Q-omics provides the consensus-scored NRAS profile across patient tissues and cancer cell-line models. NRAS expression is associated with patient survival in 29 of 34 cancer types, with the highest sampling consensus in MESO. Among the 18 cancer types available for tumor–normal comparison, NRAS is differentially expressed in 14, with the highest sampling consensus in HNSC. Additionally, NRAS protein abundance shows 21,243 significant protein co-abundance associations, with the highest sampling consensus in GBM. Together, these results highlight MESO, HNSC, and GBM as cancer lineages where NRAS 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 NRAS — synthetic lethality, tumor antigen, and pembrolizumab response.
This table summarizes NRAS survival associations across molecular data types. NRAS RNA expression shows survival associations in the most cancer types (29), followed by mutation status (8) and 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 NRAS RNA expression–survival associations across cancer types. High NRAS expression shows unfavorable associations in MESO, LIHC, ACC, LGG and PAAD, but favorable associations in KIRC. The MESO 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 MESO as the clearest survival context for NRAS RNA expression.
This table summarizes NRAS tumor–normal expression differences by data type. RNA shows broader differences across cancer types, with a lineage consensus of 14, while mass-spec protein shows differences in 5. The strongest signals are observed in KIRC for RNA and PDAC for protein.
This table ranks reproducible tumor–normal expression differences for NRAS. A negative fold-change indicates higher expression in normal tissue than in tumor tissue. NRAS shows lower tumor expression in KICH and higher tumor expression in HNSC, KIRC, BLCA, LIHC and STAD. The HNSC box plot shows higher NRAS RNA expression in tumor versus normal tissue (log2 FC = +1.042, t-test p < 0.001).
This table shows molecular features associated with NRAS in patient tissues and cancer cell lines. In patient samples, NRAS 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, NRAS RNA and mutation anchors are most strongly linked to RNA-expression features, especially in UPPER_AERODIGESTIVE_TRACT, while CRISPR and shRNA rows add functional-dependency signals in SKIN and BLOOD_Leukemia.
