Q-omics provides the consensus-scored ENDOG profile across patient tissues and cancer cell-line models. ENDOG expression is associated with patient survival in 24 of 34 cancer types, with the highest sampling consensus in KIRP. Among the 18 cancer types available for tumor–normal comparison, ENDOG is differentially expressed in 11, with the highest sampling consensus in KIRC. Additionally, ENDOG RNA expression shows 17,372 significant gene co-expression associations, with the highest sampling consensus in ACC. Together, these results highlight KIRP, KIRC, and ACC as cancer lineages where ENDOG 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 ENDOG — synthetic lethality, tumor antigen, and pembrolizumab response.
This table summarizes ENDOG survival associations across molecular data types. ENDOG RNA expression shows survival associations in the most cancer types (24), followed by mass-spec protein abundance (5). The rightmost column indicates the cancer type with the highest sampling consensus for each molecular layer.
This table ranks reproducible ENDOG RNA expression–survival associations across cancer types. High ENDOG expression shows unfavorable associations in UVM, UCS, ACC and BLCA, but favorable associations in KIRP and UCEC. 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 ENDOG RNA expression.
This table summarizes ENDOG 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 7. The strongest signals are observed in KIRC for RNA and CCRCC for protein.
This table ranks reproducible tumor–normal expression differences for ENDOG. A negative fold-change indicates higher expression in normal tissue than in tumor tissue. ENDOG shows lower tumor expression in KIRC and higher tumor expression in LUSC, STAD, BRCA, LUAD and UCEC. The KIRC box plot shows higher ENDOG RNA expression in normal versus tumor tissue (log2 FC = −0.869, t-test p < 0.001).
This table shows molecular features associated with ENDOG in patient tissues and cancer cell lines. In patient samples, ENDOG 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, ENDOG RNA and mutation anchors are most strongly linked to RNA-expression features, especially in SKIN, while CRISPR and shRNA rows add functional-dependency signals in PANCREAS and SOFT_TISSUE.
