Mutational Characterization of Cutaneous Melanoma Supports Divergent Pathways Model for Melanoma Development
According to the divergent pathway model, cutaneous melanoma comprises a nevogenic group with a propensity to melanocyte proliferation and another one associated with cumulative solar damage (CSD). While characterized clinically and epidemiologically, the differences in the molecular profiles betwee...
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| Veröffentlicht in: | Cancers 2021-10, Vol.13 (20), p.5219 |
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| creator | Millán-Esteban, David Peña-Chilet, María García-Casado, Zaida Manrique-Silva, Esperanza Requena, Celia Bañuls, José López-Guerrero, Jose Antonio Rodríguez-Hernández, Aranzazu Traves, Víctor Dopazo, Joaquín Virós, Amaya Kumar, Rajiv Nagore, Eduardo |
| description | According to the divergent pathway model, cutaneous melanoma comprises a nevogenic group with a propensity to melanocyte proliferation and another one associated with cumulative solar damage (CSD). While characterized clinically and epidemiologically, the differences in the molecular profiles between the groups have remained primarily uninvestigated. This study has used a custom gene panel and bioinformatics tools to investigate the potential molecular differences in a thoroughly characterized cohort of 119 melanoma patients belonging to nevogenic and CSD groups. We found that the nevogenic melanomas had a restricted set of mutations, with the prominently mutated gene being
. The CSD melanomas, in contrast, showed mutations in a diverse group of genes that included
,
,
, and
. We thus provide evidence that nevogenic and CSD melanomas constitute different biological entities and highlight the need to explore new targeted therapies. |
| doi_str_mv | 10.3390/cancers13205219 |
| format | Article |
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. The CSD melanomas, in contrast, showed mutations in a diverse group of genes that included
,
,
, and
. We thus provide evidence that nevogenic and CSD melanomas constitute different biological entities and highlight the need to explore new targeted therapies.</description><identifier>ISSN: 2072-6694</identifier><identifier>EISSN: 2072-6694</identifier><identifier>DOI: 10.3390/cancers13205219</identifier><identifier>PMID: 34680367</identifier><language>eng</language><publisher>Switzerland: MDPI AG</publisher><subject>Bioinformatics ; Circuits ; Classification ; Disease ; Epidemiology ; Gene expression ; Kinases ; Melanoma ; Mutation ; Patients ; Rac1 protein ; Radiation ; Tumors ; Womens health</subject><ispartof>Cancers, 2021-10, Vol.13 (20), p.5219</ispartof><rights>2021 by the authors. Licensee MDPI, Basel, Switzerland. This article is an open access article distributed under the terms and conditions of the Creative Commons Attribution (CC BY) license (https://creativecommons.org/licenses/by/4.0/). Notwithstanding the ProQuest Terms and Conditions, you may use this content in accordance with the terms of the License.</rights><rights>2021 by the authors. 