Q-omics provides the consensus-scored CNBP profile across patient tissues and cancer cell-line models. CNBP expression is associated with patient survival in 25 of 34 cancer types, with the highest sampling consensus in KIRC. Among the 18 cancer types available for tumor–normal comparison, CNBP is differentially expressed in 12, with the highest sampling consensus in HNSC. Additionally, CNBP protein abundance shows 21,834 significant protein co-abundance associations, with the highest sampling consensus in LSCC. Together, these results highlight KIRC, HNSC, and LSCC as cancer lineages where CNBP 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 CNBP — synthetic lethality, tumor antigen, and pembrolizumab response.
This table summarizes CNBP survival associations across molecular data types. CNBP RNA expression shows survival associations in the most cancer types (25), followed by mutation status (2) and mass-spec protein abundance (8). The rightmost column indicates the cancer type with the highest sampling consensus for each molecular layer.
This table ranks reproducible CNBP RNA expression–survival associations across cancer types. High CNBP expression shows unfavorable associations in KIRP, KICH, ACC and PAAD, but favorable associations in KIRC and UCS. 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 CNBP RNA expression.
This table summarizes CNBP tumor–normal expression differences by data type. RNA shows broader differences across cancer types, with a lineage consensus of 12, while mass-spec protein shows differences in 5. The strongest signals are observed in HNSC for RNA and HNSC for protein.
This table ranks reproducible tumor–normal expression differences for CNBP. A negative fold-change indicates higher expression in normal tissue than in tumor tissue. CNBP shows lower tumor expression in THCA, UCEC and KICH and higher tumor expression in HNSC, COAD and LUSC. The HNSC box plot shows higher CNBP RNA expression in tumor versus normal tissue (log2 FC = +0.869, t-test p < 0.001).
This table shows molecular features associated with CNBP in patient tissues and cancer cell lines. In patient samples, CNBP 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, CNBP RNA and mutation anchors are most strongly linked to RNA-expression features, especially in BLOOD_Leukemia, while CRISPR and shRNA rows add functional-dependency signals in SKIN and UPPER_AERODIGESTIVE_TRACT.
