Q-omics provides the consensus-scored LRMDA profile across patient tissues and cancer cell-line models. LRMDA 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, LRMDA is differentially expressed in 10, with the highest sampling consensus in KIRC. Additionally, LRMDA protein abundance shows 23,118 significant protein co-abundance associations, with the highest sampling consensus in LSCC. Together, these results highlight MESO, KIRC, and LSCC as cancer lineages where LRMDA 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 LRMDA — synthetic lethality, tumor antigen, and pembrolizumab response.
This table summarizes LRMDA survival associations across molecular data types. LRMDA RNA expression shows survival associations in the most cancer types (23), followed by mutation status (4) and mass-spec protein abundance (5). The rightmost column indicates the cancer type with the highest sampling consensus for each molecular layer.
This table ranks reproducible LRMDA RNA expression–survival associations across cancer types. High LRMDA expression shows unfavorable associations in LGG, SCLC and ACC, but favorable associations in MESO, KIRP and HNSC. The MESO Kaplan–Meier curve shows clear separation, with the low-expression group declining faster, consistent with the favorable association (log-rank p < 0.001). Together, the overview and detailed table identify MESO as the clearest survival context for LRMDA RNA expression.
This table summarizes LRMDA tumor–normal expression differences by data type. RNA shows broader differences across cancer types, with a lineage consensus of 10, while mass-spec protein shows differences in 4. The strongest signals are observed in KIRC for RNA and LSCC for protein.
This table ranks reproducible tumor–normal expression differences for LRMDA. A negative fold-change indicates higher expression in normal tissue than in tumor tissue. LRMDA shows lower tumor expression in LUAD, LUSC, UCEC and BRCA and higher tumor expression in KIRC and LIHC. The KIRC box plot shows higher LRMDA RNA expression in tumor versus normal tissue (log2 FC = +0.861, t-test p < 0.001).
This table shows molecular features associated with LRMDA in patient tissues and cancer cell lines. In patient samples, LRMDA shows the broadest associations at the RNA and protein expression levels, with LSCC recurring as the lineage with the largest associated feature set. In cancer cell lines, LRMDA RNA and mutation anchors are most strongly linked to RNA-expression features, especially in PANCREAS, while CRISPR and shRNA rows add functional-dependency signals in SKIN and BLOOD_Leukemia.
