Journal of dermatological science最新文献

{"title":"Granzyme K contributes to acute itch in psoriasis","authors":"Aoi Hiroyasu , Beni Amatya , Daisuke Tsuruta , David J. Granville , Sho Hiroyasu","doi":"10.1016/j.jdermsci.2025.08.003","DOIUrl":"10.1016/j.jdermsci.2025.08.003","url":null,"abstract":"","PeriodicalId":94076,"journal":{"name":"Journal of dermatological science","volume":"120 1","pages":"Pages 39-42"},"PeriodicalIF":4.6,"publicationDate":"2025-10-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145093354","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Prevalence of FOXA1 and ERBB2 activating mutations in extramammary Paget’s disease: A retrospective multicenter analysis of 99 cases from Japanese and Taiwanese cohorts","authors":"Michiya Omi ,&nbsp;Takuya Takeichi ,&nbsp;Yusuke Okuno ,&nbsp;Chao-Kai Hsu ,&nbsp;Cheng-Lin Wu ,&nbsp;Yi-Han Chang ,&nbsp;Shoichiro Mori ,&nbsp;Yuta Yamashita ,&nbsp;Akira Miyazaki ,&nbsp;Takaya Taira ,&nbsp;Teruki Yanagi ,&nbsp;Keitaro Fukuda ,&nbsp;Tatsuhiro Noda ,&nbsp;Yuika Suzuki ,&nbsp;Yoshinao Muro ,&nbsp;Masashi Akiyama","doi":"10.1016/j.jdermsci.2025.08.001","DOIUrl":"10.1016/j.jdermsci.2025.08.001","url":null,"abstract":"<div><h3>Background</h3><div>Extramammary Paget’s disease (EMPD) occurs in areas where apocrine glands are abundant. EMPD is associated with the known somatic hotspot mutation g.chr14:38064406 G&gt;A in the promoter region of <em>FOXA1</em> and S310F in <em>ERBB2</em>. Whether EMPD patients in non-Japanese populations have <em>FOXA1</em> driver mutations remains undetermined, and the relationship between the clinical characteristics of EMPD patients and the presence of somatic <em>FOXA1</em> driver mutations has yet to be investigated.</div></div><div><h3>Objective</h3><div>To assess the prevalence and clinical significance of the <em>FOXA1</em> and <em>ERBB2</em> hotspot somatic mutations.</div></div><div><h3>Methods</h3><div>Surgical specimens from 99 EMPD patients who underwent surgery from January 2013 to March 2024 were collected from five facilities in Japan and Taiwan. To detect the somatic mutations, amplicon sequencing was performed for <em>FOXA1</em>, and ddPCR was conducted for <em>ERBB2.</em> Immunohistochemical analysis for FOXA1 was performed on 38 samples.</div></div><div><h3>Results</h3><div>The frequencies of the <em>FOXA1</em> (g.chr14:38064406 G&gt;A) mutation and the <em>ERBB2</em> S310F mutation were 8/93 (8.6 %) and 37/93 (40.0 %), respectively, among the non-fresh-frozen specimens. <em>FOXA1</em> somatic hotspot mutation-positive cases were found at all five medical institutions. Regardless of the mutational status of the <em>FOXA1</em> promoter mutation, all examined cases immunohistochemically exhibited strong FOXA1 expression in the Paget cell nuclei. No significant correlation was found between the <em>FOXA1</em> somatic mutation or the <em>ERBB2</em> somatic mutation and any clinical parameter.</div></div><div><h3>Conclusion</h3><div>The <em>FOXA1</em> somatic hotspot mutation was found in both Japanese and Taiwanese EMPD patients. We cannot rule out the possibility that <em>FOXA1</em> might be a potential target for EMPD therapies in Japan and Taiwan.</div></div>","PeriodicalId":94076,"journal":{"name":"Journal of dermatological science","volume":"120 1","pages":"Pages 32-38"},"PeriodicalIF":4.6,"publicationDate":"2025-10-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144983949","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"NELL2-Robo3 signaling promotes keratinocyte proliferation and inhibits keratinocyte apoptosis in condyloma acuminatum through autocrine and paracrine mechanisms","authors":"Xiaohang Xie ,&nbsp;Charat Rin ,&nbsp;Yinyi Feng ,&nbsp;Yichuan Li ,&nbsp;Deqiao Qin ,&nbsp;Yuchun Cao ,&nbsp;Xiaochao Zhang ,&nbsp;Yong Zhang","doi":"10.1016/j.jdermsci.2025.09.001","DOIUrl":"10.1016/j.jdermsci.2025.09.001","url":null,"abstract":"<div><h3>Background</h3><div>Condyloma acuminatum (CA) is caused by low-risk HPV infection and characterized by benign epithelial proliferation. NELL2, as a secreted glycoprotein, is strongly linked to dermatosis, but its function in CA remains unknown.