Q-omics provides the consensus-scored HPD profile across patient tissues and cancer cell-line models. HPD expression is associated with patient survival in 22 of 34 cancer types, with the highest sampling consensus in ACC. Among the 18 cancer types available for tumor–normal comparison, HPD is differentially expressed in 15, with the highest sampling consensus in KIRC. Additionally, HPD RNA expression shows 15,910 significant gene co-expression associations, with the highest sampling consensus in ACC. Together, these results highlight ACC, and KIRC as cancer lineages where HPD 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 HPD — synthetic lethality, tumor antigen, and pembrolizumab response.
This table summarizes HPD survival associations across molecular data types. HPD RNA expression shows survival associations in the most cancer types (22), followed by mutation status (3) 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 HPD RNA expression–survival associations across cancer types. High HPD expression shows unfavorable associations in ACC, LGG, COAD, MESO, CHOL and THYM. The ACC 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 ACC as the clearest survival context for HPD RNA expression.
This table summarizes HPD tumor–normal expression differences by data type. RNA shows broader differences across cancer types, with a lineage consensus of 15, while mass-spec protein shows differences in 2. The strongest signals are observed in KIRC for RNA and CCRCC for protein.
This table ranks reproducible tumor–normal expression differences for HPD. A negative fold-change indicates higher expression in normal tissue than in tumor tissue. HPD shows lower tumor expression in KIRC, KIRP, BLCA, THCA, KICH and LUAD. The KIRC box plot shows higher HPD RNA expression in normal versus tumor tissue (log2 FC = −3.761, t-test p < 0.001).
This table shows molecular features associated with HPD in patient tissues and cancer cell lines. In patient samples, HPD shows the broadest associations at the RNA and protein expression levels, with ACC recurring as the lineage with the largest associated feature set. In cancer cell lines, HPD RNA and mutation anchors are most strongly linked to RNA-expression features, especially in LIVER, while CRISPR and shRNA rows add functional-dependency signals in SOFT_TISSUE and LARGE_INTESTINE.
