Q-omics provides the consensus-scored VPS18 profile across patient tissues and cancer cell-line models. VPS18 expression is associated with patient survival in 26 of 34 cancer types, with the highest sampling consensus in MESO. Among the 18 cancer types available for tumor–normal comparison, VPS18 is differentially expressed in 10, with the highest sampling consensus in HNSC. Additionally, VPS18 protein abundance shows 23,335 significant protein co-abundance associations, with the highest sampling consensus in LSCC. Together, these results highlight MESO, HNSC, and LSCC as cancer lineages where VPS18 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 VPS18 — synthetic lethality, tumor antigen, and pembrolizumab response.
This table summarizes VPS18 survival associations across molecular data types. VPS18 RNA expression shows survival associations in the most cancer types (26), followed by mutation status (6) and mass-spec protein abundance (5). The rightmost column indicates the cancer type with the highest sampling consensus for each molecular layer.
This table ranks reproducible VPS18 RNA expression–survival associations across cancer types. High VPS18 expression shows unfavorable associations in COAD and LUAD, but favorable associations in MESO, SARC, KIRC and UCEC. The MESO Kaplan–Meier curve shows clear separation, with the low-expression group declining faster, consistent with the favorable association (log-rank p = .002). Together, the overview and detailed table identify MESO as the clearest survival context for VPS18 RNA expression.
This table summarizes VPS18 tumor–normal expression differences by data type. RNA shows broader differences across cancer types, with a lineage consensus of 10, while mass-spec protein shows differences in 6. The strongest signals are observed in HNSC for RNA and CCRCC for protein.
This table ranks reproducible tumor–normal expression differences for VPS18. A negative fold-change indicates higher expression in normal tissue than in tumor tissue. VPS18 shows lower tumor expression in PAAD and higher tumor expression in HNSC, LIHC, CHOL, KICH and STAD. The HNSC box plot shows higher VPS18 RNA expression in tumor versus normal tissue (log2 FC = +0.766, t-test p < 0.001).
This table shows molecular features associated with VPS18 in patient tissues and cancer cell lines. In patient samples, VPS18 shows the broadest associations at the RNA and protein expression levels, with LSCC recurring as the lineage with the largest associated feature set. In cancer cell lines, VPS18 RNA and mutation anchors are most strongly linked to RNA-expression features, especially in SKIN, while CRISPR and shRNA rows add functional-dependency signals in BLOOD_Lymphoma and LARGE_INTESTINE.
