Q-omics provides the consensus-scored ALPK3 profile across patient tissues and cancer cell-line models. ALPK3 expression is associated with patient survival in 26 of 34 cancer types, with the highest sampling consensus in UVM. Among the 18 cancer types available for tumor–normal comparison, ALPK3 is differentially expressed in 13, with the highest sampling consensus in LIHC. Additionally, ALPK3 RNA expression shows 18,274 significant gene co-expression associations, with the highest sampling consensus in TGCT. Together, these results highlight UVM, LIHC, and TGCT as cancer lineages where ALPK3 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 ALPK3 — synthetic lethality, tumor antigen, and pembrolizumab response.
This table summarizes ALPK3 survival associations across molecular data types. ALPK3 RNA expression shows survival associations in the most cancer types (26), 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 ALPK3 RNA expression–survival associations across cancer types. High ALPK3 expression shows unfavorable associations in UVM, LIHC, LGG and MESO, but favorable associations in KIRC and KIRP. The UVM Kaplan–Meier curve shows clear separation, with the high-expression group declining faster, consistent with the unfavorable association (log-rank p = .001). Together, the overview and detailed table identify UVM as the clearest survival context for ALPK3 RNA expression.
This table summarizes ALPK3 tumor–normal expression differences by data type. RNA shows broader differences across cancer types, with a lineage consensus of 13, while mass-spec protein shows differences in 3. The strongest signals are observed in LIHC for RNA and LUAD for protein.
This table ranks reproducible tumor–normal expression differences for ALPK3. A negative fold-change indicates higher expression in normal tissue than in tumor tissue. ALPK3 shows lower tumor expression in BLCA, HNSC, LUSC and BRCA and higher tumor expression in LIHC and COAD. The LIHC box plot shows higher ALPK3 RNA expression in tumor versus normal tissue (log2 FC = +1.829, t-test p < 0.001).
This table shows molecular features associated with ALPK3 in patient tissues and cancer cell lines. In patient samples, ALPK3 shows the broadest associations at the RNA and protein expression levels, with TGCT recurring as the lineage with the largest associated feature set. In cancer cell lines, ALPK3 RNA and mutation anchors are most strongly linked to RNA-expression features, especially in PANCREAS, while CRISPR and shRNA rows add functional-dependency signals in SKIN and LARGE_INTESTINE.
