Q-omics provides the consensus-scored CLU profile across patient tissues and cancer cell-line models. CLU expression is associated with patient survival in 24 of 34 cancer types, with the highest sampling consensus in THCA. Among the 18 cancer types available for tumor–normal comparison, CLU is differentially expressed in 16, with the highest sampling consensus in HNSC. Additionally, CLU protein abundance shows 29,217 significant protein co-abundance associations, with the highest sampling consensus in PDAC. Together, these results highlight THCA, HNSC, and PDAC as cancer lineages where CLU 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 CLU — synthetic lethality, tumor antigen, and pembrolizumab response.
This table summarizes CLU survival associations across molecular data types. CLU RNA expression shows survival associations in the most cancer types (24), followed by mutation status (5) and mass-spec protein abundance (10). The rightmost column indicates the cancer type with the highest sampling consensus for each molecular layer.
This table ranks reproducible CLU RNA expression–survival associations across cancer types. High CLU expression shows unfavorable associations in LGG and OV, but favorable associations in THCA, SKCM, SARC and KICH. The THCA Kaplan–Meier curve shows clear separation, with the low-expression group declining faster, consistent with the favorable association (log-rank p = .001). Together, the overview and detailed table identify THCA as the clearest survival context for CLU RNA expression.
This table summarizes CLU tumor–normal expression differences by data type. RNA shows broader differences across cancer types, with a lineage consensus of 16, while mass-spec protein shows differences in 11. The strongest signals are observed in HNSC for RNA and HNSC for protein.
This table ranks reproducible tumor–normal expression differences for CLU. A negative fold-change indicates higher expression in normal tissue than in tumor tissue. CLU shows lower tumor expression in HNSC, COAD, KICH and LUAD and higher tumor expression in KIRP and THCA. The HNSC box plot shows higher CLU RNA expression in normal versus tumor tissue (log2 FC = −2.947, t-test p < 0.001).
This table shows molecular features associated with CLU in patient tissues and cancer cell lines. In patient samples, CLU 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, CLU 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 BLOOD_Lymphoma and OVARY.
