Q-omics provides the consensus-scored LPAR1 profile across patient tissues and cancer cell-line models. LPAR1 expression is associated with patient survival in 22 of 34 cancer types, with the highest sampling consensus in UVM. Among the 18 cancer types available for tumor–normal comparison, LPAR1 is differentially expressed in 13, with the highest sampling consensus in COAD. Additionally, LPAR1 RNA expression shows 17,793 significant gene co-expression associations, with the highest sampling consensus in THYM. Together, these results highlight UVM, COAD, and THYM as cancer lineages where LPAR1 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 LPAR1 — synthetic lethality, tumor antigen, and pembrolizumab response.
This table summarizes LPAR1 survival associations across molecular data types. LPAR1 RNA expression shows survival associations in the most cancer types (22), followed by mutation status (3) 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 LPAR1 RNA expression–survival associations across cancer types. High LPAR1 expression shows unfavorable associations in UVM, LGG, KIRP and ESCA, but favorable associations in UCEC and CESC. 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 LPAR1 RNA expression.
This table summarizes LPAR1 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 COAD for RNA and COAD for protein.
This table ranks reproducible tumor–normal expression differences for LPAR1. A negative fold-change indicates higher expression in normal tissue than in tumor tissue. LPAR1 shows lower tumor expression in COAD, KIRC, THCA, BLCA, KICH and BRCA. The COAD box plot shows higher LPAR1 RNA expression in normal versus tumor tissue (log2 FC = −1.978, t-test p < 0.001).
This table shows molecular features associated with LPAR1 in patient tissues and cancer cell lines. In patient samples, LPAR1 shows the broadest associations at the RNA and protein expression levels, with THYM recurring as the lineage with the largest associated feature set. In cancer cell lines, LPAR1 RNA and mutation anchors are most strongly linked to RNA-expression features, especially in LIVER, while CRISPR and shRNA rows add functional-dependency signals in PANCREAS and SOFT_TISSUE.
