Q-omics provides the consensus-scored CNTNAP4 profile across patient tissues and cancer cell-line models. CNTNAP4 expression is associated with patient survival in 21 of 34 cancer types, with the highest sampling consensus in KIRP. Among the 18 cancer types available for tumor–normal comparison, CNTNAP4 is differentially expressed in 13, with the highest sampling consensus in HNSC. Additionally, CNTNAP4 RNA expression shows 10,970 significant gene co-expression associations, with the highest sampling consensus in TGCT. Together, these results highlight KIRP, HNSC, and TGCT as cancer lineages where CNTNAP4 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 CNTNAP4 — synthetic lethality, tumor antigen, and pembrolizumab response.
This table summarizes CNTNAP4 survival associations across molecular data types. CNTNAP4 RNA expression shows survival associations in the most cancer types (21), followed by mutation status (8). The rightmost column indicates the cancer type with the highest sampling consensus for each molecular layer.
This table ranks reproducible CNTNAP4 RNA expression–survival associations across cancer types. High CNTNAP4 expression shows unfavorable associations in KIRP, LUSC and OV, but favorable associations in PAAD, LUAD and DLBC. The KIRP 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 KIRP as the clearest survival context for CNTNAP4 RNA expression.
This table summarizes CNTNAP4 tumor–normal expression differences by data type. RNA shows broader differences across cancer types, with a lineage consensus of 13. The strongest signals are observed in HNSC for RNA.
This table ranks reproducible tumor–normal expression differences for CNTNAP4. A negative fold-change indicates higher expression in normal tissue than in tumor tissue. CNTNAP4 shows lower tumor expression in KICH, KIRC, COAD and BRCA and higher tumor expression in HNSC and LIHC. The HNSC box plot shows higher CNTNAP4 RNA expression in tumor versus normal tissue (log2 FC = +0.097, t-test p = .001).
This table shows molecular features associated with CNTNAP4 in patient tissues and cancer cell lines. In patient samples, CNTNAP4 shows the broadest associations at the RNA and protein expression levels, with TGCT recurring as the lineage with the largest associated feature set. In cancer cell lines, CNTNAP4 RNA and mutation anchors are most strongly linked to RNA-expression features, especially in PANCREAS, while CRISPR and shRNA rows add functional-dependency signals in LARGE_INTESTINE and BLOOD_Leukemia.