2021</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c421t-19f3ebca50d4afcd477cf757cf3f928e6906af64950a696f9b969fb9bf3dba293</citedby><cites>FETCH-LOGICAL-c421t-19f3ebca50d4afcd477cf757cf3f928e6906af64950a696f9b969fb9bf3dba293</cites><orcidid>0000-0002-0990-7608 ; 0000-0002-8066-1444 ; 0000-0003-3318-120X ; 0000-0002-6445-9617 ; 0000-0003-3433-8707 ; 0000-0002-7369-8388 ; 0000-0002-6093-0395</orcidid></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC8533762/pdf/$$EPDF$$P50$$Gpubmedcentral$$Hfree_for_read</linktopdf><linktohtml>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC8533762/$$EHTML$$P50$$Gpubmedcentral$$Hfree_for_read</linktohtml><link.rule.ids>230,314,727,780,784,885,27924,27925,53791,53793</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/34680367$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Millán-Esteban, David</creatorcontrib><creatorcontrib>Peña-Chilet, María</creatorcontrib><creatorcontrib>García-Casado, Zaida</creatorcontrib><creatorcontrib>Manrique-Silva, Esperanza</creatorcontrib><creatorcontrib>Requena, Celia</creatorcontrib><creatorcontrib>Bañuls, José</creatorcontrib><creatorcontrib>López-Guerrero, Jose Antonio</creatorcontrib><creatorcontrib>Rodríguez-Hernández, Aranzazu</creatorcontrib><creatorcontrib>Traves, Víctor</creatorcontrib><creatorcontrib>Dopazo, Joaquín</creatorcontrib><creatorcontrib>Virós, Amaya</creatorcontrib><creatorcontrib>Kumar, Rajiv</creatorcontrib><creatorcontrib>Nagore, Eduardo</creatorcontrib><title>Mutational Characterization of Cutaneous Melanoma Supports Divergent Pathways Model for Melanoma Development</title><title>Cancers</title><addtitle>Cancers (Basel)</addtitle><description>According to the divergent pathway model, cutaneous melanoma comprises a nevogenic group with a propensity to melanocyte proliferation and another one associated with cumulative solar damage (CSD). While characterized clinically and epidemiologically, the differences in the molecular profiles between the groups have remained primarily uninvestigated. This study has used a custom gene panel and bioinformatics tools to investigate the potential molecular differences in a thoroughly characterized cohort of 119 melanoma patients belonging to nevogenic and CSD groups. We found that the nevogenic melanomas had a restricted set of mutations, with the prominently mutated gene being
. The CSD melanomas, in contrast, showed mutations in a diverse group of genes that included
,
,
, and
. We thus provide evidence that nevogenic and CSD melanomas constitute different biological entities and highlight the need to explore new targeted therapies.</description><subject>Bioinformatics</subject><subject>Circuits</subject><subject>Classification</subject><subject>Disease</subject><subject>Epidemiology</subject><subject>Gene expression</subject><subject>Kinases</subject><subject>Melanoma</subject><subject>Mutation</subject><subject>Patients</subject><subject>Rac1 protein</subject><subject>Radiation</subject><subject>Tumors</subject><subject>Womens health</subject><issn>2072-6694</issn><issn>2072-6694</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2021</creationdate><recordtype>article</recordtype><sourceid>8G5</sourceid><sourceid>ABUWG</sourceid><sourceid>AFKRA</sourceid><sourceid>AZQEC</sourceid><sourceid>BENPR</sourceid><sourceid>CCPQU</sourceid><sourceid>DWQXO</sourceid><sourceid>GNUQQ</sourceid><sourceid>GUQSH</sourceid><sourceid>M2O</sourceid><recordid>eNpdkU1P3DAQhq0KVBBw7q2K1AuXLbYnsdeXSmhpC9IikNqerYljs0FOnNrJIvrra1g-FnywrZlnXo_nJeQTo18BFD0x2BsbEwNOK87UB7LPqeQzIVS5s3XfI0cp3dK8AJgU8iPZg1LMKQi5T_zlNOLYhh59sVhhRDPa2P57DBXBFYuc7m2YUnFpPfahw-LXNAwhjqk4a9c23th-LK5xXN3hfYZCY33hQnzFz-za-jB0mTskuw59skdP5wH58-P778X5bHn182JxupyZkrNxxpQDWxusaFOiM00ppXGyyhs4xedWKCrQiVJVFIUSTtVKKFer2kFTI1dwQL5tdIep7mxj8tMRvR5i22G81wFb_TbTtyt9E9Z6XgFIwbPA8ZNADH8nm0bdtclY7zez0Lyal1JlEDL65R16G6aYx7mhoATJWKZONpSJIaVo3UszjOoHM_U7M3PF5-0_vPDP1sF_CLmfLg</recordid><startdate>20211018</startdate><enddate>20211018</enddate><creator>Millán-Esteban, David</creator><creator>Peña-Chilet, María</creator><creator>García-Casado, Zaida</creator><creator>Manrique-Silva, Esperanza</creator><creator>Requena, Celia</creator><creator>Bañuls, José</creator><creator>López-Guerrero, Jose