Q-omics provides the consensus-scored VPS13D profile across patient tissues and cancer cell-line models. VPS13D expression is associated with patient survival in 24 of 34 cancer types, with the highest sampling consensus in KIRC. Among the 18 cancer types available for tumor–normal comparison, VPS13D is differentially expressed in 14, with the highest sampling consensus in KIRC. Additionally, VPS13D protein abundance shows 22,331 significant protein co-abundance associations, with the highest sampling consensus in GBM. Together, these results highlight KIRC, and GBM as cancer lineages where VPS13D 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 VPS13D — synthetic lethality, tumor antigen, and pembrolizumab response.
This table summarizes VPS13D survival associations across molecular data types. VPS13D RNA expression shows survival associations in the most cancer types (24), followed by mutation status (8) 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 VPS13D RNA expression–survival associations across cancer types. High VPS13D expression shows unfavorable associations in ACC, but favorable associations in KIRC, HNSC, LUAD, LGG and SCLC. 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 VPS13D RNA expression.
This table summarizes VPS13D tumor–normal expression differences by data type. RNA shows broader differences across cancer types, with a lineage consensus of 14, while mass-spec protein shows differences in 4. The strongest signals are observed in KIRC for RNA and CCRCC for protein.
This table ranks reproducible tumor–normal expression differences for VPS13D. A negative fold-change indicates higher expression in normal tissue than in tumor tissue. VPS13D shows lower tumor expression in KIRC, COAD, BRCA, LUAD and HNSC and higher tumor expression in LIHC. The KIRC box plot shows higher VPS13D RNA expression in normal versus tumor tissue (log2 FC = −0.930, t-test p < 0.001).
This table shows molecular features associated with VPS13D in patient tissues and cancer cell lines. In patient samples, VPS13D shows the broadest associations at the RNA and protein expression levels, with GBM recurring as the lineage with the largest associated feature set. In cancer cell lines, VPS13D RNA and mutation anchors are most strongly linked to RNA-expression features, especially in STOMACH, while CRISPR and shRNA rows add functional-dependency signals in LIVER and BLOOD_Leukemia.
