Q-omics provides the consensus-scored CTSV profile across patient tissues and cancer cell-line models. CTSV expression is associated with patient survival in 30 of 34 cancer types, with the highest sampling consensus in ACC. Among the 18 cancer types available for tumor–normal comparison, CTSV is differentially expressed in 13, with the highest sampling consensus in HNSC. Additionally, CTSV RNA expression shows 17,943 significant protein co-abundance associations, with the highest sampling consensus in LSCC. Together, these results highlight ACC, HNSC, and LSCC as cancer lineages where CTSV 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 CTSV — synthetic lethality, tumor antigen, and pembrolizumab response.
This table summarizes CTSV survival associations across molecular data types. CTSV RNA expression shows survival associations in the most cancer types (30), followed by mutation status (2) 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 CTSV RNA expression–survival associations across cancer types. High CTSV expression shows unfavorable associations in ACC, BLCA, PAAD, LIHC and LUAD, but favorable associations in UCEC. The ACC Kaplan–Meier curve shows clear separation, with the high-expression group declining faster, consistent with the unfavorable association (log-rank p < 0.001). Together, the overview and detailed table identify ACC as the clearest survival context for CTSV RNA expression.
This table summarizes CTSV 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 HNSC for RNA and HNSC for protein.
This table ranks reproducible tumor–normal expression differences for CTSV. A negative fold-change indicates higher expression in normal tissue than in tumor tissue. CTSV shows lower tumor expression in KIRC, KICH and KIRP and higher tumor expression in HNSC, LUAD and LUSC. The HNSC box plot shows higher CTSV RNA expression in tumor versus normal tissue (log2 FC = +3.448, t-test p < 0.001).
This table shows molecular features associated with CTSV in patient tissues and cancer cell lines. In patient samples, CTSV 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, CTSV RNA and mutation anchors are most strongly linked to RNA-expression features, especially in LIVER, while CRISPR and shRNA rows add functional-dependency signals in SOFT_TISSUE and BLOOD_Lymphoma.
