Q-omics provides the consensus-scored HPR profile across patient tissues and cancer cell-line models. HPR expression is associated with patient survival in 23 of 34 cancer types, with the highest sampling consensus in MESO. Among the 18 cancer types available for tumor–normal comparison, HPR is differentially expressed in 13, with the highest sampling consensus in LUAD. Additionally, HPR protein abundance shows 20,688 significant protein co-abundance associations, with the highest sampling consensus in PDAC. Together, these results highlight MESO, LUAD, and PDAC as cancer lineages where HPR 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 HPR — synthetic lethality, tumor antigen, and pembrolizumab response.
This table summarizes HPR survival associations across molecular data types. HPR RNA expression shows survival associations in the most cancer types (23), followed by mutation status (4) and mass-spec protein abundance (8). The rightmost column indicates the cancer type with the highest sampling consensus for each molecular layer.
This table ranks reproducible HPR RNA expression–survival associations across cancer types. High HPR expression shows unfavorable associations in LUSC and KIRC, but favorable associations in MESO, UCEC, LIHC and ACC. The MESO 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 MESO as the clearest survival context for HPR RNA expression.
This table summarizes HPR tumor–normal expression differences by data type. RNA shows broader differences across cancer types, with a lineage consensus of 13, while mass-spec protein shows differences in 6. The strongest signals are observed in LUAD for RNA and HNSC for protein.
This table ranks reproducible tumor–normal expression differences for HPR. A negative fold-change indicates higher expression in normal tissue than in tumor tissue. HPR shows lower tumor expression in LUAD, LUSC, KIRP, UCEC, BRCA and CHOL. The LUAD box plot shows higher HPR RNA expression in normal versus tumor tissue (log2 FC = −0.877, t-test p < 0.001).
This table shows molecular features associated with HPR in patient tissues and cancer cell lines. In patient samples, HPR 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, HPR RNA and mutation anchors are most strongly linked to RNA-expression features, especially in OESOPHAGUS, while CRISPR and shRNA rows add functional-dependency signals in BLOOD_Leukemia and SKIN.
