraviolet B for the Treatment of Progressive Non-Segmental Vitiligo: A Prospective, Controlled, Open-Label Study","authors":"Zhonghui Hu, Lu Lu, Jindi Feng, Hongbin Song, Shiyu Zhang, Lu Yang, Yuehua Liu, Tao Wang","doi":"10.1111/pcmr.13209","DOIUrl":"10.1111/pcmr.13209","url":null,"abstract":"Vitiligo is a chronic autoimmune disease, and current treatments for vitiligo have limited efficacy. Janus kinase (JAK) inhibitors could offer new therapeutic options. To evaluate the efficacy and safety of baricitinib, an oral JAK1/2 inhibitor, combined with narrow-band ultraviolet B (NB-UVB) in vitiligo treatment. This prospective, controlled, open-label study included adults with progressive non-segmental vitiligo (NSV). Patients were assigned to combination therapy with baricitinib 2 mg daily and NB-UVB three times a week or NB-UVB alone three times a week (control). The primary endpoint was the proportion of patients achieving 50% or greater improvement from baseline in the total Vitiligo Area Scoring Index (T-VASI50) at week 16. Of the 33 patients (mean age, 34.1 years; 27.3% women) who completed the study, 12 of 17 (70.6%) patients in the combination group and 2 of 16 (12.5%) in the control group had a T-VASI50 response at week 16 (relative risk [RR] = 5.6; 95% CI = 1.5–21.4; p = 0.001). Adverse events were minor, including erythema, mild blister after phototherapy and acne. Combination therapy with low-dose baricitinib and NB-UVB was effective and well tolerated in adults with progressive NSV.","PeriodicalId":219,"journal":{"name":"Pigment Cell & Melanoma Research","volume":"38 1","pages":""},"PeriodicalIF":3.9,"publicationDate":"2024-10-23","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11681843/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142491758","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

25th Annual meeting of the European Society for Pigment Cell Research, Marseille, France 第 25 届欧洲色素细胞研究学会年会，法国马赛

IF 3.9 3区医学

Pigment Cell & Melanoma Research Pub Date : 2024-10-14 DOI: 10.1111/pcmr.13192

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PASPCR 2024 Annual Meeting, New York, NY PASPCR 2024 年年会，纽约州纽约市

IF 3.9 3区医学

Pigment Cell & Melanoma Research Pub Date : 2024-10-14 DOI: 10.1111/pcmr.13191

引用次数: 0

Meeting Report From the 2023 Cure Ocular Melanoma (CURE OM) Global Science Meeting, Philadelphia, PA, November 2023 2023 年治疗眼部黑色素瘤（CURE OM）全球科学会议报告，宾夕法尼亚州费城，2023 年 11 月。

IF 3.9 3区医学

Pigment Cell & Melanoma Research Pub Date : 2024-10-09 DOI: 10.1111/pcmr.13205

Rino S. Seedor, Andrew E. Aplin, Corine Bertolotto, Richard D. Carvajal, Nigel Deacon, Katie Doble, Omid Hamid, Rizwan Haq, Miriam Kadosh, Shaheer Khan, Jacqueline Kraska, Jose Lutzky, Meredith McKean, Kamaneh Montazeri, Justin Moser, Michael Onken, Marlana Orloff, Joseph J. Sacco, Keiran Smalley, Sara M. Selig

引用次数: 0

Sex Differences in Acral Lentiginous Melanoma: A Retrospective Cohort Analysis of 3617 Cases From the Surveillance, Epidemiology, and End Results Database 口腔扁平状黑色素瘤的性别差异：对监测、流行病学和最终结果数据库中 3617 例病例的回顾性队列分析。

IF 3.9 3区医学

Pigment Cell & Melanoma Research Pub Date : 2024-10-01 DOI: 10.1111/pcmr.13200

Jennifer M. Fernandez, Mitchell A. Taylor, Katherine Plampton, Erin X. Wei, Ashley Wysong

引用次数: 0

LL37-DNA Complex Drives Vitiligo Progression Through TLR9-MyD88 Signaling Pathways LL37-DNA复合物通过TLR9-MyD88信号通路驱动白癜风进展

