Q-omics provides the consensus-scored APLN profile across patient tissues and cancer cell-line models. APLN expression is associated with patient survival in 27 of 34 cancer types, with the highest sampling consensus in KICH. Among the 18 cancer types available for tumor–normal comparison, APLN is differentially expressed in 15, with the highest sampling consensus in KIRC. Additionally, APLN RNA expression shows 17,104 significant gene co-expression associations, with the highest sampling consensus in ACC. Together, these results highlight KICH, KIRC, and ACC as cancer lineages where APLN 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 APLN — synthetic lethality, tumor antigen, and pembrolizumab response.
This table summarizes APLN survival associations across molecular data types. APLN RNA expression shows survival associations in the most cancer types (27), followed by mutation status (2) and mass-spec protein abundance (2). The rightmost column indicates the cancer type with the highest sampling consensus for each molecular layer.
This table ranks reproducible APLN RNA expression–survival associations across cancer types. High APLN expression shows unfavorable associations in KICH, LUSC, CESC, KIRP, UVM and ESCA. The KICH 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 KICH as the clearest survival context for APLN RNA expression.
This table summarizes APLN 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 1. The strongest signals are observed in KIRC for RNA and LSCC for protein.
This table ranks reproducible tumor–normal expression differences for APLN. A negative fold-change indicates higher expression in normal tissue than in tumor tissue. APLN shows lower tumor expression in KIRP and higher tumor expression in KIRC, HNSC, COAD, STAD and LIHC. The KIRC box plot shows higher APLN RNA expression in tumor versus normal tissue (log2 FC = +3.276, t-test p < 0.001).
This table shows molecular features associated with APLN in patient tissues and cancer cell lines. In patient samples, APLN shows the broadest associations at the RNA and protein expression levels, with ACC recurring as the lineage with the largest associated feature set. In cancer cell lines, APLN RNA and mutation anchors are most strongly linked to RNA-expression features, especially in KIDNEY, while CRISPR and shRNA rows add functional-dependency signals in UPPER_AERODIGESTIVE_TRACT and SOFT_TISSUE.
