Q-omics provides the consensus-scored LHPP profile across patient tissues and cancer cell-line models. LHPP expression is associated with patient survival in 22 of 34 cancer types, with the highest sampling consensus in LIHC. Among the 18 cancer types available for tumor–normal comparison, LHPP is differentially expressed in 13, with the highest sampling consensus in KICH. Additionally, LHPP protein abundance shows 30,159 significant protein co-abundance associations, with the highest sampling consensus in PDAC. Together, these results highlight LIHC, KICH, and PDAC as cancer lineages where LHPP 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 LHPP — synthetic lethality, tumor antigen, and pembrolizumab response.
This table summarizes LHPP survival associations across molecular data types. LHPP RNA expression shows survival associations in the most cancer types (22), followed by mutation status (5) and mass-spec protein abundance (7). The rightmost column indicates the cancer type with the highest sampling consensus for each molecular layer.
This table ranks reproducible LHPP RNA expression–survival associations across cancer types. High LHPP expression shows unfavorable associations in UCS and KIRC, but favorable associations in LIHC, LGG, SCLC and KIRP. The LIHC Kaplan–Meier curve shows clear separation, with the low-expression group declining faster, consistent with the favorable association (log-rank p = .003). Together, the overview and detailed table identify LIHC as the clearest survival context for LHPP RNA expression.
This table summarizes LHPP 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 5. The strongest signals are observed in KICH for RNA and CCRCC for protein.
This table ranks reproducible tumor–normal expression differences for LHPP. A negative fold-change indicates higher expression in normal tissue than in tumor tissue. LHPP shows lower tumor expression in KICH, KIRC, BLCA, COAD, THCA and BRCA. The KICH box plot shows higher LHPP RNA expression in normal versus tumor tissue (log2 FC = −2.663, t-test p < 0.001).
This table shows molecular features associated with LHPP in patient tissues and cancer cell lines. In patient samples, LHPP 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, LHPP RNA and mutation anchors are most strongly linked to RNA-expression features, especially in BREAST, while CRISPR and shRNA rows add functional-dependency signals in LUNG_NSCLC_LUAD and BLOOD_Lymphoma.
