Q-omics provides the consensus-scored CTSL profile across patient tissues and cancer cell-line models. CTSL expression is associated with patient survival in 24 of 34 cancer types, with the highest sampling consensus in HNSC. Among the 18 cancer types available for tumor–normal comparison, CTSL is differentially expressed in 10, with the highest sampling consensus in HNSC. Additionally, CTSL protein abundance shows 28,763 significant protein co-abundance associations, with the highest sampling consensus in LSCC. Together, these results highlight HNSC, and LSCC as cancer lineages where CTSL 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 CTSL — synthetic lethality, tumor antigen, and pembrolizumab response.
This table summarizes CTSL survival associations across molecular data types. CTSL RNA expression shows survival associations in the most cancer types (24), followed by mutation status (7) and mass-spec protein abundance (7). The rightmost column indicates the cancer type with the highest sampling consensus for each molecular layer.
This table ranks reproducible CTSL RNA expression–survival associations across cancer types. High CTSL expression shows unfavorable associations in HNSC, LUAD, LUSC, GBM and LGG, but favorable associations in KIRC. The HNSC 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 HNSC as the clearest survival context for CTSL RNA expression.
This table summarizes CTSL 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 HNSC for RNA and CCRCC for protein.
This table ranks reproducible tumor–normal expression differences for CTSL. A negative fold-change indicates higher expression in normal tissue than in tumor tissue. CTSL shows lower tumor expression in THCA, KICH and UCEC and higher tumor expression in HNSC, KIRC and KIRP. The HNSC box plot shows higher CTSL RNA expression in tumor versus normal tissue (log2 FC = +2.366, t-test p < 0.001).
This table shows molecular features associated with CTSL in patient tissues and cancer cell lines. In patient samples, CTSL 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, CTSL RNA and mutation anchors are most strongly linked to RNA-expression features, especially in BONE, while CRISPR and shRNA rows add functional-dependency signals in OVARY and CNS.
