Q-omics provides the consensus-scored CLN8 profile across patient tissues and cancer cell-line models. CLN8 expression is associated with patient survival in 23 of 34 cancer types, with the highest sampling consensus in MESO. Among the 18 cancer types available for tumor–normal comparison, CLN8 is differentially expressed in 11, with the highest sampling consensus in LUAD. Additionally, CLN8 RNA expression shows 19,365 significant gene co-expression associations, with the highest sampling consensus in ACC. Together, these results highlight MESO, LUAD, and ACC as cancer lineages where CLN8 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 CLN8 — synthetic lethality, tumor antigen, and pembrolizumab response.
This table summarizes CLN8 survival associations across molecular data types. CLN8 RNA expression shows survival associations in the most cancer types (23), followed by mutation status (4) and mass-spec protein abundance (6). The rightmost column indicates the cancer type with the highest sampling consensus for each molecular layer.
This table ranks reproducible CLN8 RNA expression–survival associations across cancer types. High CLN8 expression shows unfavorable associations in MESO, LUAD, THCA and STAD, but favorable associations in HNSC and KIRC. The MESO 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 MESO as the clearest survival context for CLN8 RNA expression.
This table summarizes CLN8 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 2. The strongest signals are observed in KIRC for RNA and CCRCC for protein.
This table ranks reproducible tumor–normal expression differences for CLN8. A negative fold-change indicates higher expression in normal tissue than in tumor tissue. CLN8 shows lower tumor expression in LUAD, KIRC, BRCA, BLCA and LUSC and higher tumor expression in KICH. The LUAD box plot shows higher CLN8 RNA expression in normal versus tumor tissue (log2 FC = −0.615, t-test p < 0.001).
This table shows molecular features associated with CLN8 in patient tissues and cancer cell lines. In patient samples, CLN8 shows the broadest associations at the RNA and protein expression levels, with ACC recurring as the lineage with the largest associated feature set. In cancer cell lines, CLN8 RNA and mutation anchors are most strongly linked to RNA-expression features, especially in LUNG_NSCLC_LUAD, while CRISPR and shRNA rows add functional-dependency signals in LARGE_INTESTINE and BLOOD_Lymphoma.
