Q-omics provides the consensus-scored ESD profile across patient tissues and cancer cell-line models. ESD expression is associated with patient survival in 23 of 34 cancer types, with the highest sampling consensus in HNSC. Among the 18 cancer types available for tumor–normal comparison, ESD is differentially expressed in 13, with the highest sampling consensus in THCA. Additionally, ESD protein abundance shows 27,354 significant protein co-abundance associations, with the highest sampling consensus in LUAD. Together, these results highlight HNSC, THCA, and LUAD as cancer lineages where ESD 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 ESD — synthetic lethality, tumor antigen, and pembrolizumab response.
This table summarizes ESD survival associations across molecular data types. ESD RNA expression shows survival associations in the most cancer types (23), followed by mutation status (3) and mass-spec protein abundance (7). The rightmost column indicates the cancer type with the highest sampling consensus for each molecular layer.
This table ranks reproducible ESD RNA expression–survival associations across cancer types. High ESD expression shows unfavorable associations in HNSC, BLCA, CESC and ACC, but favorable associations in KIRC and KIRP. The HNSC 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 HNSC as the clearest survival context for ESD RNA expression.
This table summarizes ESD 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 THCA for RNA and COAD for protein.
This table ranks reproducible tumor–normal expression differences for ESD. A negative fold-change indicates higher expression in normal tissue than in tumor tissue. ESD shows lower tumor expression in THCA, UCEC, BLCA and LUAD and higher tumor expression in KIRC and HNSC. The THCA box plot shows higher ESD RNA expression in normal versus tumor tissue (log2 FC = −0.913, t-test p < 0.001).
This table shows molecular features associated with ESD in patient tissues and cancer cell lines. In patient samples, ESD 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, ESD RNA and mutation anchors are most strongly linked to RNA-expression features, especially in LUNG_SCLC, while CRISPR and shRNA rows add functional-dependency signals in UPPER_AERODIGESTIVE_TRACT and CNS.
