vesicle transport through interaction with t-SNAREs 1AGenealiases: MMDS3 · MVti1 · VTI1RP2 · Vti1-rp2
Q-omics provides the consensus-scored VTI1A profile across patient tissues and cancer cell-line models. VTI1A expression is associated with patient survival in 26 of 34 cancer types, with the highest sampling consensus in KIRC. Among the 18 cancer types available for tumor–normal comparison, VTI1A is differentially expressed in 13, with the highest sampling consensus in KIRC. Additionally, VTI1A RNA expression shows 20,408 significant gene co-expression associations, with the highest sampling consensus in ACC. Together, these results highlight KIRC, and ACC as cancer lineages where VTI1A 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 VTI1A — synthetic lethality, tumor antigen, and pembrolizumab response.
This table summarizes VTI1A survival associations across molecular data types. VTI1A RNA expression shows survival associations in the most cancer types (26), followed by mutation status (4) and mass-spec protein abundance (4). The rightmost column indicates the cancer type with the highest sampling consensus for each molecular layer.
This table ranks reproducible VTI1A RNA expression–survival associations across cancer types. High VTI1A expression shows unfavorable associations in ACC, BLCA and LIHC, but favorable associations in KIRC, SCLC and BRCA. 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 VTI1A RNA expression.
This table summarizes VTI1A tumor–normal expression differences by data type. RNA shows broader differences across cancer types, with a lineage consensus of 13, while mass-spec protein shows differences in 5. The strongest signals are observed in KIRC for RNA and HNSC for protein.
This table ranks reproducible tumor–normal expression differences for VTI1A. A negative fold-change indicates higher expression in normal tissue than in tumor tissue. VTI1A shows lower tumor expression in KIRC and THCA and higher tumor expression in LIHC, STAD, LUAD and HNSC. The KIRC box plot shows higher VTI1A RNA expression in normal versus tumor tissue (log2 FC = −0.665, t-test p < 0.001).
This table shows molecular features associated with VTI1A in patient tissues and cancer cell lines. In patient samples, VTI1A shows the broadest associations at the RNA and protein expression levels, with ACC recurring as the lineage with the largest associated feature set. In cancer cell lines, VTI1A RNA and mutation anchors are most strongly linked to RNA-expression features, especially in KIDNEY, while CRISPR and shRNA rows add functional-dependency signals in URINARY_TRACT and BLOOD_Leukemia.
