Pigment Cell & Melanoma Research最新文献

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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
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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
{"title":"Meeting Report From the 2023 Cure Ocular Melanoma (CURE OM) Global Science Meeting, Philadelphia, PA, November 2023","authors":"Rino S. Seedor,&nbsp;Andrew E. Aplin,&nbsp;Corine Bertolotto,&nbsp;Richard D. Carvajal,&nbsp;Nigel Deacon,&nbsp;Katie Doble,&nbsp;Omid Hamid,&nbsp;Rizwan Haq,&nbsp;Miriam Kadosh,&nbsp;Shaheer Khan,&nbsp;Jacqueline Kraska,&nbsp;Jose Lutzky,&nbsp;Meredith McKean,&nbsp;Kamaneh Montazeri,&nbsp;Justin Moser,&nbsp;Michael Onken,&nbsp;Marlana Orloff,&nbsp;Joseph J. Sacco,&nbsp;Keiran Smalley,&nbsp;Sara M. Selig","doi":"10.1111/pcmr.13205","DOIUrl":"10.1111/pcmr.13205","url":null,"abstract":"<p>The 2023 Cure Ocular Melanoma (CURE OM) Global Science Meeting was held in Philadelphia on November 6, 2023. There is increased awareness and dedicated research in uveal melanoma (UM), but unmet needs remain in the prevention, detection, and treatment of UM. The purpose of this meeting was to provide an international forum for the exchange of research ideas, to allow for discussion of basic science as well as clinical research on UM, and to gather input about advocacy and patient needs.</p>","PeriodicalId":219,"journal":{"name":"Pigment Cell & Melanoma Research","volume":"38 1","pages":""},"PeriodicalIF":3.9,"publicationDate":"2024-10-09","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1111/pcmr.13205","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142386801","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
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
{"title":"Sex Differences in Acral Lentiginous Melanoma: A Retrospective Cohort Analysis of 3617 Cases From the Surveillance, Epidemiology, and End Results Database","authors":"Jennifer M. Fernandez,&nbsp;Mitchell A. Taylor,&nbsp;Katherine Plampton,&nbsp;Erin X. Wei,&nbsp;Ashley Wysong","doi":"10.1111/pcmr.13200","DOIUrl":"10.1111/pcmr.13200","url":null,"abstract":"","PeriodicalId":219,"journal":{"name":"Pigment Cell & Melanoma Research","volume":"38 1","pages":""},"PeriodicalIF":3.9,"publicationDate":"2024-10-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142363597","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
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,&nbsp;Hanxiao Mao,&nbsp;Rulan Liu,&nbsp;Ziyuan Zeng,&nbsp;Lvsha Xie,&nbsp;Yan Yang,&nbsp;Yuanmin He","doi":"10.1111/pcmr.13202","DOIUrl":"10.1111/pcmr.13202","url":null,"abstract":"<div>\u0000 \u0000 <p>Vitiligo is an autoimmune disorder characterized by chronic depigmentation and milk-white patches on the skin. Skin infiltration by autoreactive CD8<sup>+</sup> 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 H<sub>2</sub>O<sub>2</sub>. 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<sup>+</sup> 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.