Q-omics provides the consensus-scored LGMN profile across patient tissues and cancer cell-line models. LGMN expression is associated with patient survival in 22 of 34 cancer types, with the highest sampling consensus in KIRC. Among the 18 cancer types available for tumor–normal comparison, LGMN is differentially expressed in 11, with the highest sampling consensus in THCA. Additionally, LGMN protein abundance shows 27,936 significant protein co-abundance associations, with the highest sampling consensus in PDAC. Together, these results highlight KIRC, THCA, and PDAC as cancer lineages where LGMN 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 LGMN — synthetic lethality, tumor antigen, and pembrolizumab response.
This table summarizes LGMN survival associations across molecular data types. LGMN RNA expression shows survival associations in the most cancer types (22), followed by mutation status (3) and mass-spec protein abundance (8). The rightmost column indicates the cancer type with the highest sampling consensus for each molecular layer.
This table ranks reproducible LGMN RNA expression–survival associations across cancer types. High LGMN expression shows unfavorable associations in UVM, HNSC, ACC and BLCA, but favorable associations in KIRC and SKCM. The KIRC 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 KIRC as the clearest survival context for LGMN RNA expression.
This table summarizes LGMN tumor–normal expression differences by data type. RNA shows broader differences across cancer types, with a lineage consensus of 11, while mass-spec protein shows differences in 6. The strongest signals are observed in THCA for RNA and LUAD for protein.
This table ranks reproducible tumor–normal expression differences for LGMN. A negative fold-change indicates higher expression in normal tissue than in tumor tissue. LGMN shows lower tumor expression in THCA and LUSC and higher tumor expression in HNSC, STAD, KICH and UCEC. The THCA box plot shows higher LGMN RNA expression in normal versus tumor tissue (log2 FC = −1.844, t-test p < 0.001).
This table shows molecular features associated with LGMN in patient tissues and cancer cell lines. In patient samples, LGMN shows the broadest associations at the RNA and protein expression levels, with PDAC recurring as the lineage with the largest associated feature set. In cancer cell lines, LGMN RNA and mutation anchors are most strongly linked to RNA-expression features, especially in LUNG_NSCLC_LUAD, while CRISPR and shRNA rows add functional-dependency signals in LUNG_SCLC and BLOOD_Leukemia.