IF 3.9 3区医学

Pigment Cell & Melanoma Research Pub Date : 2024-09-30 DOI: 10.1111/pcmr.13202

Jingying Wang, Hanxiao Mao, Rulan Liu, Ziyuan Zeng, Lvsha Xie, Yan Yang, Yuanmin He

{"title":"LL37-DNA Complex Drives Vitiligo Progression Through TLR9-MyD88 Signaling Pathways","authors":"Jingying Wang, Hanxiao Mao, Rulan Liu, Ziyuan Zeng, Lvsha Xie, Yan Yang, Yuanmin He","doi":"10.1111/pcmr.13202","DOIUrl":"10.1111/pcmr.13202","url":null,"abstract":"<div>\u0000 \u0000 Vitiligo is an autoimmune disorder characterized by chronic depigmentation and milk-white patches on the skin. Skin infiltration by autoreactive CD8+ T cells causes melanocyte destruction in vitiligo. Multiple risk factors, particularly immune-related inflammatory factors, are involved in the disappearance of melanocytes. LL37 is a classic damage-associated molecular pattern molecule that is involved in the development of various autoimmune diseases. An enhanced expression of LL37 in vitiligo is known; however, the exact role of LL37 in melanocyte loss has not yet been elucidated. In the present study, we detected increased LL37 expression in vitiligo serum and lesions. Furthermore, we confirmed that cultured keratinocytes released LL37 after treatment with H2O2. Moreover, the LL37-DNA complex enhanced the secretion of CXCL9, CXCL10, and CXCL16 from keratinocytes via the TLR9-MyD88 signaling pathway and facilitated the migration of CD8+ T cells. Altogether, our study demonstrates that LL37 released from keratinocytes binds to DNA and contributes to melanocyte destruction under oxidative stress-induced autoimmunity in vitiligo.\u0000 </div>","PeriodicalId":219,"journal":{"name":"Pigment Cell & Melanoma Research","volume":"38 1","pages":""},"PeriodicalIF":3.9,"publicationDate":"2024-09-30","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142338013","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Cholinergic Signaling Mediated by Muscarinic Receptors Triggers the Ultraviolet-Induced Release of Melanosome in Cultured Melanoma Cells 由毒蕈碱受体介导的胆碱能信号在培养的黑色素瘤细胞中触发紫外线诱导的黑色素体释放。

IF 3.9 3区医学

Pigment Cell & Melanoma Research Pub Date : 2024-09-30 DOI: 10.1111/pcmr.13201

Maggie Suisui Guo, Qiyun Wu, Yingjie Xia, Jiahui Wu, Xiaoyang Wang, Gary Ka Wing Yuen, Tina Tingxia Dong, Jin Gao, Karl Wah Keung Tsim

{"title":"Cholinergic Signaling Mediated by Muscarinic Receptors Triggers the Ultraviolet-Induced Release of Melanosome in Cultured Melanoma Cells","authors":"Maggie Suisui Guo, Qiyun Wu, Yingjie Xia, Jiahui Wu, Xiaoyang Wang, Gary Ka Wing Yuen, Tina Tingxia Dong, Jin Gao, Karl Wah Keung Tsim","doi":"10.1111/pcmr.13201","DOIUrl":"10.1111/pcmr.13201","url":null,"abstract":"In skin, melanin is synthesized and stored in melanosomes. In epidermal melanocytes, melanosomes are transported to and internalized by the neighboring keratinocytes, subsequently leading to skin pigmentation. Ultraviolet (UV) radiation induces the release of acetylcholine (ACh) from keratinocytes, which in turn activates ACh receptors (AChRs) on nearby melanocytes, forming a proposed “skin synapse”. Here, we illustrated that the UV-induced melanosome release from cultured B16F10 melanoma cells could be mediated by co-actions of ACh. In the cell cultures, UV exposure robustly elicited melanosome release. Applied bethanechol (BeCh), an agonist of muscarinic AChR (mAChR), could significantly enhance the release. In parallel, the intracellular Ca2+ mobilization was regulated. The applied antagonists of M1 and/or M3 mAChRs could block the UV-induced melanosome release and the mobilization of intracellular Ca2+. The phosphorylation of PKC, triggered by UV and BeCh treatments, could be suppressed by the applied mAChR antagonists. The expressions of tethering complex for exocytosis, for example, Sec8, Exo70, and Rab11b, as well as synaptotagmin, were increased under UV exposure together with mAChR agonist: The inductions were fully abolished by M1 or M3 antagonist. Here, we hypothesize that the cholinergic signaling is playing roles in UV-induced exocytosis of melanosomes.","PeriodicalId":219,"journal":{"name":"Pigment Cell & Melanoma Research","volume":"38 1","pages":""},"PeriodicalIF":3.9,"publicationDate":"2024-09-30","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11681844/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142338012","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Pathogenic Germline Variants in Uveal Melanoma Driver and BAP1-Associated Genes in Finnish Patients with Uveal Melanoma 芬兰葡萄膜黑色素瘤患者中葡萄膜黑色素瘤驱动基因和 BAP1 相关基因的致病性基因变异。

