Q-omics provides the consensus-scored LPA profile across patient tissues and cancer cell-line models. LPA 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, LPA is differentially expressed in 13, with the highest sampling consensus in KIRP. Additionally, LPA RNA expression shows 14,695 significant gene co-expression associations, with the highest sampling consensus in TGCT. Together, these results highlight ACC, KIRP, and TGCT as cancer lineages where LPA 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 LPA — synthetic lethality, tumor antigen, and pembrolizumab response.
This table summarizes LPA survival associations across molecular data types. LPA RNA expression shows survival associations in the most cancer types (22), followed by mutation status (11) and mass-spec protein abundance (4). The rightmost column indicates the cancer type with the highest sampling consensus for each molecular layer.
This table ranks reproducible LPA RNA expression–survival associations across cancer types. High LPA expression shows unfavorable associations in ACC, CHOL and OV, but favorable associations in LGG, READ and LIHC. 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 LPA RNA expression.
This table summarizes LPA 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 4. The strongest signals are observed in KIRP for RNA and LUAD for protein.
This table ranks reproducible tumor–normal expression differences for LPA. A negative fold-change indicates higher expression in normal tissue than in tumor tissue. LPA shows lower tumor expression in KIRP, KIRC, THCA, LIHC, KICH and LUAD. The KIRP box plot shows higher LPA RNA expression in normal versus tumor tissue (log2 FC = −1.036, t-test p < 0.001).
This table shows molecular features associated with LPA in patient tissues and cancer cell lines. In patient samples, LPA shows the broadest associations at the RNA and protein expression levels, with TGCT recurring as the lineage with the largest associated feature set. In cancer cell lines, LPA RNA and mutation anchors are most strongly linked to RNA-expression features, especially in OVARY, while CRISPR and shRNA rows add functional-dependency signals in SOFT_TISSUE and BLOOD_Leukemia.