</div></div><div><h3>Objective</h3><div>To investigate the expression, function and mechanism of NELL2 in CA.</div></div><div><h3>Methods</h3><div>The expression of NELL2 was detected in CA and normal skin tissues. HaCaT cells stably expressing HPV11-E7 (HPV11-E7-HaCaT) and control group (Vector-HaCaT) were constructed to explore the relationship between HPV infection and NELL2 expression. We downregulated <em>NELL2</em> expression in HPV11-E7-HaCaT cells and added recombinant human NELL2 to medium of Vector-HaCaT and HPV11-E7-HaCaT cells to examine the effects of NELL2 on cell proliferation and apoptosis. The activation of MAPK pathway and the role of Robo3 were evaluated to explore the mechanisms underlying these effects.</div></div><div><h3>Results</h3><div>NELL2 was overexpressed in CA, and increased NELL2 expression was positively associated with high HPV copy number and high Ki67 expression. HPV11-E7 induced the expression of NELL2 in HaCaT cells. In addition, NELL2 promoted proliferation and inhibited apoptosis in HPV11-E7-HaCaT and Vector-HaCaT cells through autocrine and paracrine mechanisms. NELL2 treatment activated the ERK pathway, and ERK inhibition by U0126 confirmed that ERK pathway was essential for the function of NELL2 in CA. Moreover, Robo3 acts as the NELL2 receptor in CA.</div></div><div><h3>Conclusion</h3><div>NELL2 binds Robo3 to promote keratinocyte proliferation and inhibit keratinocyte apoptosis in CA through autocrine and paracrine mechanisms. NELL2-Robo3 signaling may be regarded as a potential target for CA treatment in the future.</div></div>","PeriodicalId":94076,"journal":{"name":"Journal of dermatological science","volume":"120 1","pages":"Pages 21-31"},"PeriodicalIF":4.6,"publicationDate":"2025-10-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145152463","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Eupatilin attenuates vemurafenib resistance through inhibition of ABCB1 in melanoma","authors":"Daishi Li ,&nbsp;Sitao Liu ,&nbsp;Yi Ge ,&nbsp;Hui Li ,&nbsp;Xinchen Ke ,&nbsp;Dongsheng Cao ,&nbsp;Guangtong Deng ,&nbsp;Lixia Lu ,&nbsp;Juan Su","doi":"10.1016/j.jdermsci.2025.06.003","DOIUrl":"10.1016/j.jdermsci.2025.06.003","url":null,"abstract":"<div><h3>Background</h3><div>The clinical efficacy of vemurafenib<span> in melanoma patients has been hindered by the development of acquired resistance.</span></div></div><div><h3>Objectives</h3><div>To comprehend the molecular signaling pathways underlying this resistance and identify potential strategies to overcome it.</div></div><div><h3>Methods</h3><div><span>We first constructed the vemurafenib-resistant melanoma cell lines A375R and identified ABCB1 as a potential driver through </span>RNA sequence<span>. ABCB1 knockdown on vemurafenib<span> sensitivity was assessed by CCK-8 and colony formation. FDA-approved eupatilin was identified as a novel ABCB1 inhibitor by employing the quantitative structure-activity relationship model and ADMETlab 2.0. The combined effect of eupatilin and vemurafenib was detected in in vitro and in vivo.</span></span></div></div><div><h3>Results</h3><div>The expression of ABCB1 was upregulated in A375R. The genetic inhibition of ABCB1 could restore sensitivity to vemurafenib in resistant cells. Eupatilin was a previously unexplored compound that can selectively target ABCB1 and exhibit favorable safety profiles. Notably, we identified eupatilin as a therapeutic intervention to counteract acquired resistance to vemurafenib in cell and animal experiments, resulting in the inhibition of tumor growth. Furthermore, we found upregulation of ABCB1 in resistant cells due to the activation of the PI3K-AKT-mTOR pathway.</div></div><div><h3>Conclusion</h3><div>These findings provided valuable insights into a novel molecular mechanism underlying vemurafenib resistance and highlighted potential ABCB1 as a viable target, in conjunction with its novel inhibitor eupatilin, to enhance effectiveness of vemurafenib.