Q-omics provides the consensus-scored APOL3 profile across patient tissues and cancer cell-line models. APOL3 expression is associated with patient survival in 23 of 34 cancer types, with the highest sampling consensus in SKCM. Among the 18 cancer types available for tumor–normal comparison, APOL3 is differentially expressed in 11, with the highest sampling consensus in KICH. Additionally, APOL3 protein abundance shows 17,561 significant protein co-abundance associations, with the highest sampling consensus in LSCC. Together, these results highlight SKCM, KICH, and LSCC as cancer lineages where APOL3 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 APOL3 — synthetic lethality, tumor antigen, and pembrolizumab response.
This table summarizes APOL3 survival associations across molecular data types. APOL3 RNA expression shows survival associations in the most cancer types (23), followed by mutation status (4) and mass-spec protein abundance (9). The rightmost column indicates the cancer type with the highest sampling consensus for each molecular layer.
This table ranks reproducible APOL3 RNA expression–survival associations across cancer types. High APOL3 expression shows unfavorable associations in UVM and KIRP, but favorable associations in SKCM, KIRC, CESC and BRCA. The SKCM 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 SKCM as the clearest survival context for APOL3 RNA expression.
This table summarizes APOL3 tumor–normal expression differences by data type. RNA shows broader differences across cancer types, with a lineage consensus of 11, while mass-spec protein shows differences in 5. The strongest signals are observed in KICH for RNA and CCRCC for protein.
This table ranks reproducible tumor–normal expression differences for APOL3. A negative fold-change indicates higher expression in normal tissue than in tumor tissue. APOL3 shows lower tumor expression in KICH, KIRP, THCA, LUSC and LUAD and higher tumor expression in KIRC. The KICH box plot shows higher APOL3 RNA expression in normal versus tumor tissue (log2 FC = −1.826, t-test p < 0.001).
This table shows molecular features associated with APOL3 in patient tissues and cancer cell lines. In patient samples, APOL3 shows the broadest associations at the RNA and protein expression levels, with LSCC recurring as the lineage with the largest associated feature set. In cancer cell lines, APOL3 RNA and mutation anchors are most strongly linked to RNA-expression features, especially in LIVER, while CRISPR and shRNA rows add functional-dependency signals in BLOOD_Leukemia and SOFT_TISSUE.
