Q-omics provides the consensus-scored LPAR2 profile across patient tissues and cancer cell-line models. LPAR2 expression is associated with patient survival in 27 of 34 cancer types, with the highest sampling consensus in ACC. Among the 18 cancer types available for tumor–normal comparison, LPAR2 is differentially expressed in 16, with the highest sampling consensus in HNSC. Additionally, LPAR2 RNA expression shows 18,902 significant gene co-expression associations, with the highest sampling consensus in ACC. Together, these results highlight ACC, and HNSC as cancer lineages where LPAR2 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 LPAR2 — synthetic lethality, tumor antigen, and pembrolizumab response.
This table summarizes LPAR2 survival associations across molecular data types. LPAR2 RNA expression shows survival associations in the most cancer types (27), followed by mutation status (1) 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 LPAR2 RNA expression–survival associations across cancer types. High LPAR2 expression shows unfavorable associations in ACC, KIRC and MESO, but favorable associations in HNSC, OV and STAD. 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 LPAR2 RNA expression.
This table summarizes LPAR2 tumor–normal expression differences by data type. RNA shows broader differences across cancer types, with a lineage consensus of 16, while mass-spec protein shows differences in 4. The strongest signals are observed in HNSC for RNA and LSCC for protein.
This table ranks reproducible tumor–normal expression differences for LPAR2. A negative fold-change indicates higher expression in normal tissue than in tumor tissue. LPAR2 shows higher tumor expression in HNSC, COAD, LUAD, BLCA, LUSC and KIRC. The HNSC box plot shows higher LPAR2 RNA expression in tumor versus normal tissue (log2 FC = +1.353, t-test p < 0.001).
This table shows molecular features associated with LPAR2 in patient tissues and cancer cell lines. In patient samples, LPAR2 shows the broadest associations at the RNA and protein expression levels, with ACC recurring as the lineage with the largest associated feature set. In cancer cell lines, LPAR2 RNA and mutation anchors are most strongly linked to RNA-expression features, especially in URINARY_TRACT, while CRISPR and shRNA rows add functional-dependency signals in BONE and LARGE_INTESTINE.
