Q-omics provides the consensus-scored LMOD3 profile across patient tissues and cancer cell-line models. LMOD3 expression is associated with patient survival in 27 of 34 cancer types, with the highest sampling consensus in UVM. Among the 18 cancer types available for tumor–normal comparison, LMOD3 is differentially expressed in 11, with the highest sampling consensus in BLCA. Additionally, LMOD3 RNA expression shows 20,538 significant protein co-abundance associations, with the highest sampling consensus in LSCC. Together, these results highlight UVM, BLCA, and LSCC as cancer lineages where LMOD3 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 LMOD3 — synthetic lethality, tumor antigen, and pembrolizumab response.
This table summarizes LMOD3 survival associations across molecular data types. LMOD3 RNA expression shows survival associations in the most cancer types (27), followed by mutation status (6) and mass-spec protein abundance (1). The rightmost column indicates the cancer type with the highest sampling consensus for each molecular layer.
This table ranks reproducible LMOD3 RNA expression–survival associations across cancer types. High LMOD3 expression shows unfavorable associations in UVM, HNSC, KIRC, KICH and CESC, but favorable associations in LUAD. 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 LMOD3 RNA expression.
This table summarizes LMOD3 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 2. The strongest signals are observed in LUAD for RNA and HNSC for protein.
This table ranks reproducible tumor–normal expression differences for LMOD3. A negative fold-change indicates higher expression in normal tissue than in tumor tissue. LMOD3 shows lower tumor expression in BLCA, LUAD, HNSC, LUSC and KICH and higher tumor expression in COAD. The BLCA box plot shows higher LMOD3 RNA expression in normal versus tumor tissue (log2 FC = −2.188, t-test p < 0.001).
This table shows molecular features associated with LMOD3 in patient tissues and cancer cell lines. In patient samples, LMOD3 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, LMOD3 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 OVARY and LARGE_INTESTINE.
