Q-omics provides the consensus-scored HPSE profile across patient tissues and cancer cell-line models. HPSE expression is associated with patient survival in 20 of 34 cancer types, with the highest sampling consensus in UVM. Among the 18 cancer types available for tumor–normal comparison, HPSE is differentially expressed in 10, with the highest sampling consensus in UCEC. Additionally, HPSE RNA expression shows 18,019 significant gene co-expression associations, with the highest sampling consensus in UVM. Together, these results highlight UVM, and UCEC as cancer lineages where HPSE 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.
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This table summarizes HPSE survival associations across molecular data types. HPSE RNA expression shows survival associations in the most cancer types (20), followed by mutation status (6) and mass-spec protein abundance (3). The rightmost column indicates the cancer type with the highest sampling consensus for each molecular layer.
This table ranks reproducible HPSE RNA expression–survival associations across cancer types. High HPSE expression shows unfavorable associations in UVM, BLCA, LUAD and UCEC, but favorable associations in KIRC and SCLC. The UVM 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 UVM as the clearest survival context for HPSE RNA expression.
This table summarizes HPSE tumor–normal expression differences by data type. RNA shows broader differences across cancer types, with a lineage consensus of 10, while mass-spec protein shows differences in 3. The strongest signals are observed in THCA for RNA and HNSC for protein.
This table ranks reproducible tumor–normal expression differences for HPSE. A negative fold-change indicates higher expression in normal tissue than in tumor tissue. HPSE shows lower tumor expression in UCEC, COAD and KIRP and higher tumor expression in STAD, THCA and BRCA. The UCEC box plot shows higher HPSE RNA expression in normal versus tumor tissue (log2 FC = −1.359, t-test p < 0.001).
This table shows molecular features associated with HPSE in patient tissues and cancer cell lines. In patient samples, HPSE shows the broadest associations at the RNA and protein expression levels, with UVM recurring as the lineage with the largest associated feature set. In cancer cell lines, HPSE RNA and mutation anchors are most strongly linked to RNA-expression features, especially in LUNG_SCLC, while CRISPR and shRNA rows add functional-dependency signals in OVARY and LARGE_INTESTINE.