Q-omics provides the consensus-scored ALAD profile across patient tissues and cancer cell-line models. ALAD expression is associated with patient survival in 22 of 34 cancer types, with the highest sampling consensus in KIRC. Among the 18 cancer types available for tumor–normal comparison, ALAD is differentially expressed in 16, with the highest sampling consensus in KIRC. Additionally, ALAD protein abundance shows 26,132 significant protein co-abundance associations, with the highest sampling consensus in GBM. Together, these results highlight KIRC, and GBM as cancer lineages where ALAD 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 ALAD — synthetic lethality, tumor antigen, and pembrolizumab response.
This table summarizes ALAD survival associations across molecular data types. ALAD RNA expression shows survival associations in the most cancer types (22), followed by mutation status (5) and mass-spec protein abundance (4). The rightmost column indicates the cancer type with the highest sampling consensus for each molecular layer.
This table ranks reproducible ALAD RNA expression–survival associations across cancer types. High ALAD expression shows unfavorable associations in BLCA, but favorable associations in KIRC, LIHC, LUAD, SARC and SKCM. The KIRC 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 KIRC as the clearest survival context for ALAD RNA expression.
This table summarizes ALAD tumor–normal expression differences by data type. RNA shows broader differences across cancer types, with a lineage consensus of 16, while mass-spec protein shows differences in 7. The strongest signals are observed in KIRC for RNA and COAD for protein.
This table ranks reproducible tumor–normal expression differences for ALAD. A negative fold-change indicates higher expression in normal tissue than in tumor tissue. ALAD shows lower tumor expression in KIRC, KIRP, THCA, KICH, LUAD and BLCA. The KIRC box plot shows higher ALAD RNA expression in normal versus tumor tissue (log2 FC = −0.986, t-test p < 0.001).
This table shows molecular features associated with ALAD in patient tissues and cancer cell lines. In patient samples, ALAD shows the broadest associations at the RNA and protein expression levels, with GBM recurring as the lineage with the largest associated feature set. In cancer cell lines, ALAD 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 LIVER and UPPER_AERODIGESTIVE_TRACT.
