Q-omics provides the consensus-scored ARHGAP24 profile across patient tissues and cancer cell-line models. ARHGAP24 expression is associated with patient survival in 24 of 34 cancer types, with the highest sampling consensus in KIRC. Among the 18 cancer types available for tumor–normal comparison, ARHGAP24 is differentially expressed in 15, with the highest sampling consensus in KIRC. Additionally, ARHGAP24 protein abundance shows 31,467 significant protein co-abundance associations, with the highest sampling consensus in LUAD. Together, these results highlight KIRC, and LUAD as cancer lineages where ARHGAP24 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 ARHGAP24 — synthetic lethality, tumor antigen, and pembrolizumab response.
This table summarizes ARHGAP24 survival associations across molecular data types. ARHGAP24 RNA expression shows survival associations in the most cancer types (24), followed by mutation status (4) 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 ARHGAP24 RNA expression–survival associations across cancer types. High ARHGAP24 expression shows unfavorable associations in BLCA and MESO, but favorable associations in KIRC, KIRP, LUSC and ACC. 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 ARHGAP24 RNA expression.
This table summarizes ARHGAP24 tumor–normal expression differences by data type. RNA shows broader differences across cancer types, with a lineage consensus of 15, while mass-spec protein shows differences in 8. The strongest signals are observed in KIRC for RNA and CCRCC for protein.
This table ranks reproducible tumor–normal expression differences for ARHGAP24. A negative fold-change indicates higher expression in normal tissue than in tumor tissue. ARHGAP24 shows lower tumor expression in KIRC, THCA, KICH, LUAD, KIRP and BLCA. The KIRC box plot shows higher ARHGAP24 RNA expression in normal versus tumor tissue (log2 FC = −1.466, t-test p < 0.001).
This table shows molecular features associated with ARHGAP24 in patient tissues and cancer cell lines. In patient samples, ARHGAP24 shows the broadest associations at the RNA and protein expression levels, with LUAD recurring as the lineage with the largest associated feature set. In cancer cell lines, ARHGAP24 RNA and mutation anchors are most strongly linked to RNA-expression features, especially in BLOOD_Leukemia, while CRISPR and shRNA rows add functional-dependency signals in STOMACH and BONE.
