Q-omics provides the consensus-scored OCLN profile across patient tissues and cancer cell-line models. OCLN expression is associated with patient survival in 18 of 34 cancer types, with the highest sampling consensus in KIRC. Among the 18 cancer types available for tumor–normal comparison, OCLN is differentially expressed in 13, with the highest sampling consensus in KIRC. Additionally, OCLN protein abundance shows 19,433 significant protein co-abundance associations, with the highest sampling consensus in LUAD. Together, these results highlight KIRC, and LUAD as cancer lineages where OCLN 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 OCLN — synthetic lethality, tumor antigen, and pembrolizumab response.
This table summarizes OCLN survival associations across molecular data types. OCLN RNA expression shows survival associations in the most cancer types (18), followed by mutation status (2) 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 OCLN RNA expression–survival associations across cancer types. High OCLN expression shows unfavorable associations in ESCA, but favorable associations in KIRC, COAD, LUAD, HNSC and BRCA. The KIRC 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 KIRC as the clearest survival context for OCLN RNA expression.
This table summarizes OCLN 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 6. The strongest signals are observed in KIRC for RNA and CCRCC for protein.
This table ranks reproducible tumor–normal expression differences for OCLN. A negative fold-change indicates higher expression in normal tissue than in tumor tissue. OCLN shows lower tumor expression in KIRC, HNSC, LUSC and KICH and higher tumor expression in STAD and BRCA. The KIRC box plot shows higher OCLN RNA expression in normal versus tumor tissue (log2 FC = −1.928, t-test p < 0.001).
This table shows molecular features associated with OCLN in patient tissues and cancer cell lines. In patient samples, OCLN shows the broadest associations at the RNA and protein expression levels, with LUAD recurring as the lineage with the largest associated feature set. In cancer cell lines, OCLN 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 STOMACH and BREAST.