IF 3.9 3区医学

Pigment Cell & Melanoma Research Pub Date : 2024-09-30 DOI: 10.1111/pcmr.13198

Pauliina E. Repo, Eveliina Jakkula, Juho Hiltunen, Heidi Putkuri, Aleksandra Staskiewicz-Tuikkanen, Reetta-Stiina Järvinen, Martin Täll, Virpi Raivio, Rana'a T. Al-Jamal, Tero T. Kivelä, Joni A. Turunen

{"title":"Pathogenic Germline Variants in Uveal Melanoma Driver and BAP1-Associated Genes in Finnish Patients with Uveal Melanoma","authors":"Pauliina E. Repo, Eveliina Jakkula, Juho Hiltunen, Heidi Putkuri, Aleksandra Staskiewicz-Tuikkanen, Reetta-Stiina Järvinen, Martin Täll, Virpi Raivio, Rana'a T. Al-Jamal, Tero T. Kivelä, Joni A. Turunen","doi":"10.1111/pcmr.13198","DOIUrl":"10.1111/pcmr.13198","url":null,"abstract":"Uveal melanoma (UM) is a rare yet aggressive eye cancer causing over 50% mortality from metastasis. Familial UM, amounting to 1%–6% of patients in Finland and the United States, mostly lack identified genetic cause, while 8% show associations with other cancer syndromes. We searched novel genetic associations for predisposition to UM, additional to already studied BAP1 and MBD4, by using targeted amplicon sequencing of 19 genes associated with UM, BAP1, or renal cell carcinoma in 270 consecutively enrolled Finnish patients with UM. Key UM drivers GNAQ, GNA11, CYSLTR2, PLCB4, EIF1AX, and SF3B1 lacked pathogenic germline variants. One patient carried the pathogenic BRCA1 variant c.3626del p.(Leu1209*), and one harbored a novel truncating MET variant c.252C > G p.(Tyr84*), classified as likely pathogenic. FLCN and BRCA2, previously identified with pathogenic variants in patients with UM, did not have such variants in our cohort. Two patients were heterozygous for a pathogenic recessive BLM variant c.2824-2A > T. None of the carriers of identified variants had familial UM. We identified BRCA1 and MET as genes with pathogenic germline variants in Finnish UM patients, each with a frequency of 0.4% (95% confidence interval, 0–2).","PeriodicalId":219,"journal":{"name":"Pigment Cell & Melanoma Research","volume":"38 1","pages":""},"PeriodicalIF":3.9,"publicationDate":"2024-09-30","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11681845/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142338014","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Germline Variants in Patients Affected by Both Uveal and Cutaneous Melanoma 葡萄膜黑色素瘤和皮肤黑色素瘤患者的基因变异

IF 3.9 3区医学

Pigment Cell & Melanoma Research Pub Date : 2024-09-24 DOI: 10.1111/pcmr.13199

Peter A. Johansson, Jane M. Palmer, Lindsay McGrath, Sunil Warrier, Hayley R. Hamilton, Timothy Beckman, Matthew G. D'Mellow, Kelly M. Brooks, William Glasson, Nicholas K. Hayward, Antonia L. Pritchard

