{"database":"biostudies-literature","file_versions":[],"scores":null,"additional":{"submitter":["Lavoro A"],"funding":["Italian Ministry of Health (IT-MOH) through 'Ricerca Corrente', grant numbers M2/2 and L2-1","European Union - NextGenerationEU through the Italian Ministry of University and Research under PNRR M4C2-Action 1.4-Call \"Potenziamento strutture di ricerca e creazione di \"campioni nazionali di R&S\"-Project \"National Center for Gene Therapy and Drugs bas","2017POCSICILIA1/5/5.4/9.2.3/AVV6.22/0001 (CUP: G61I0002200095)"],"pagination":["887"],"full_dataset_link":["https://www.ebi.ac.uk/biostudies/studies/S-EPMC11445995"],"repository":["biostudies-literature"],"omics_type":["Unknown"],"volume":["22(1)"],"pubmed_abstract":["

Background

Cancer onset and progression are driven by genetic and epigenetic alterations leading to oncogene activation and the silencing of tumor suppressor genes. Among epigenetic mechanisms, DNA methylation (methDNA) is gaining growing interest in cancer. Promoter hypomethylation is associated with oncogene activation while intragenic methDNA can be involved in transcriptional elongation, alternative spicing, and the activation of cryptic start sites. Several genes involved in the modulation of the tumor microenvironment are regulated by methDNA, including the Solute Carrier Family 22 Member 17 (SLC22A17), which is involved in iron trafficking and extracellular matrix remodeling cooperating with the Gelatinase-Associated Lipocalin (NGAL) ligand. However, the exact role of intrag"],"journal":["Journal of translational medicine"],"pubmed_title":["Identification of SLC22A17 DNA methylation hotspot as a potential biomarker in cutaneous melanoma."],"pmcid":["PMC11445995"],"funding_grant_id":["Italian Ministry of Health (IT-MOH) through 'Ricerca Corrente', grant numbers M2/2 and L2-1","European Union - NextGenerationEU through the Italian Ministry of University and Research under PNRR M4C2-Action 1.4-Call \"Potenziamento strutture di ricerca e creazione di \"campioni nazionali di R&S\"-Project \"National Center for Gene Therapy and Drugs bas","2017POCSICILIA1/5/5.4/9.2.3/AVV6.22/0001 (CUP: G61I0002200095)"],"pubmed_authors":["Candido S","Falzone L","Libra M","Caltabiano R","Ascierto PA","Gattuso G","Capone M","Conti GN","Madonna G","McCubrey JA","Lavoro A"],"additional_accession":[]},"is_claimable":false,"name":"Identification of SLC22A17 DNA methylation hotspot as a potential biomarker in cutaneous melanoma.","description":"

Background

Cancer onset and progression are driven by genetic and epigenetic alterations leading to oncogene activation and the silencing of tumor suppressor genes. Among epigenetic mechanisms, DNA methylation (methDNA) is gaining growing interest in cancer. Promoter hypomethylation is associated with oncogene activation while intragenic methDNA can be involved in transcriptional elongation, alternative spicing, and the activation of cryptic start sites. Several genes involved in the modulation of the tumor microenvironment are regulated by methDNA, including the Solute Carrier Family 22 Member 17 (SLC22A17), which is involved in iron trafficking and extracellular matrix remodeling cooperating with the Gelatinase-Associated Lipocalin (NGAL) ligand. However, the exact role of intrag","dates":{"release":"2024-01-01T00:00:00Z","publication":"2024 Oct","modification":"2026-06-08T03:30:44.748Z","creation":"2025-04-04T00:34:29.5Z"},"accession":"S-EPMC11445995","cross_references":{"pubmed":["39358721"],"doi":["10.1186/s12967-024-05622-9"]}}