Q-omics provides the consensus-scored CLPX profile across patient tissues and cancer cell-line models. CLPX expression is associated with patient survival in 20 of 34 cancer types, with the highest sampling consensus in KIRC. Among the 18 cancer types available for tumor–normal comparison, CLPX is differentially expressed in 9, with the highest sampling consensus in BLCA. Additionally, CLPX protein abundance shows 29,926 significant protein co-abundance associations, with the highest sampling consensus in LSCC. Together, these results highlight KIRC, BLCA, and LSCC as cancer lineages where CLPX 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 CLPX — synthetic lethality, tumor antigen, and pembrolizumab response.
This table summarizes CLPX survival associations across molecular data types. CLPX RNA expression shows survival associations in the most cancer types (20), followed by mutation status (2) and mass-spec protein abundance (2). The rightmost column indicates the cancer type with the highest sampling consensus for each molecular layer.
This table ranks reproducible CLPX RNA expression–survival associations across cancer types. High CLPX expression shows unfavorable associations in PAAD, UVM and ACC, but favorable associations in KIRC, BRCA and GBM. The KIRC Kaplan–Meier curve shows clear separation, with the low-expression group declining faster, consistent with the favorable association (log-rank p < 0.001). Together, the overview and detailed table identify KIRC as the clearest survival context for CLPX RNA expression.
This table summarizes CLPX tumor–normal expression differences by data type. RNA shows broader differences across cancer types, with a lineage consensus of 9, while mass-spec protein shows differences in 7. The strongest signals are observed in BLCA for RNA and CCRCC for protein.
This table ranks reproducible tumor–normal expression differences for CLPX. A negative fold-change indicates higher expression in normal tissue than in tumor tissue. CLPX shows lower tumor expression in KIRC and KICH and higher tumor expression in BLCA, LUSC, LUAD and COAD. The BLCA box plot shows higher CLPX RNA expression in tumor versus normal tissue (log2 FC = +0.487, t-test p < 0.001).
This table shows molecular features associated with CLPX in patient tissues and cancer cell lines. In patient samples, CLPX 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, CLPX RNA and mutation anchors are most strongly linked to RNA-expression features, especially in CNS, while CRISPR and shRNA rows add functional-dependency signals in OVARY and BLOOD_Leukemia.
