Q-omics provides the consensus-scored HPDL profile across patient tissues and cancer cell-line models. HPDL expression is associated with patient survival in 27 of 34 cancer types, with the highest sampling consensus in OV. Among the 18 cancer types available for tumor–normal comparison, HPDL is differentially expressed in 15, with the highest sampling consensus in BLCA. Additionally, HPDL RNA expression shows 18,609 significant protein co-abundance associations, with the highest sampling consensus in LSCC. Together, these results highlight OV, BLCA, and LSCC as cancer lineages where HPDL 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 HPDL — synthetic lethality, tumor antigen, and pembrolizumab response.
This table summarizes HPDL survival associations across molecular data types. HPDL RNA expression shows survival associations in the most cancer types (27), followed by mutation status (2) 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 HPDL RNA expression–survival associations across cancer types. High HPDL expression shows unfavorable associations in SKCM, ACC, PAAD, UCEC and LGG, but favorable associations in OV. The OV 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 OV as the clearest survival context for HPDL RNA expression.
This table summarizes HPDL 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 1. The strongest signals are observed in BLCA for RNA and COAD for protein.
This table ranks reproducible tumor–normal expression differences for HPDL. A negative fold-change indicates higher expression in normal tissue than in tumor tissue. HPDL shows lower tumor expression in THCA and KIRC and higher tumor expression in BLCA, LUAD, LUSC and STAD. The BLCA box plot shows higher HPDL RNA expression in tumor versus normal tissue (log2 FC = +1.224, t-test p < 0.001).
This table shows molecular features associated with HPDL in patient tissues and cancer cell lines. In patient samples, HPDL shows the broadest associations at the RNA and protein expression levels, with LSCC recurring as the lineage with the largest associated feature set. In cancer cell lines, HPDL RNA and mutation anchors are most strongly linked to RNA-expression features, especially in LUNG_NSCLC_LUAD, while CRISPR and shRNA rows add functional-dependency signals in BREAST and BONE.
