Q-omics provides the consensus-scored VPS26C profile across patient tissues and cancer cell-line models. VPS26C expression is associated with patient survival in 25 of 34 cancer types, with the highest sampling consensus in KIRC. Among the 18 cancer types available for tumor–normal comparison, VPS26C is differentially expressed in 12, with the highest sampling consensus in COAD. Additionally, VPS26C protein abundance shows 23,308 significant protein co-abundance associations, with the highest sampling consensus in LSCC. Together, these results highlight KIRC, COAD, and LSCC as cancer lineages where VPS26C 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 VPS26C — synthetic lethality, tumor antigen, and pembrolizumab response.
This table summarizes VPS26C survival associations across molecular data types. VPS26C RNA expression shows survival associations in the most cancer types (25), 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 VPS26C RNA expression–survival associations across cancer types. High VPS26C expression shows unfavorable associations in CESC, BRCA, LIHC, HNSC and MESO, but favorable associations in KIRC. 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 VPS26C RNA expression.
This table summarizes VPS26C tumor–normal expression differences by data type. RNA shows broader differences across cancer types, with a lineage consensus of 12, while mass-spec protein shows differences in 7. The strongest signals are observed in THCA for RNA and CCRCC for protein.
This table ranks reproducible tumor–normal expression differences for VPS26C. A negative fold-change indicates higher expression in normal tissue than in tumor tissue. VPS26C shows lower tumor expression in COAD, THCA, KICH and LUAD and higher tumor expression in HNSC and LIHC. The COAD box plot shows higher VPS26C RNA expression in normal versus tumor tissue (log2 FC = −0.619, t-test p < 0.001).
This table shows molecular features associated with VPS26C in patient tissues and cancer cell lines. In patient samples, VPS26C 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, VPS26C RNA and mutation anchors are most strongly linked to RNA-expression features, especially in PANCREAS, while CRISPR and shRNA rows add functional-dependency signals in URINARY_TRACT and BLOOD_Leukemia.
