ArfGAP with coiled-coil, ankyrin repeat and PH domains 2Genealiases: CENTB2 · CNT-B2
Q-omics provides the consensus-scored ACAP2 profile across patient tissues and cancer cell-line models. ACAP2 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, ACAP2 is differentially expressed in 12, with the highest sampling consensus in KIRC. Additionally, ACAP2 protein abundance shows 22,563 significant protein co-abundance associations, with the highest sampling consensus in GBM. Together, these results highlight KIRC, and GBM as cancer lineages where ACAP2 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 ACAP2 — synthetic lethality, tumor antigen, and pembrolizumab response.
This table summarizes ACAP2 survival associations across molecular data types. ACAP2 RNA expression shows survival associations in the most cancer types (24), followed by mutation status (6) 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 ACAP2 RNA expression–survival associations across cancer types. High ACAP2 expression shows unfavorable associations in ACC, KICH and MESO, but favorable associations in KIRC, LUSC and HNSC. 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 ACAP2 RNA expression.
This table summarizes ACAP2 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 6. The strongest signals are observed in KIRC for RNA and CCRCC for protein.
This table ranks reproducible tumor–normal expression differences for ACAP2. A negative fold-change indicates higher expression in normal tissue than in tumor tissue. ACAP2 shows higher tumor expression in KIRC, LIHC, LUSC, HNSC, BLCA and CHOL. The KIRC box plot shows higher ACAP2 RNA expression in tumor versus normal tissue (log2 FC = +0.443, t-test p < 0.001).
This table shows molecular features associated with ACAP2 in patient tissues and cancer cell lines. In patient samples, ACAP2 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, ACAP2 RNA and mutation anchors are most strongly linked to RNA-expression features, especially in LUNG_SCLC, while CRISPR and shRNA rows add functional-dependency signals in URINARY_TRACT and LARGE_INTESTINE.
