Q-omics provides the consensus-scored ASPDH profile across patient tissues and cancer cell-line models. ASPDH expression is associated with patient survival in 29 of 34 cancer types, with the highest sampling consensus in KIRP. Among the 18 cancer types available for tumor–normal comparison, ASPDH is differentially expressed in 11, with the highest sampling consensus in KIRP. Additionally, ASPDH RNA expression shows 18,240 significant gene co-expression associations, with the highest sampling consensus in TGCT. Together, these results highlight KIRP, and TGCT as cancer lineages where ASPDH 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 ASPDH — synthetic lethality, tumor antigen, and pembrolizumab response.
This table summarizes ASPDH survival associations across molecular data types. ASPDH RNA expression shows survival associations in the most cancer types (29), followed by mutation status (4) and mass-spec protein abundance (1). The rightmost column indicates the cancer type with the highest sampling consensus for each molecular layer.
This table ranks reproducible ASPDH RNA expression–survival associations across cancer types. High ASPDH expression shows unfavorable associations in UCEC, THCA and COAD, but favorable associations in KIRP, LIHC and KIRC. The KIRP 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 KIRP as the clearest survival context for ASPDH RNA expression.
This table summarizes ASPDH 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 1. The strongest signals are observed in KIRP for RNA and CCRCC for protein.
This table ranks reproducible tumor–normal expression differences for ASPDH. A negative fold-change indicates higher expression in normal tissue than in tumor tissue. ASPDH shows lower tumor expression in KIRP, LIHC, KIRC, KICH, UCEC and BRCA. The KIRP box plot shows higher ASPDH RNA expression in normal versus tumor tissue (log2 FC = −4.810, t-test p < 0.001).
This table shows molecular features associated with ASPDH in patient tissues and cancer cell lines. In patient samples, ASPDH 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, ASPDH RNA and mutation anchors are most strongly linked to RNA-expression features, especially in SOFT_TISSUE, while CRISPR and shRNA rows add functional-dependency signals in OVARY and BLOOD_Leukemia.
