Q-omics provides the consensus-scored SNX18 profile across patient tissues and cancer cell-line models. SNX18 expression is associated with patient survival in 21 of 34 cancer types, with the highest sampling consensus in KIRC. Among the 18 cancer types available for tumor–normal comparison, SNX18 is differentially expressed in 9, with the highest sampling consensus in KIRC. Additionally, SNX18 protein abundance shows 24,475 significant protein co-abundance associations, with the highest sampling consensus in COAD. Together, these results highlight KIRC, and COAD as cancer lineages where SNX18 shows reproducible signals across survival, tumor–normal expression, and patient cross-omics analyses.
Every result is evaluated using two consensus scores. Sampling consensus measures how consistently a finding is reproduced within a cancer lineage across different conditions. Lineage consensus measures how broadly the result is shared across cancer types, distinguishing pan-cancer signals from lineage-specific patterns.
Premium analyses for SNX18 — synthetic lethality, tumor antigen, and pembrolizumab response.
This table summarizes SNX18 survival associations across molecular data types. SNX18 RNA expression shows survival associations in the most cancer types (21), followed by mutation status (4) and mass-spec protein abundance (7). The rightmost column indicates the cancer type with the highest sampling consensus for each molecular layer.
This table ranks reproducible SNX18 RNA expression–survival associations across cancer types. High SNX18 expression shows unfavorable associations in KICH and HNSC, but favorable associations in KIRC, LGG, ACC and LUAD. The KIRC Kaplan–Meier curve shows clear separation, with the low-expression group declining faster, consistent with the favorable association (log-rank p < 0.001). Together, the overview and detailed table identify KIRC as the clearest survival context for SNX18 RNA expression.
This table summarizes SNX18 tumor–normal expression differences by data type. RNA shows broader differences across cancer types, with a lineage consensus of 9, while mass-spec protein shows differences in 6. The strongest signals are observed in KIRC for RNA and COAD for protein.
This table ranks reproducible tumor–normal expression differences for SNX18. A negative fold-change indicates higher expression in normal tissue than in tumor tissue. SNX18 shows lower tumor expression in KIRC, KIRP, LUSC, BRCA and UCEC and higher tumor expression in LIHC. The KIRC box plot shows higher SNX18 RNA expression in normal versus tumor tissue (log2 FC = −0.769, t-test p < 0.001).
This table shows molecular features associated with SNX18 in patient tissues and cancer cell lines. In patient samples, SNX18 shows the broadest associations at the RNA and protein expression levels, with COAD recurring as the lineage with the largest associated feature set. In cancer cell lines, SNX18 RNA and mutation anchors are most strongly linked to RNA-expression features, especially in OVARY, while CRISPR and shRNA rows add functional-dependency signals in LARGE_INTESTINE and CNS.