Q-omics provides the consensus-scored ELMOD2 profile across patient tissues and cancer cell-line models. ELMOD2 expression is associated with patient survival in 20 of 34 cancer types, with the highest sampling consensus in KIRC. Among the 18 cancer types available for tumor–normal comparison, ELMOD2 is differentially expressed in 11, with the highest sampling consensus in KIRC. Additionally, ELMOD2 RNA expression shows 20,625 significant gene co-expression associations, with the highest sampling consensus in ACC. Together, these results highlight KIRC, and ACC as cancer lineages where ELMOD2 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 ELMOD2 — synthetic lethality, tumor antigen, and pembrolizumab response.
This table summarizes ELMOD2 survival associations across molecular data types. ELMOD2 RNA expression shows survival associations in the most cancer types (20), followed by mutation status (6) 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 ELMOD2 RNA expression–survival associations across cancer types. High ELMOD2 expression shows unfavorable associations in LGG, LIHC and KICH, but favorable associations in KIRC, UCEC and READ. 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 ELMOD2 RNA expression.
This table summarizes ELMOD2 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 LUAD for protein.
This table ranks reproducible tumor–normal expression differences for ELMOD2. A negative fold-change indicates higher expression in normal tissue than in tumor tissue. ELMOD2 shows lower tumor expression in THCA and higher tumor expression in KIRC, HNSC, LIHC, KIRP and STAD. The KIRC box plot shows higher ELMOD2 RNA expression in tumor versus normal tissue (log2 FC = +0.888, t-test p < 0.001).
This table shows molecular features associated with ELMOD2 in patient tissues and cancer cell lines. In patient samples, ELMOD2 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, ELMOD2 RNA and mutation anchors are most strongly linked to RNA-expression features, especially in BLOOD_Lymphoma, while CRISPR and shRNA rows add functional-dependency signals in LUNG_NSCLC_LUAD and BLOOD_Leukemia.