</div></div>","PeriodicalId":94076,"journal":{"name":"Journal of dermatological science","volume":"119 3","pages":"Pages 112-121"},"PeriodicalIF":4.6,"publicationDate":"2025-09-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144593248","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Difamilast induces human beta defensin 3 production via CREB and NRF2 in human keratinocytes","authors":"Gaku Tsuji ,&nbsp;Ayako Yumine ,&nbsp;Masaki Takemura ,&nbsp;Takeshi Nakahara","doi":"10.1016/j.jdermsci.2025.07.003","DOIUrl":"10.1016/j.jdermsci.2025.07.003","url":null,"abstract":"","PeriodicalId":94076,"journal":{"name":"Journal of dermatological science","volume":"119 3","pages":"Pages 135-138"},"PeriodicalIF":4.6,"publicationDate":"2025-09-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144812757","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Preferential CD101 expression on resident memory regulatory T cells and IFN-γ-producing CD8+ resident memory T cells in human epidermis","authors":"Takuya Sato ,&nbsp;Youichi Ogawa ,&nbsp;Manao Kinoshita ,&nbsp;Yuka Nagasaka ,&nbsp;Shinji Shimada ,&nbsp;Akira Momosawa ,&nbsp;Tatsuyoshi Kawamura","doi":"10.1016/j.jdermsci.2025.07.002","DOIUrl":"10.1016/j.jdermsci.2025.07.002","url":null,"abstract":"","PeriodicalId":94076,"journal":{"name":"Journal of dermatological science","volume":"119 3","pages":"Pages 132-134"},"PeriodicalIF":4.6,"publicationDate":"2025-09-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144818867","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Integrative genomic and transcriptomic profiling reveals dysregulation of FOXA1-AGR2 axis in penoscrotal extramammary Paget's disease","authors":"Daoning Zhang ,&nbsp;Sini Gao ,&nbsp;Chunxia Zhao ,&nbsp;Xiaomin Cai ,&nbsp;Ruiqin Mai ,&nbsp;Guohong Zhang ,&nbsp;Hang Li","doi":"10.1016/j.jdermsci.2025.06.002","DOIUrl":"10.1016/j.jdermsci.2025.06.002","url":null,"abstract":"<div><h3>Background</h3><div>Extramammary Paget's disease (EMPD) is a rare cutaneous mucinous adenocarcinoma primarily affect the penoscrotal skin, characterized by the presence of Paget cells scattered within the epidermis. The molecular features of Paget cells remain poorly understood.</div></div><div><h3>Objectives</h3><div>To describe the genomic and transcriptomic landscape of penoscrotal EMPD, identify the driver mutation or core transcription factor through integrative analysis, identify biological markers and provide new insights for the pathogenesis of penoscrotal EMPD.</div></div><div><h3>Methods</h3><div>Whole exome sequencing was performed on penoscrotal EMPD tissues from 37 patients, of whom 28 patients also underwent RNA sequencing, and the findings was validated in an additional 72 patients, encompassing 120 multi-region tumor tissues to identify core transcription factors. The dysregulation was further confirmed by immunohistochemistry.</div></div><div><h3>Results</h3><div>Genomic landscape did not reveal <em>FOXA1</em> or <em>SPDEF</em> mutations penoscrotal EMPD. Transcriptomic profiling identified the upregulation of lineage-specific transcription factors <em>FOXA1</em> and <em>SPDEF,</em> along with their targeted genes <em>AGR2</em> and <em>MUC5AC</em>. Upregulation of <em>FOXA1</em>, <em>SPDEF</em> and <em>AGR2</em> without gene fusion were consistently replicated in the validation cohort. Further analysis of multiple tissue regions confirmed <em>FOXA1</em> and <em>SPDEF</em> as driver transcription factors in penoscrotal EMPD. We identify key transcription factors regulating co-expressed modules <em>FOXA1-SPDEF-AGR2</em>, suggesting goblet cells features of penoscrotal EMPD. The immunohistochemistry confirmed the co-expression of FOXA1-AGR2 pattern in Paget cells.</div></div><div><h3>Conclusions</h3><div>Our study provides novel insights into the molecular characteristics of Paget cells, and also highlights the critical role of FOXA1 in Paget cell development in EMPD.