Q-omics provides the consensus-scored LEMD3 profile across patient tissues and cancer cell-line models. LEMD3 expression is associated with patient survival in 26 of 34 cancer types, with the highest sampling consensus in KIRC. Among the 18 cancer types available for tumor–normal comparison, LEMD3 is differentially expressed in 10, with the highest sampling consensus in HNSC. Additionally, LEMD3 RNA expression shows 21,112 significant gene co-expression associations, with the highest sampling consensus in ACC. Together, these results highlight KIRC, HNSC, and ACC as cancer lineages where LEMD3 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 LEMD3 — synthetic lethality, tumor antigen, and pembrolizumab response.
This table summarizes LEMD3 survival associations across molecular data types. LEMD3 RNA expression shows survival associations in the most cancer types (26), followed by mutation status (6) and mass-spec protein abundance (6). The rightmost column indicates the cancer type with the highest sampling consensus for each molecular layer.
This table ranks reproducible LEMD3 RNA expression–survival associations across cancer types. High LEMD3 expression shows unfavorable associations in CESC, UVM, LIHC and HNSC, but favorable associations in KIRC and UCS. 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 LEMD3 RNA expression.
This table summarizes LEMD3 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 HNSC for RNA and COAD for protein.
This table ranks reproducible tumor–normal expression differences for LEMD3. A negative fold-change indicates higher expression in normal tissue than in tumor tissue. LEMD3 shows lower tumor expression in THCA and higher tumor expression in HNSC, STAD, LIHC, BLCA and CHOL. The HNSC box plot shows higher LEMD3 RNA expression in tumor versus normal tissue (log2 FC = +0.797, t-test p < 0.001).
This table shows molecular features associated with LEMD3 in patient tissues and cancer cell lines. In patient samples, LEMD3 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, LEMD3 RNA and mutation anchors are most strongly linked to RNA-expression features, especially in BLOOD_Leukemia, while CRISPR and shRNA rows add functional-dependency signals in BONE and LARGE_INTESTINE.