{"title":"Germline Variants in Patients Affected by Both Uveal and Cutaneous Melanoma","authors":"Peter A. Johansson, Jane M. Palmer, Lindsay McGrath, Sunil Warrier, Hayley R. Hamilton, Timothy Beckman, Matthew G. D'Mellow, Kelly M. Brooks, William Glasson, Nicholas K. Hayward, Antonia L. Pritchard","doi":"10.1111/pcmr.13199","DOIUrl":"10.1111/pcmr.13199","url":null,"abstract":"Uveal melanoma (UM) and nonacral cutaneous melanoma (CM) are distinct entities with varied genetic landscapes despite both arising from melanocytes. There are, however, similarities in that they most frequently affect people of European ancestry, and high penetrance germline variants in BAP1, POT1 and CDKN2A have been shown to predispose to both UM and CM. This study aims to further explore germline variants in patients affected by both UM and CM, shedding light on the underlying genetic mechanism causing these diseases. Using exome sequencing we analysed germline DNA samples from a cohort of 83 Australian patients diagnosed with both UM and CM. Eight (10%) patients were identified that carried pathogenic mutations in known melanoma predisposition genes POT1, MITF, OCA2, SLC45A2 and TYR. Three (4%) patients carried pathogenic variants in genes previously linked with other cancer syndromes (ATR, BRIP1 and MSH6) and another three cases carried monoallelic pathogenic variants in recessive cancer genes (xeroderma pigmentosum and Fanconi anaemia), indicating that reduced penetrance of phenotype in these individuals may contribute to the development of both UM and CM. These findings highlight the need for further studies characterising the role of these genes in melanoma susceptibility.","PeriodicalId":219,"journal":{"name":"Pigment Cell & Melanoma Research","volume":"38 1","pages":""},"PeriodicalIF":3.9,"publicationDate":"2024-09-24","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11681841/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142306808","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

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Segregation Between an Ornamental and a Disease Driver Gene Provides Insights Into Pigment Cell Regulation 观赏基因与疾病驱动基因之间的分离为色素细胞调控提供了启示

IF 3.9 3区医学

Pigment Cell & Melanoma Research Pub Date : 2024-09-17 DOI: 10.1111/pcmr.13196

Erika Soria, Qiusheng Lu, Will Boswell, Kang Du, Yanting Xing, Mikki Boswell, Korri S. Weldon, Zhao Lai, Markita Savage, Manfred Schartl, Yuan Lu

{"title":"Segregation Between an Ornamental and a Disease Driver Gene Provides Insights Into Pigment Cell Regulation","authors":"Erika Soria, Qiusheng Lu, Will Boswell, Kang Du, Yanting Xing, Mikki Boswell, Korri S. Weldon, Zhao Lai, Markita Savage, Manfred Schartl, Yuan Lu","doi":"10.1111/pcmr.13196","DOIUrl":"10.1111/pcmr.13196","url":null,"abstract":"Genetic interactions are adaptive within a species. Hybridization can disrupt such species-specific genetic interactions and creates novel interactions that alter the hybrid progeny overall fitness. Hybrid incompatibility, which refers to degenerative genetic interactions that decrease the overall hybrid survival and sterility, is one of the results from combining two diverged genomes in hybrids. The discovery of spontaneous lethal tumorigenesis and underlying genetic interactions in select hybrids between diverged Xiphophorus species showed that lethal pathological process can result from degenerative genetic interactions. Such genetic interactions leading to lethal phenotype are thought to shield gene flow between diverged species. However, hybrids between certain Xiphophorus species do not develop such tumors. Here we report the identification of a locus residing in the genome of one Xiphophorus species that represses an oncogene from a different species. Our finding provides insights into normal and pathological pigment cell development, regulation and a molecular mechanism in hybrid incompatibility.","PeriodicalId":219,"journal":{"name":"Pigment Cell & Melanoma Research","volume":"38 1","pages":""},"PeriodicalIF":3.9,"publicationDate":"2024-09-17","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1111/pcmr.13196","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142247998","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0