Q-omics provides the consensus-scored RRAS2 profile across patient tissues and cancer cell-line models. RRAS2 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, RRAS2 is differentially expressed in 12, with the highest sampling consensus in HNSC. Additionally, RRAS2 protein abundance shows 23,749 significant protein co-abundance associations, with the highest sampling consensus in GBM. Together, these results highlight HNSC, and GBM as cancer lineages where RRAS2 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 RRAS2 — synthetic lethality, tumor antigen, and pembrolizumab response.
This table summarizes RRAS2 survival associations across molecular data types. RRAS2 RNA expression shows survival associations in the most cancer types (23), followed by mutation status (2) and mass-spec protein abundance (10). The rightmost column indicates the cancer type with the highest sampling consensus for each molecular layer.
This table ranks reproducible RRAS2 RNA expression–survival associations across cancer types. High RRAS2 expression shows unfavorable associations in HNSC, ACC, PAAD, LIHC, KIRP and SARC. 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 RRAS2 RNA expression.
This table summarizes RRAS2 tumor–normal expression differences by data type. RNA shows broader differences across cancer types, with a lineage consensus of 12, while mass-spec protein shows differences in 10. The strongest signals are observed in HNSC for RNA and CCRCC for protein.
This table ranks reproducible tumor–normal expression differences for RRAS2. A negative fold-change indicates higher expression in normal tissue than in tumor tissue. RRAS2 shows lower tumor expression in THCA, KICH, BRCA and COAD and higher tumor expression in HNSC and KIRP. The HNSC box plot shows higher RRAS2 RNA expression in tumor versus normal tissue (log2 FC = +1.440, t-test p < 0.001).
This table shows molecular features associated with RRAS2 in patient tissues and cancer cell lines. In patient samples, RRAS2 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, RRAS2 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 BONE and BREAST.
