Q-omics provides the consensus-scored VPS35 profile across patient tissues and cancer cell-line models. VPS35 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, VPS35 is differentially expressed in 15, with the highest sampling consensus in KIRP. Additionally, VPS35 protein abundance shows 21,565 significant protein co-abundance associations, with the highest sampling consensus in GBM. Together, these results highlight KIRC, KIRP, and GBM as cancer lineages where VPS35 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 VPS35 — synthetic lethality, tumor antigen, and pembrolizumab response.
This table summarizes VPS35 survival associations across molecular data types. VPS35 RNA expression shows survival associations in the most cancer types (21), followed by mutation status (5) and mass-spec protein abundance (6). The rightmost column indicates the cancer type with the highest sampling consensus for each molecular layer.
This table ranks reproducible VPS35 RNA expression–survival associations across cancer types. High VPS35 expression shows unfavorable associations in MESO, STAD, LIHC and HNSC, but favorable associations in KIRC and COAD. 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 VPS35 RNA expression.
This table summarizes VPS35 tumor–normal expression differences by data type. RNA shows broader differences across cancer types, with a lineage consensus of 15, while mass-spec protein shows differences in 5. The strongest signals are observed in KIRP for RNA and CCRCC for protein.
This table ranks reproducible tumor–normal expression differences for VPS35. A negative fold-change indicates higher expression in normal tissue than in tumor tissue. VPS35 shows higher tumor expression in KIRP, HNSC, LIHC, LUAD, BRCA and CHOL. The KIRP box plot shows higher VPS35 RNA expression in tumor versus normal tissue (log2 FC = +1.174, t-test p < 0.001).
This table shows molecular features associated with VPS35 in patient tissues and cancer cell lines. In patient samples, VPS35 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, VPS35 RNA and mutation anchors are most strongly linked to RNA-expression features, especially in CNS, while CRISPR and shRNA rows add functional-dependency signals in SOFT_TISSUE and BLOOD_Leukemia.
