Q-omics provides the consensus-scored RASL11B profile across patient tissues and cancer cell-line models. RASL11B expression is associated with patient survival in 27 of 34 cancer types, with the highest sampling consensus in KIRP. Among the 18 cancer types available for tumor–normal comparison, RASL11B is differentially expressed in 13, with the highest sampling consensus in KIRC. Additionally, RASL11B RNA expression shows 17,505 significant gene co-expression associations, with the highest sampling consensus in UVM. Together, these results highlight KIRP, KIRC, and UVM as cancer lineages where RASL11B 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 RASL11B — synthetic lethality, tumor antigen, and pembrolizumab response.
This table summarizes RASL11B survival associations across molecular data types. RASL11B RNA expression shows survival associations in the most cancer types (27), followed by mutation status (2). The rightmost column indicates the cancer type with the highest sampling consensus for each molecular layer.
This table ranks reproducible RASL11B RNA expression–survival associations across cancer types. High RASL11B expression shows unfavorable associations in KIRP, UVM and THCA, but favorable associations in ACC, BRCA and ESCA. The KIRP 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 KIRP as the clearest survival context for RASL11B RNA expression.
This table summarizes RASL11B tumor–normal expression differences by data type. RNA shows broader differences across cancer types, with a lineage consensus of 13. The strongest signals are observed in KIRC for RNA.
This table ranks reproducible tumor–normal expression differences for RASL11B. A negative fold-change indicates higher expression in normal tissue than in tumor tissue. RASL11B shows lower tumor expression in KIRC, KICH and KIRP and higher tumor expression in HNSC, BLCA and BRCA. The KIRC box plot shows higher RASL11B RNA expression in normal versus tumor tissue (log2 FC = −4.432, t-test p < 0.001).
This table shows molecular features associated with RASL11B in patient tissues and cancer cell lines. In patient samples, RASL11B shows the broadest associations at the RNA and protein expression levels, with UVM recurring as the lineage with the largest associated feature set. In cancer cell lines, RASL11B 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 OESOPHAGUS and SOFT_TISSUE.
