Q-omics provides the consensus-scored CNTN1 profile across patient tissues and cancer cell-line models. CNTN1 expression is associated with patient survival in 20 of 34 cancer types, with the highest sampling consensus in BLCA. Among the 18 cancer types available for tumor–normal comparison, CNTN1 is differentially expressed in 13, with the highest sampling consensus in KIRC. Additionally, CNTN1 protein abundance shows 35,073 significant protein co-abundance associations, with the highest sampling consensus in GBM. Together, these results highlight BLCA, KIRC, and GBM as cancer lineages where CNTN1 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 CNTN1 — synthetic lethality, tumor antigen, and pembrolizumab response.
This table summarizes CNTN1 survival associations across molecular data types. CNTN1 RNA expression shows survival associations in the most cancer types (20), followed by mutation status (8) 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 CNTN1 RNA expression–survival associations across cancer types. High CNTN1 expression shows unfavorable associations in BLCA, STAD and KIRP, but favorable associations in UVM, LGG and CHOL. The BLCA 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 BLCA as the clearest survival context for CNTN1 RNA expression.
This table summarizes CNTN1 tumor–normal expression differences by data type. RNA shows broader differences across cancer types, with a lineage consensus of 13, while mass-spec protein shows differences in 7. The strongest signals are observed in KIRC for RNA and CCRCC for protein.
This table ranks reproducible tumor–normal expression differences for CNTN1. A negative fold-change indicates higher expression in normal tissue than in tumor tissue. CNTN1 shows lower tumor expression in KIRC, KICH, KIRP, COAD and THCA and higher tumor expression in HNSC. The KIRC box plot shows higher CNTN1 RNA expression in normal versus tumor tissue (log2 FC = −3.235, t-test p < 0.001).
This table shows molecular features associated with CNTN1 in patient tissues and cancer cell lines. In patient samples, CNTN1 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, CNTN1 RNA and mutation anchors are most strongly linked to RNA-expression features, especially in BREAST, while CRISPR and shRNA rows add functional-dependency signals in URINARY_TRACT and LARGE_INTESTINE.
