Q-omics provides the consensus-scored CNTN6 profile across patient tissues and cancer cell-line models. CNTN6 expression is associated with patient survival in 20 of 34 cancer types, with the highest sampling consensus in KIRP. Among the 18 cancer types available for tumor–normal comparison, CNTN6 is differentially expressed in 11, with the highest sampling consensus in KIRP. Additionally, CNTN6 RNA expression shows 14,652 significant protein co-abundance associations, with the highest sampling consensus in LSCC. Together, these results highlight KIRP, and LSCC as cancer lineages where CNTN6 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 CNTN6 — synthetic lethality, tumor antigen, and pembrolizumab response.
This table summarizes CNTN6 survival associations across molecular data types. CNTN6 RNA expression shows survival associations in the most cancer types (20), followed by mutation status (9) and mass-spec protein abundance (4). The rightmost column indicates the cancer type with the highest sampling consensus for each molecular layer.
This table ranks reproducible CNTN6 RNA expression–survival associations across cancer types. High CNTN6 expression shows unfavorable associations in LUSC, LIHC and TGCT, but favorable associations in KIRP, LGG and CHOL. The KIRP 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 KIRP as the clearest survival context for CNTN6 RNA expression.
This table summarizes CNTN6 tumor–normal expression differences by data type. RNA shows broader differences across cancer types, with a lineage consensus of 11, while mass-spec protein shows differences in 5. The strongest signals are observed in LUAD for RNA and CCRCC for protein.
This table ranks reproducible tumor–normal expression differences for CNTN6. A negative fold-change indicates higher expression in normal tissue than in tumor tissue. CNTN6 shows lower tumor expression in LUAD, LUSC, BRCA, COAD and THCA and higher tumor expression in KIRP. The KIRP box plot shows higher CNTN6 RNA expression in tumor versus normal tissue (log2 FC = +3.179, t-test p < 0.001).
This table shows molecular features associated with CNTN6 in patient tissues and cancer cell lines. In patient samples, CNTN6 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, CNTN6 RNA and mutation anchors are most strongly linked to RNA-expression features, especially in LUNG_SCLC, while CRISPR and shRNA rows add functional-dependency signals in LARGE_INTESTINE and SOFT_TISSUE.
