Q-omics provides the consensus-scored CTSC profile across patient tissues and cancer cell-line models. CTSC expression is associated with patient survival in 22 of 34 cancer types, with the highest sampling consensus in UVM. Among the 18 cancer types available for tumor–normal comparison, CTSC is differentially expressed in 10, with the highest sampling consensus in HNSC. Additionally, CTSC protein abundance shows 29,113 significant protein co-abundance associations, with the highest sampling consensus in PDAC. Together, these results highlight UVM, HNSC, and PDAC as cancer lineages where CTSC 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 CTSC — synthetic lethality, tumor antigen, and pembrolizumab response.
This table summarizes CTSC survival associations across molecular data types. CTSC RNA expression shows survival associations in the most cancer types (22), followed by mutation status (6) 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 CTSC RNA expression–survival associations across cancer types. High CTSC expression shows unfavorable associations in UVM, KICH, LIHC and LGG, but favorable associations in KIRC and SKCM. The UVM 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 UVM as the clearest survival context for CTSC RNA expression.
This table summarizes CTSC 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 9. The strongest signals are observed in HNSC for RNA and CCRCC for protein.
This table ranks reproducible tumor–normal expression differences for CTSC. A negative fold-change indicates higher expression in normal tissue than in tumor tissue. CTSC shows lower tumor expression in KICH and higher tumor expression in HNSC, THCA, BLCA, KIRP and STAD. The HNSC box plot shows higher CTSC RNA expression in tumor versus normal tissue (log2 FC = +1.958, t-test p < 0.001).
This table shows molecular features associated with CTSC in patient tissues and cancer cell lines. In patient samples, CTSC shows the broadest associations at the RNA and protein expression levels, with PDAC recurring as the lineage with the largest associated feature set. In cancer cell lines, CTSC RNA and mutation anchors are most strongly linked to RNA-expression features, especially in SOFT_TISSUE, while CRISPR and shRNA rows add functional-dependency signals in UPPER_AERODIGESTIVE_TRACT and BREAST.
