Q-omics provides the consensus-scored CLPB profile across patient tissues and cancer cell-line models. CLPB expression is associated with patient survival in 24 of 34 cancer types, with the highest sampling consensus in UVM. Among the 18 cancer types available for tumor–normal comparison, CLPB is differentially expressed in 16, with the highest sampling consensus in HNSC. Additionally, CLPB RNA expression shows 18,329 significant gene co-expression associations, with the highest sampling consensus in ACC. Together, these results highlight UVM, HNSC, and ACC as cancer lineages where CLPB 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 CLPB — synthetic lethality, tumor antigen, and pembrolizumab response.
This table summarizes CLPB survival associations across molecular data types. CLPB RNA expression shows survival associations in the most cancer types (24), followed by mutation status (9) and mass-spec protein abundance (5). The rightmost column indicates the cancer type with the highest sampling consensus for each molecular layer.
This table ranks reproducible CLPB RNA expression–survival associations across cancer types. High CLPB expression shows unfavorable associations in UVM, KICH, BLCA, PAAD and CESC, but favorable associations in KIRC. 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 CLPB RNA expression.
This table summarizes CLPB 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 6. The strongest signals are observed in HNSC for RNA and CCRCC for protein.
This table ranks reproducible tumor–normal expression differences for CLPB. A negative fold-change indicates higher expression in normal tissue than in tumor tissue. CLPB shows higher tumor expression in HNSC, COAD, BLCA, STAD, LUAD and LUSC. The HNSC box plot shows higher CLPB RNA expression in tumor versus normal tissue (log2 FC = +1.017, t-test p < 0.001).
This table shows molecular features associated with CLPB in patient tissues and cancer cell lines. In patient samples, CLPB shows the broadest associations at the RNA and protein expression levels, with ACC recurring as the lineage with the largest associated feature set. In cancer cell lines, CLPB 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 OVARY and BONE.