</div></div>","PeriodicalId":94076,"journal":{"name":"Journal of dermatological science","volume":"119 3","pages":"Pages 122-131"},"PeriodicalIF":4.6,"publicationDate":"2025-09-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144700776","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"17β-Estradiol promotes LL37-induced rosacea-like skin inflammation via G protein-coupled estrogen receptor 30","authors":"Jin Tang ,&nbsp;Peng Chen ,&nbsp;Chuchu Huang ,&nbsp;Wanjing Wang ,&nbsp;Ben Wang ,&nbsp;Wei Shi ,&nbsp;Yan Tang ,&nbsp;Zhili Deng ,&nbsp;Yiya Zhang ,&nbsp;Ji Li ,&nbsp;Dan Jian","doi":"10.1016/j.jdermsci.2025.05.005","DOIUrl":"10.1016/j.jdermsci.2025.05.005","url":null,"abstract":"<div><h3>Background</h3><div>Rosacea is a common chronic inflammatory skin condition that predominantly affects females, though its underlying mechanisms remain unclear.</div></div><div><h3>Objective</h3><div>To explore the role of 17β-estradiol (E2) and the G-coupled estrogen receptor 30 (GPR30) in the pathogenesis of rosacea.</div></div><div><h3>Methods</h3><div>We conducted a cross-sectional analysis of UK Biobank data to investigate the association between exogenous hormone use and rosacea risk in females. Additionally, ovariectomized (OVX) LL37-induced rosacea mouse models were utilized to evaluate the effects of ovarian E2 loss and exogenous E2 supplementation. GPR30 expression was measured in rosacea skin lesions, LL37-treated mice, and HaCaT keratinocytes. The impact of GPR30 deletion on rosacea inflammation was assessed using GPR30 knockout mice. Finally, the efficacy of GPR30 inhibition or silencing in reducing inflammation was examined in LL37 or LL37 plus E2 treated mice and HaCaT cells.</div></div><div><h3>Results</h3><div>UK Biobank data revealed significant associations between oral contraceptive use (OR: 1.20; 95 % CI: 1.06, 1.37) and hormone-replacement therapy (OR: 1.31; 95 % CI: 1.18, 1.46) with increased rosacea risk. OVX mice exhibited reduced skin erythema and dermal infiltration, effects reversed by E2 supplementation, which exacerbated rosacea inflammation. GPR30 was overexpressed in rosacea lesions, LL37-treated mice, and HaCaT cells, with TFAP2C potentially mediating this effect. GPR30-deficient mice showed reduced inflammation, while GPR30 inhibition or knockdown significantly improved rosacea-like inflammation in LL37 or LL37 plus E2 treated models.</div></div><div><h3>Conclusion</h3><div>Activation of the E2/GPR30 pathway plays a significant role in rosacea inflammation, and GPR30 inhibition may represent a novel therapeutic strategy for rosacea.</div></div>","PeriodicalId":94076,"journal":{"name":"Journal of dermatological science","volume":"119 3","pages":"Pages 101-111"},"PeriodicalIF":4.6,"publicationDate":"2025-09-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144651667","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Mast cells express IL17A, IL17F and RORC in lesional psoriatic skin, are activated before therapy and persist in high numbers in a resting state with IL-17A positivity after treatment","authors":"Theresa Benezeder ,&nbsp;Natalie Bordag ,&nbsp;Johannes Woltsche ,&nbsp;Andrea Teufelberger ,&nbsp;Isabella Perchthaler ,&nbsp;Wolfgang Weger ,&nbsp;Wolfgang Salmhofer ,&nbsp;Alexandra Gruber-Wackernagel ,&nbsp;Clemens Painsi ,&nbsp;Qian Zhan ,&nbsp;Amin El-Heliebi ,&nbsp;Magda Babina ,&nbsp;Rachael Clark ,&nbsp;Peter Wolf","doi":"10.1016/j.jdermsci.2025.05.006","DOIUrl":"10.1016/j.jdermsci.2025.05.006","url":null,"abstract":"<div><h3>Background</h3><div>The proinflammatory cytokine IL-17 is known to play an important role in psoriasis pathogenesis, but little is known about its regulation in psoriasis or after treatment.</div></div><div><h3>Objective</h3><div>Aiming to investigate the role of IL-17 regulation in the resolution of psoriasis, we analyzed biopsy samples from patients with plaque psoriasis, including non-lesional and lesional skin at baseline and after anti-IL-17 and -IL-23 antibody, topical dithranol or UVB treatment as well as skin from healthy donors.</div></div><div><h3>Methods</h3><div>Skin biopsy samples were analyzed using immunostaining, RNA sequencing and in situ mRNA detection. In addition, we investigated IL-17 concentration of primary human skin mast cell supernatants after stimulation with the pro-inflammatory cytokines TNFα, IL-22, IL-23 and IFNγ.