Q-omics provides the consensus-scored CNTN3 profile across patient tissues and cancer cell-line models. CNTN3 expression is associated with patient survival in 22 of 34 cancer types, with the highest sampling consensus in ACC. Among the 18 cancer types available for tumor–normal comparison, CNTN3 is differentially expressed in 11, with the highest sampling consensus in COAD. Additionally, CNTN3 RNA expression shows 18,101 significant protein co-abundance associations, with the highest sampling consensus in GBM. Together, these results highlight ACC, COAD, and GBM as cancer lineages where CNTN3 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 CNTN3 — synthetic lethality, tumor antigen, and pembrolizumab response.
This table summarizes CNTN3 survival associations across molecular data types. CNTN3 RNA expression shows survival associations in the most cancer types (22), followed by mutation status (6) and mass-spec protein abundance (3). The rightmost column indicates the cancer type with the highest sampling consensus for each molecular layer.
This table ranks reproducible CNTN3 RNA expression–survival associations across cancer types. High CNTN3 expression shows unfavorable associations in STAD, but favorable associations in ACC, UVM, HNSC, SCLC and LGG. The ACC 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 ACC as the clearest survival context for CNTN3 RNA expression.
This table summarizes CNTN3 tumor–normal expression differences by data type. RNA shows broader differences across cancer types, with a lineage consensus of 11. The strongest signals are observed in COAD for RNA.
This table ranks reproducible tumor–normal expression differences for CNTN3. A negative fold-change indicates higher expression in normal tissue than in tumor tissue. CNTN3 shows lower tumor expression in COAD, KIRC, THCA, BLCA, READ and LIHC. The COAD box plot shows higher CNTN3 RNA expression in normal versus tumor tissue (log2 FC = −2.322, t-test p < 0.001).
This table shows molecular features associated with CNTN3 in patient tissues and cancer cell lines. In patient samples, CNTN3 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, CNTN3 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 UPPER_AERODIGESTIVE_TRACT and LARGE_INTESTINE.
