Q-omics provides the consensus-scored ALPK2 profile across patient tissues and cancer cell-line models. ALPK2 expression is associated with patient survival in 21 of 34 cancer types, with the highest sampling consensus in MESO. Among the 18 cancer types available for tumor–normal comparison, ALPK2 is differentially expressed in 8, with the highest sampling consensus in KIRC. Additionally, ALPK2 RNA expression shows 17,976 significant protein co-abundance associations, with the highest sampling consensus in PDAC. Together, these results highlight MESO, KIRC, and PDAC as cancer lineages where ALPK2 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 ALPK2 — synthetic lethality, tumor antigen, and pembrolizumab response.
This table summarizes ALPK2 survival associations across molecular data types. ALPK2 RNA expression shows survival associations in the most cancer types (21), followed by mutation status (10) 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 ALPK2 RNA expression–survival associations across cancer types. High ALPK2 expression shows unfavorable associations in MESO, LGG, UCEC and ACC, but favorable associations in LUAD and ESCA. The MESO 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 MESO as the clearest survival context for ALPK2 RNA expression.
This table summarizes ALPK2 tumor–normal expression differences by data type. RNA shows broader differences across cancer types, with a lineage consensus of 8, while mass-spec protein shows differences in 1. The strongest signals are observed in KIRC for RNA and CCRCC for protein.
This table ranks reproducible tumor–normal expression differences for ALPK2. A negative fold-change indicates higher expression in normal tissue than in tumor tissue. ALPK2 shows lower tumor expression in KICH and higher tumor expression in KIRC, COAD, LUAD, LUSC and UCEC. The KIRC box plot shows higher ALPK2 RNA expression in tumor versus normal tissue (log2 FC = +2.203, t-test p < 0.001).
This table shows molecular features associated with ALPK2 in patient tissues and cancer cell lines. In patient samples, ALPK2 shows the broadest associations at the RNA and protein expression levels, with PDAC recurring as the lineage with the largest associated feature set. In cancer cell lines, ALPK2 RNA and mutation anchors are most strongly linked to RNA-expression features, especially in OESOPHAGUS, while CRISPR and shRNA rows add functional-dependency signals in SKIN and BONE.
