Q-omics provides the consensus-scored LPAR3 profile across patient tissues and cancer cell-line models. LPAR3 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, LPAR3 is differentially expressed in 11, with the highest sampling consensus in HNSC. Additionally, LPAR3 RNA expression shows 14,244 significant gene co-expression associations, with the highest sampling consensus in THYM. Together, these results highlight MESO, HNSC, and THYM as cancer lineages where LPAR3 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 LPAR3 — synthetic lethality, tumor antigen, and pembrolizumab response.
This table summarizes LPAR3 survival associations across molecular data types. LPAR3 RNA expression shows survival associations in the most cancer types (23), followed by mutation status (6). The rightmost column indicates the cancer type with the highest sampling consensus for each molecular layer.
This table ranks reproducible LPAR3 RNA expression–survival associations across cancer types. High LPAR3 expression shows unfavorable associations in MESO, HNSC, LGG and STAD, but favorable associations in OV and UVM. The MESO Kaplan–Meier curve shows clear separation, with the high-expression group declining faster, consistent with the unfavorable association (log-rank p = .001). Together, the overview and detailed table identify MESO as the clearest survival context for LPAR3 RNA expression.
This table summarizes LPAR3 tumor–normal expression differences by data type. RNA shows broader differences across cancer types, with a lineage consensus of 11. The strongest signals are observed in HNSC for RNA.
This table ranks reproducible tumor–normal expression differences for LPAR3. A negative fold-change indicates higher expression in normal tissue than in tumor tissue. LPAR3 shows lower tumor expression in LUAD, COAD and KIRP and higher tumor expression in HNSC, LUSC and BLCA. The HNSC box plot shows higher LPAR3 RNA expression in tumor versus normal tissue (log2 FC = +1.859, t-test p < 0.001).
This table shows molecular features associated with LPAR3 in patient tissues and cancer cell lines. In patient samples, LPAR3 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, LPAR3 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 OVARY and LUNG_SCLC.
