Q-omics provides the consensus-scored ALPL profile across patient tissues and cancer cell-line models. ALPL expression is associated with patient survival in 24 of 34 cancer types, with the highest sampling consensus in LUSC. Among the 18 cancer types available for tumor–normal comparison, ALPL is differentially expressed in 11, with the highest sampling consensus in KICH. Additionally, ALPL protein abundance shows 15,558 significant protein co-abundance associations, with the highest sampling consensus in PDAC. Together, these results highlight LUSC, KICH, and PDAC as cancer lineages where ALPL 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 ALPL — synthetic lethality, tumor antigen, and pembrolizumab response.
This table summarizes ALPL survival associations across molecular data types. ALPL RNA expression shows survival associations in the most cancer types (24), followed by mutation status (5) and mass-spec protein abundance (6). The rightmost column indicates the cancer type with the highest sampling consensus for each molecular layer.
This table ranks reproducible ALPL RNA expression–survival associations across cancer types. High ALPL expression shows unfavorable associations in LUSC, ACC and STAD, but favorable associations in HNSC, KIRC and LGG. The LUSC 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 LUSC as the clearest survival context for ALPL RNA expression.
This table summarizes ALPL 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 4. The strongest signals are observed in LUAD for RNA and HNSC for protein.
This table ranks reproducible tumor–normal expression differences for ALPL. A negative fold-change indicates higher expression in normal tissue than in tumor tissue. ALPL shows lower tumor expression in KICH, LUAD, KIRP, LUSC and LIHC and higher tumor expression in THCA. The KICH box plot shows higher ALPL RNA expression in normal versus tumor tissue (log2 FC = −3.692, t-test p < 0.001).
This table shows molecular features associated with ALPL in patient tissues and cancer cell lines. In patient samples, ALPL 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, ALPL RNA and mutation anchors are most strongly linked to RNA-expression features, especially in BLOOD_Lymphoma, while CRISPR and shRNA rows add functional-dependency signals in OVARY and LARGE_INTESTINE.
