ENAapplication/xmlftp://ftp.sra.ebi.ac.uk/vol1/fastq/SRR563/003/SRR5638583/SRR5638583_1.fastq.gzftp://ftp.sra.ebi.ac.uk/vol1/fastq/SRR563/000/SRR5638580/SRR5638580_2.fastq.gzftp://ftp.sra.ebi.ac.uk/vol1/fastq/SRR563/005/SRR5638585/SRR5638585_1.fastq.gzftp://ftp.sra.ebi.ac.uk/vol1/fastq/SRR563/001/SRR5638581/SRR5638581_1.fastq.gzftp://ftp.sra.ebi.ac.uk/vol1/fastq/SRR563/002/SRR5638582/SRR5638582_1.fastq.gzftp://ftp.sra.ebi.ac.uk/vol1/fastq/SRR563/006/SRR5638586/SRR5638586_1.fastq.gzftp://ftp.sra.ebi.ac.uk/vol1/fastq/SRR563/003/SRR5638583/SRR5638583_2.fastq.gzftp://ftp.sra.ebi.ac.uk/vol1/fastq/SRR563/002/SRR5638582/SRR5638582_2.fastq.gzftp://ftp.sra.ebi.ac.uk/vol1/fastq/SRR563/001/SRR5638581/SRR5638581_2.fastq.gzftp://ftp.sra.ebi.ac.uk/vol1/fastq/SRR563/009/SRR5638589/SRR5638589_2.fastq.gzftp://ftp.sra.ebi.ac.uk/vol1/fastq/SRR563/004/SRR5638584/SRR5638584_1.fastq.gzftp://ftp.sra.ebi.ac.uk/vol1/fastq/SRR563/007/SRR5638587/SRR5638587_2.fastq.gzftp://ftp.sra.ebi.ac.uk/vol1/fastq/SRR563/009/SRR5638579/SRR5638579_2.fastq.gzftp://ftp.sra.ebi.ac.uk/vol1/fastq/SRR563/008/SRR5638588/SRR5638588_2.fastq.gzftp://ftp.sra.ebi.ac.uk/vol1/fastq/SRR563/006/SRR5638586/SRR5638586_2.fastq.gzftp://ftp.sra.ebi.ac.uk/vol1/fastq/SRR563/009/SRR5638589/SRR5638589_1.fastq.gzftp://ftp.sra.ebi.ac.uk/vol1/fastq/SRR563/008/SRR5638578/SRR5638578_2.fastq.gzftp://ftp.sra.ebi.ac.uk/vol1/fastq/SRR563/007/SRR5638587/SRR5638587_1.fastq.gzftp://ftp.sra.ebi.ac.uk/vol1/fastq/SRR563/004/SRR5638584/SRR5638584_2.fastq.gzftp://ftp.sra.ebi.ac.uk/vol1/fastq/SRR563/008/SRR5638578/SRR5638578_1.fastq.gzftp://ftp.sra.ebi.ac.uk/vol1/fastq/SRR563/005/SRR5638585/SRR5638585_2.fastq.gzftp://ftp.sra.ebi.ac.uk/vol1/fastq/SRR563/000/SRR5638580/SRR5638580_1.fastq.gzftp://ftp.sra.ebi.ac.uk/vol1/fastq/SRR563/008/SRR5638588/SRR5638588_1.fastq.gzftp://ftp.sra.ebi.ac.uk/vol1/fastq/SRR563/009/SRR5638579/SRR5638579_1.fastq.gzprimaryOK200GenomicsCenter of Applied Genomics, Children's Hospital of Philadelphiahttps://www.ebi.ac.uk/ena/browser/view/PRJNA388966Homo sapiensTelomerase promoter mutations are highly prevalent in human tumors including melanoma. Telomere transcriptional signatures are enriched in a subset of therapy-naïve melanomas associated with worse overall survival, in BRAF-mutant intrinsically resistant melanoma cells that evade MAPK inhibitors (MAPKi), as well as in a subset of post-treatment tumor biopsies derived from patients who have disease progression on MAPKi or the immune checkpoint inhibitors, anti-CTLA-4 or anti-PD1. We demonstrate the efficacy of a telomerase-directed nucleoside, 6-thio-2'-deoxyguanosine (6-thio-dG) that results in telomere dysfunction and cell death in various models of therapy-resistant cells. Furthermore, 6-thio-dG significantly inhibits tumor growth of primary tumor biopsy cultures derived from patients who had disease progression on multiple therapies including anti-CTLA-4 or anti-PD1. Overall design: A375 and LOX-IMVI BR melanoma cells were treated with the control, 6-Thio-dG and BIBR 1532. RNA was purified from two biological replicates for RNA sequencing.xref:PubMed:29563139ENAfalseHomo sapiensGene Expression Analysis of Melanoma Cells Treated with 6-Thio-dG In Vitro2025-09-242017-06-04PRJNA388966GSE99552960629563139