Q-omics provides the consensus-scored CTSS profile across patient tissues and cancer cell-line models. CTSS expression is associated with patient survival in 26 of 34 cancer types, with the highest sampling consensus in BLCA. Among the 18 cancer types available for tumor–normal comparison, CTSS is differentially expressed in 10, with the highest sampling consensus in KIRC. Additionally, CTSS protein abundance shows 22,111 significant protein co-abundance associations, with the highest sampling consensus in LSCC. Together, these results highlight BLCA, KIRC, and LSCC as cancer lineages where CTSS 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 CTSS — synthetic lethality, tumor antigen, and pembrolizumab response.
This table summarizes CTSS survival associations across molecular data types. CTSS RNA expression shows survival associations in the most cancer types (26), followed by mutation status (3) 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 CTSS RNA expression–survival associations across cancer types. High CTSS expression shows unfavorable associations in LGG and UVM, but favorable associations in BLCA, HNSC, SKCM and KIRC. The BLCA Kaplan–Meier curve shows clear separation, with the low-expression group declining faster, consistent with the favorable association (log-rank p = .002). Together, the overview and detailed table identify BLCA as the clearest survival context for CTSS RNA expression.
This table summarizes CTSS tumor–normal expression differences by data type. RNA shows broader differences across cancer types, with a lineage consensus of 10, 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 CTSS. A negative fold-change indicates higher expression in normal tissue than in tumor tissue. CTSS shows lower tumor expression in COAD, LUAD and LUSC and higher tumor expression in KIRC, THCA and STAD. The KIRC box plot shows higher CTSS RNA expression in tumor versus normal tissue (log2 FC = +2.394, t-test p < 0.001).
This table shows molecular features associated with CTSS in patient tissues and cancer cell lines. In patient samples, CTSS 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, CTSS RNA and mutation anchors are most strongly linked to RNA-expression features, especially in BREAST, while CRISPR and shRNA rows add functional-dependency signals in LARGE_INTESTINE and BLOOD_Leukemia.