</div></div><div><h3>Results</h3><div>A high number of IL-17A+ mast cells persisted in resolved lesions after treatment and correlated inversely with the time span in remission. IL-17A+ mast cells were found in T cell-rich areas and near resident memory T cells in active and resolved lesions. CIBERSORTx deconvolution of RNA-seq data of active and dithranol-treated psoriasis lesions showed that activated mast cells were increased in psoriatic skin but returned to normal levels after treatment. Primary skin mast cells responded with an increased release of IL-17A after stimulation with the pro-inflammatory cytokines and in situ mRNA detection revealed positive signals for <em>IL17A, IL17F</em> and <em>RORC</em> in mast cells.</div></div><div><h3>Conclusion</h3><div>Thus, together with T cells, mast cells seem to be important players of the IL-23/IL17 axis underlying psoriasis pathogenesis and relevant for early disease recurrence.</div></div>","PeriodicalId":94076,"journal":{"name":"Journal of dermatological science","volume":"119 2","pages":"Pages 53-63"},"PeriodicalIF":4.6,"publicationDate":"2025-08-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144340712","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Salivary metabolomics for skin cancer screening","authors":"Masahiro Hayashi ,&nbsp;Shigeo Ishikawa ,&nbsp;Masahiro Sugimoto ,&nbsp;Naoki Okuyama ,&nbsp;Kaoru Edamatsu ,&nbsp;Kazuyuki Yusa ,&nbsp;Tomoharu Hemmi ,&nbsp;Takayuki Konno ,&nbsp;Ken Okamura ,&nbsp;Yuta Araki ,&nbsp;Mariko Nikaido ,&nbsp;Yoriko Yaguchi ,&nbsp;Toru Saito ,&nbsp;Shoko Nakano ,&nbsp;Ami Hemmi ,&nbsp;Yutaka Hozumi ,&nbsp;Tamio Suzuki","doi":"10.1016/j.jdermsci.2025.05.003","DOIUrl":"10.1016/j.jdermsci.2025.05.003","url":null,"abstract":"<div><h3>Background</h3><div>If skin cancer (SC) can be screened using saliva, it would be extremely important for improving the prognosis of skin cancer. However, there is currently no available data on salivary screening for SC.</div></div><div><h3>Objective</h3><div>This study aimed to identify salivary metabolomic<span> biomarkers for SC screening by comparing tissue and saliva samples.</span></div></div><div><h3>Methods</h3><div>This single-center study involved SC patients from Yamagata University Hospital, enrolled between May 2017 and April 2020. For the healthy controls (HCs), our database comprising salivary metabolomics data of HCs was used. Whole unstimulated saliva samples were collected from patients with SC (n = 75) and HCs (n = 77). Paired tumor and control tissues after SC resection were obtained from the same patients who donated saliva. Hydrophilic metabolites in the tissue and saliva samples were comprehensively analyzed using capillary electrophoresis–mass spectrometry. Using these candidate metabolites, a multiple logistic regression (MLR) model was developed to differentiate SC from HCs</div></div><div><h3>Results</h3><div>Sixty-six and 12 metabolites showed significant differences in tissues and saliva, respectively. Of these, six metabolites were commonly different between SC and HCs. Spermidine<span><span><span>, 2-aminobutyric acid, and isoleucine were selected to develop the MLR model. The model exhibited a large area under the receiver operating characteristic curve (0.802, 95 % confidence interval: 0.731–0.874, P &lt; 0.0001). Additionally, no significant differences were shown in candidate salivary metabolites between stages in both </span>malignant melanoma and </span>squamous cell carcinoma.</span></div></div><div><h3>Conclusions</h3><div>The salivary metabolomic profiles between SC and HCs differed clearly. This combination of salivary metabolites could serve as non-invasive biomarkers for screening SC.</div></div>","PeriodicalId":94076,"journal":{"name":"Journal of dermatological science","volume":"119 2","pages":"Pages 90-96"},"PeriodicalIF":4.6,"publicationDate":"2025-08-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144251610","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}