</p>\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,&nbsp;Qiyun Wu,&nbsp;Yingjie Xia,&nbsp;Jiahui Wu,&nbsp;Xiaoyang Wang,&nbsp;Gary Ka Wing Yuen,&nbsp;Tina Tingxia Dong,&nbsp;Jin Gao,&nbsp;Karl Wah Keung Tsim","doi":"10.1111/pcmr.13201","DOIUrl":"10.1111/pcmr.13201","url":null,"abstract":"<p>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 Ca<sup>2+</sup> mobilization was regulated. The applied antagonists of M1 and/or M3 mAChRs could block the UV-induced melanosome release and the mobilization of intracellular Ca<sup>2+</sup>. 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.</p>","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,&nbsp;Eveliina Jakkula,&nbsp;Juho Hiltunen,&nbsp;Heidi Putkuri,&nbsp;Aleksandra Staskiewicz-Tuikkanen,&nbsp;Reetta-Stiina Järvinen,&nbsp;Martin Täll,&nbsp;Virpi Raivio,&nbsp;Rana'a T. Al-Jamal,&nbsp;Tero T. Kivelä,&nbsp;Joni A. Turunen","doi":"10.1111/pcmr.13198","DOIUrl":"10.1111/pcmr.13198","url":null,"abstract":"<p>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 <i>BAP1</i> and <i>MBD4</i>, 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 <i>GNAQ</i>, <i>GNA11</i>, <i>CYSLTR2</i>, <i>PLCB4</i>, <i>EIF1AX</i>, and <i>SF3B1</i> lacked pathogenic germline variants. One patient carried the pathogenic <i>BRCA1</i> variant c.3626del p.(Leu1209*), and one harbored a novel truncating <i>MET</i> variant c.252C &gt; G p.(Tyr84*), classified as likely pathogenic. <i>FLCN</i> and <i>BRCA2</i>, 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 <i>BLM</i> variant c.2824-2A &gt; T. None of the carriers of identified variants had familial UM. We identified <i>BRCA1</i> and <i>MET</i> as genes with pathogenic germline variants in Finnish UM patients, each with a frequency of 0.4% (95% confidence interval, 0–2).</p>","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,&nbsp;Jane M. Palmer,&nbsp;Lindsay McGrath,&nbsp;Sunil Warrier,&nbsp;Hayley R. Hamilton,&nbsp;Timothy Beckman,&nbsp;Matthew G. D'Mellow,&nbsp;Kelly M. Brooks,&nbsp;William Glasson,&nbsp;Nicholas K. Hayward,&nbsp;Antonia L. Pritchard","doi":"10.1111/pcmr.13199","DOIUrl":"10.1111/pcmr.13199","url":null,"abstract":"<p>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 <i>BAP1</i>, <i>POT1</i> and <i>CDKN2A</i> 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 <i>POT1</i>, <i>MITF</i>, <i>OCA2</i>, <i>SLC45A2</i> and <i>TYR</i>. Three (4%) patients carried pathogenic variants in genes previously linked with other cancer syndromes (<i>ATR</i>, <i>BRIP1</i> and <i>MSH6</i>) 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.</p>","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}
引用次数: 0
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,&nbsp;Qiusheng Lu,&nbsp;Will Boswell,&nbsp;Kang Du,&nbsp;Yanting Xing,&nbsp;Mikki Boswell,&nbsp;Korri S. Weldon,&nbsp;Zhao Lai,&nbsp;Markita Savage,&nbsp;Manfred Schartl,&nbsp;Yuan Lu","doi":"10.1111/pcmr.13196","DOIUrl":"10.1111/pcmr.13196","url":null,"abstract":"<p>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 <i>Xiphophorus</i> 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 <i>Xiphophorus</i> species do not develop such tumors. Here we report the identification of a locus residing in the genome of one <i>Xiphophorus</i> 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.</p>","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
An In Vivo Study of LNS8801, a GPER Agonist, in a Spontaneous Melanoma-Prone Mouse Model, TGS GPER 激动剂 LNS8801 在自发性黑色素瘤小鼠模型中的体内研究,TGS.
