Q-omics provides the consensus-scored ARHGAP42P2 profile across patient tissues and cancer cell-line models. ARHGAP42P2 expression is associated with patient survival in 18 of 34 cancer types, with the highest sampling consensus in KIRC. Among the 18 cancer types available for tumor–normal comparison, ARHGAP42P2 is differentially expressed in 6, with the highest sampling consensus in KIRC. Additionally, ARHGAP42P2 RNA expression shows 10,817 significant gene co-expression associations, with the highest sampling consensus in THYM. Together, these results highlight KIRC, and THYM as cancer lineages where ARHGAP42P2 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 ARHGAP42P2 — synthetic lethality, tumor antigen, and pembrolizumab response.
This table summarizes ARHGAP42P2 survival associations across molecular data types. ARHGAP42P2 RNA expression shows survival associations in the most cancer types (18). The rightmost column indicates the cancer type with the highest sampling consensus for each molecular layer.
This table ranks reproducible ARHGAP42P2 RNA expression–survival associations across cancer types. High ARHGAP42P2 expression shows unfavorable associations in DLBC, UVM, STAD and LIHC, but favorable associations in KIRC and BRCA. The KIRC Kaplan–Meier curve shows clear separation, with the low-expression group declining faster, consistent with the favorable association (log-rank p = .001). Together, the overview and detailed table identify KIRC as the clearest survival context for ARHGAP42P2 RNA expression.
This table summarizes ARHGAP42P2 tumor–normal expression differences by data type. RNA shows broader differences across cancer types, with a lineage consensus of 6. The strongest signals are observed in KIRC for RNA.
This table ranks reproducible tumor–normal expression differences for ARHGAP42P2. A negative fold-change indicates higher expression in normal tissue than in tumor tissue. ARHGAP42P2 shows lower tumor expression in READ and higher tumor expression in KIRC, BRCA, PRAD, STAD and THCA. The KIRC box plot shows higher ARHGAP42P2 RNA expression in tumor versus normal tissue (log2 FC = +0.055, t-test p < 0.001).
This table shows molecular features associated with ARHGAP42P2 in patient tissues and cancer cell lines. In patient samples, ARHGAP42P2 shows the broadest associations at the RNA and protein expression levels, with THYM recurring as the lineage with the largest associated feature set.
