Q-omics provides the consensus-scored CNTNAP2 profile across patient tissues and cancer cell-line models. CNTNAP2 expression is associated with patient survival in 23 of 34 cancer types, with the highest sampling consensus in KIRP. Among the 18 cancer types available for tumor–normal comparison, CNTNAP2 is differentially expressed in 14, with the highest sampling consensus in HNSC. Additionally, CNTNAP2 RNA expression shows 16,691 significant protein co-abundance associations, with the highest sampling consensus in GBM. Together, these results highlight KIRP, HNSC, and GBM as cancer lineages where CNTNAP2 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 CNTNAP2 — synthetic lethality, tumor antigen, and pembrolizumab response.
This table summarizes CNTNAP2 survival associations across molecular data types. CNTNAP2 RNA expression shows survival associations in the most cancer types (23), followed by mutation status (10) and mass-spec protein abundance (1). The rightmost column indicates the cancer type with the highest sampling consensus for each molecular layer.
This table ranks reproducible CNTNAP2 RNA expression–survival associations across cancer types. High CNTNAP2 expression shows unfavorable associations in KIRP, UCEC, BLCA and LUAD, but favorable associations in LGG and KIRC. 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 CNTNAP2 RNA expression.
This table summarizes CNTNAP2 tumor–normal expression differences by data type. RNA shows broader differences across cancer types, with a lineage consensus of 14. The strongest signals are observed in KIRC for RNA.
This table ranks reproducible tumor–normal expression differences for CNTNAP2. A negative fold-change indicates higher expression in normal tissue than in tumor tissue. CNTNAP2 shows lower tumor expression in KIRC and higher tumor expression in HNSC, BRCA, LUSC, KICH and LUAD. The HNSC box plot shows higher CNTNAP2 RNA expression in tumor versus normal tissue (log2 FC = +2.780, t-test p < 0.001).
This table shows molecular features associated with CNTNAP2 in patient tissues and cancer cell lines. In patient samples, CNTNAP2 shows the broadest associations at the RNA and protein expression levels, with GBM recurring as the lineage with the largest associated feature set. In cancer cell lines, CNTNAP2 RNA and mutation anchors are most strongly linked to RNA-expression features, especially in OVARY, while CRISPR and shRNA rows add functional-dependency signals in LARGE_INTESTINE and LUNG_SCLC.
