{"database":"biostudies-literature","file_versions":[],"scores":null,"additional":{"omics_type":["Unknown"],"volume":["14(2)"],"submitter":["Qiu Q"],"pubmed_abstract":["The expression level of PD-L1 does not accurately predict the prognosis of advanced colorectal cancer (CRC) patients, but it still reflects the tumor microenvironment to some extent. By stratifying PD-L1 status, gene subtypes in PD-L1 positivity-related pathological pathways were analyzed for their relationship to MSI or TMB to provide more individualized treatment options for CRCs. A total of 752 advanced CRCs were included, and their genomic variance was measured by a targeted next generation sequencing panel in this study. MSI and TMB were both measured by NGS, while PD-L1 expression level was measured using the PD-L1 colon 22C3 pharmDx kit. We found RTK/RAS pathway was positively related to high PD-L1 expression, with <i>BRAF V600E</i> and most <i>KRAS</i> mutations (G12 and G13) subtypes showing a significant correlation. Conversely, the Wnt and p53 pathways were negatively related to high PD-L1 expression, with <i>APC</i> C-terminal alterations and other non-inactivation mutations in <i>TP53</i> making a primary contribution with significant statistical significance. Major subtypes showing a significantly higher proportion of TMB-H or MSI-H were irrespective of PD-L1 status. These findings demonstrate pathological pathways associated with high PD-L1 expression, suggesting that pathway-induced oncogenic constructive PD-L1 upregulation may be the reason for the corresponding patients' primary resistance to immune checkpoint inhibitors (ICIs), rather than a lack of pre-existing immune responses."],"journal":["American journal of cancer research"],"pagination":["796-808"],"full_dataset_link":["https://www.ebi.ac.uk/biostudies/studies/S-EPMC10915335"],"repository":["biostudies-literature"],"pubmed_title":["Clinical implications of PD-L1 expression and pathway-related molecular subtypes in advanced Asian colorectal cancer patients."],"pmcid":["PMC10915335"],"pubmed_authors":["Wang M","Chen Q","Li J","Zhang D","Zhou R","Qiu Q","Tan D","Yang P","Gong Z","Wen W","Zhao X"],"additional_accession":[]},"is_claimable":false,"name":"Clinical implications of PD-L1 expression and pathway-related molecular subtypes in advanced Asian colorectal cancer patients.","description":"The expression level of PD-L1 does not accurately predict the prognosis of advanced colorectal cancer (CRC) patients, but it still reflects the tumor microenvironment to some extent. By stratifying PD-L1 status, gene subtypes in PD-L1 positivity-related pathological pathways were analyzed for their relationship to MSI or TMB to provide more individualized treatment options for CRCs. A total of 752 advanced CRCs were included, and their genomic variance was measured by a targeted next generation sequencing panel in this study. MSI and TMB were both measured by NGS, while PD-L1 expression level was measured using the PD-L1 colon 22C3 pharmDx kit. We found RTK/RAS pathway was positively related to high PD-L1 expression, with <i>BRAF V600E</i> and most <i>KRAS</i> mutations (G12 and G13) subtypes showing a significant correlation. Conversely, the Wnt and p53 pathways were negatively related to high PD-L1 expression, with <i>APC</i> C-terminal alterations and other non-inactivation mutations in <i>TP53</i> making a primary contribution with significant statistical significance. Major subtypes showing a significantly higher proportion of TMB-H or MSI-H were irrespective of PD-L1 status. These findings demonstrate pathological pathways associated with high PD-L1 expression, suggesting that pathway-induced oncogenic constructive PD-L1 upregulation may be the reason for the corresponding patients' primary resistance to immune checkpoint inhibitors (ICIs), rather than a lack of pre-existing immune responses.","dates":{"release":"2024-01-01T00:00:00Z","publication":"2024","modification":"2026-05-29T12:06:02.009Z","creation":"2024-11-20T23:50:17.262Z"},"accession":"S-EPMC10915335","cross_references":{"pubmed":["38455414"],"doi":["10.62347/fssf9938"]}}