Antonio</creator><creator>Rodríguez-Hernández, Aranzazu</creator><creator>Traves, Víctor</creator><creator>Dopazo, Joaquín</creator><creator>Virós, Amaya</creator><creator>Kumar, Rajiv</creator><creator>Nagore, Eduardo</creator><general>MDPI AG</general><general>MDPI</general><scope>NPM</scope><scope>AAYXX</scope><scope>CITATION</scope><scope>3V.</scope><scope>7T5</scope><scope>7TO</scope><scope>7XB</scope><scope>8FE</scope><scope>8FH</scope><scope>8FK</scope><scope>8G5</scope><scope>ABUWG</scope><scope>AFKRA</scope><scope>AZQEC</scope><scope>BBNVY</scope><scope>BENPR</scope><scope>BHPHI</scope><scope>CCPQU</scope><scope>DWQXO</scope><scope>GNUQQ</scope><scope>GUQSH</scope><scope>H94</scope><scope>HCIFZ</scope><scope>LK8</scope><scope>M2O</scope><scope>M7P</scope><scope>MBDVC</scope><scope>PIMPY</scope><scope>PQEST</scope><scope>PQQKQ</scope><scope>PQUKI</scope><scope>PRINS</scope><scope>Q9U</scope><scope>7X8</scope><scope>5PM</scope><orcidid>https://orcid.org/0000-0002-0990-7608</orcidid><orcidid>https://orcid.org/0000-0002-8066-1444</orcidid><orcidid>https://orcid.org/0000-0003-3318-120X</orcidid><orcidid>https://orcid.org/0000-0002-6445-9617</orcidid><orcidid>https://orcid.org/0000-0003-3433-8707</orcidid><orcidid>https://orcid.org/0000-0002-7369-8388</orcidid><orcidid>https://orcid.org/0000-0002-6093-0395</orcidid></search><sort><creationdate>20211018</creationdate><title>Mutational Characterization of Cutaneous Melanoma Supports Divergent Pathways Model for Melanoma Development</title><author>Millán-Esteban, David ; 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While characterized clinically and epidemiologically, the differences in the molecular profiles between the groups have remained primarily uninvestigated. This study has used a custom gene panel and bioinformatics tools to investigate the potential molecular differences in a thoroughly characterized cohort of 119 melanoma patients belonging to nevogenic and CSD groups. We found that the nevogenic melanomas had a restricted set of mutations, with the prominently mutated gene being
. The CSD melanomas, in contrast, showed mutations in a diverse group of genes that included
,
,
, and
. We thus provide evidence that nevogenic and CSD melanomas constitute different biological entities and highlight the need to explore new targeted therapies.</abstract><cop>Switzerland</cop><pub>MDPI AG</pub><pmid>34680367</pmid><doi>10.3390/cancers13205219</doi><orcidid>https://orcid.org/0000-0002-0990-7608</orcidid><orcidid>https://orcid.org/0000-0002-8066-1444</orcidid><orcidid>https://orcid.org/0000-0003-3318-120X</orcidid><orcidid>https://orcid.org/0000-0002-6445-9617</orcidid><orcidid>https://orcid.org/0000-0003-3433-8707</orcidid><orcidid>https://orcid.org/0000-0002-7369-8388</orcidid><orcidid>https://orcid.org/0000-0002-6093-0395</orcidid><oa>free_for_read</oa></addata></record> |
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| subjects | Bioinformatics Circuits Classification Disease Epidemiology Gene expression Kinases Melanoma Mutation Patients Rac1 protein Radiation Tumors Womens health |
| title | Mutational Characterization of Cutaneous Melanoma Supports Divergent Pathways Model for Melanoma Development |
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