Q-omics provides the consensus-scored CST5 profile across patient tissues and cancer cell-line models. CST5 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, CST5 is differentially expressed in 13, with the highest sampling consensus in THCA. Additionally, CST5 RNA expression shows 10,542 significant protein co-abundance associations, with the highest sampling consensus in LUAD. Together, these results highlight UVM, THCA, and LUAD as cancer lineages where CST5 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 CST5 — synthetic lethality, tumor antigen, and pembrolizumab response.
This table summarizes CST5 survival associations across molecular data types. CST5 RNA expression shows survival associations in the most cancer types (22), followed by mutation status (2). The rightmost column indicates the cancer type with the highest sampling consensus for each molecular layer.
This table ranks reproducible CST5 RNA expression–survival associations across cancer types. High CST5 expression shows unfavorable associations in UVM, DLBC, KIRP and ACC, but favorable associations in MESO and CHOL. The UVM Kaplan–Meier curve shows clear separation, with the high-expression group declining faster, consistent with the unfavorable association (log-rank p = .002). Together, the overview and detailed table identify UVM as the clearest survival context for CST5 RNA expression.
This table summarizes CST5 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 1. The strongest signals are observed in THCA for RNA and HNSC for protein.
This table ranks reproducible tumor–normal expression differences for CST5. A negative fold-change indicates higher expression in normal tissue than in tumor tissue. CST5 shows lower tumor expression in LUSC, LUAD and KICH and higher tumor expression in THCA, COAD and BRCA. The THCA box plot shows higher CST5 RNA expression in tumor versus normal tissue (log2 FC = +2.288, t-test p < 0.001).
This table shows molecular features associated with CST5 in patient tissues and cancer cell lines. In patient samples, CST5 shows the broadest associations at the RNA and protein expression levels, with LUAD recurring as the lineage with the largest associated feature set. In cancer cell lines, CST5 RNA and mutation anchors are most strongly linked to RNA-expression features, especially in BLOOD_Lymphoma, while CRISPR and shRNA rows add functional-dependency signals in BREAST and LUNG_NSCLC_LUSC.
