Q-omics provides the consensus-scored ORM2 profile across patient tissues and cancer cell-line models. ORM2 expression is associated with patient survival in 23 of 34 cancer types, with the highest sampling consensus in KIRC. Among the 18 cancer types available for tumor–normal comparison, ORM2 is differentially expressed in 9, with the highest sampling consensus in COAD. Additionally, ORM2 protein abundance shows 20,408 significant protein co-abundance associations, with the highest sampling consensus in GBM. Together, these results highlight KIRC, COAD, and GBM as cancer lineages where ORM2 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 ORM2 — synthetic lethality, tumor antigen, and pembrolizumab response.
This table summarizes ORM2 survival associations across molecular data types. ORM2 RNA expression shows survival associations in the most cancer types (23), followed by mutation status (2) and mass-spec protein abundance (8). The rightmost column indicates the cancer type with the highest sampling consensus for each molecular layer.
This table ranks reproducible ORM2 RNA expression–survival associations across cancer types. High ORM2 expression shows unfavorable associations in KIRC, UVM, BRCA, CHOL and PAAD, but favorable associations in UCEC. The KIRC 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 KIRC as the clearest survival context for ORM2 RNA expression.
This table summarizes ORM2 tumor–normal expression differences by data type. RNA shows broader differences across cancer types, with a lineage consensus of 9, while mass-spec protein shows differences in 6. The strongest signals are observed in COAD for RNA and HNSC for protein.
This table ranks reproducible tumor–normal expression differences for ORM2. A negative fold-change indicates higher expression in normal tissue than in tumor tissue. ORM2 shows lower tumor expression in LIHC, LUSC and CHOL and higher tumor expression in COAD, UCEC and BRCA. The COAD box plot shows higher ORM2 RNA expression in tumor versus normal tissue (log2 FC = +0.755, t-test p < 0.001).
This table shows molecular features associated with ORM2 in patient tissues and cancer cell lines. In patient samples, ORM2 shows the broadest associations at the RNA and protein expression levels, with GBM recurring as the lineage with the largest associated feature set. In cancer cell lines, ORM2 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 LIVER and BREAST.