IF 3.9 3区 医学
Pigment Cell & Melanoma Research Pub Date : 2024-09-16 DOI: 10.1111/pcmr.13197
Christina Marinaro, John Sauer, Christopher A. Natale, Todd Ridky, Suzie Chen
{"title":"An In Vivo Study of LNS8801, a GPER Agonist, in a Spontaneous Melanoma-Prone Mouse Model, TGS","authors":"Christina Marinaro,&nbsp;John Sauer,&nbsp;Christopher A. Natale,&nbsp;Todd Ridky,&nbsp;Suzie Chen","doi":"10.1111/pcmr.13197","DOIUrl":"10.1111/pcmr.13197","url":null,"abstract":"<p>Melanoma is the most aggressive and deadly form of skin cancer that arises from the transformation of melanocytes, the pigment producing cells of the skin. In the year 2024 there will be approximately 10,000 new cases of melanoma diagnosed and approximately 8,000 deaths attributed to melanoma in the United States. In this study we treated a group of male and female transgenic mice that spontaneously develop metastatic melanoma, TGS, with a G-protein-coupled estrogen receptor agonist LNS8801 to assess the efficacy on disease progression. A second group of male and female TGS mice was also exposed to UVB irradiation to mimic exposure to sunlight. Over the course of the 32-week experiment, visible images were taken by the small animal imaging IVIS system to track tumor progression, and blood and tissue samples were collected for molecular analyses. Results showed that sex-biased effects were observed in the efficacy of LNS8801 and that LNS8801 shows a UV-protective influence in both male and female TGS mice.</p>","PeriodicalId":219,"journal":{"name":"Pigment Cell & Melanoma Research","volume":"38 1","pages":""},"PeriodicalIF":3.9,"publicationDate":"2024-09-16","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11681840/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142277689","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
MetFinder: A Tool for Automated Quantitation of Metastatic Burden in Histological Sections From Preclinical Models MetFinder:临床前模型组织切片转移负荷自动定量工具
IF 3.9 3区 医学
Pigment Cell & Melanoma Research Pub Date : 2024-09-10 DOI: 10.1111/pcmr.13195
Alcida Karz, Nicolas Coudray, Erol Bayraktar, Kristyn Galbraith, George Jour, Arman Alberto Sorin Shadaloey, Nicole Eskow, Andrey Rubanov, Maya Navarro, Rana Moubarak, Gillian Baptiste, Grace Levinson, Valeria Mezzano, Mark Alu, Cynthia Loomis, Daniel Lima, Adam Rubens, Lucia Jilaveanu, Aristotelis Tsirigos, Eva Hernando
{"title":"MetFinder: A Tool for Automated Quantitation of Metastatic Burden in Histological Sections From Preclinical Models","authors":"Alcida Karz,&nbsp;Nicolas Coudray,&nbsp;Erol Bayraktar,&nbsp;Kristyn Galbraith,&nbsp;George Jour,&nbsp;Arman Alberto Sorin Shadaloey,&nbsp;Nicole Eskow,&nbsp;Andrey Rubanov,&nbsp;Maya Navarro,&nbsp;Rana Moubarak,&nbsp;Gillian Baptiste,&nbsp;Grace Levinson,&nbsp;Valeria Mezzano,&nbsp;Mark Alu,&nbsp;Cynthia Loomis,&nbsp;Daniel Lima,&nbsp;Adam Rubens,&nbsp;Lucia Jilaveanu,&nbsp;Aristotelis Tsirigos,&nbsp;Eva Hernando","doi":"10.1111/pcmr.13195","DOIUrl":"10.1111/pcmr.13195","url":null,"abstract":"<div>\u0000 \u0000 <p>As efforts to study the mechanisms of melanoma metastasis and novel therapeutic approaches multiply, researchers need accurate, high-throughput methods to evaluate the effects on tumor burden resulting from specific interventions. We show that automated quantification of tumor content from whole slide images is a compelling solution to assess in vivo experiments. In order to increase the outflow of data collection from preclinical studies, we assembled a large dataset with annotations and trained a deep neural network for the quantitative analysis of melanoma tumor content on histopathological sections of murine models. After assessing its performance in segmenting these images, the tool obtained consistent results with an orthogonal method (bioluminescence) of measuring metastasis in an experimental setting. This AI-based algorithm, made freely available to academic laboratories through a web-interface called MetFinder, promises to become an asset for melanoma researchers and pathologists interested in accurate, quantitative assessment of metastasis burden.</p>\u0000 </div>","PeriodicalId":219,"journal":{"name":"Pigment Cell & Melanoma Research","volume":"38 1","pages":""},"PeriodicalIF":3.9,"publicationDate":"2024-09-10","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142215777","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
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