Q-omics provides the consensus-scored MSL3 profile across patient tissues and cancer cell-line models. MSL3 expression is associated with patient survival in 27 of 34 cancer types, with the highest sampling consensus in BLCA. Among the 18 cancer types available for tumor–normal comparison, MSL3 is differentially expressed in 11, with the highest sampling consensus in KIRC. Additionally, MSL3 RNA expression shows 19,577 significant gene co-expression associations, with the highest sampling consensus in KIRP. Together, these results highlight BLCA, KIRC, and KIRP as cancer lineages where MSL3 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 MSL3 — synthetic lethality, tumor antigen, and pembrolizumab response.
This table summarizes MSL3 survival associations across molecular data types. MSL3 RNA expression shows survival associations in the most cancer types (27), followed by mutation status (3) 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 MSL3 RNA expression–survival associations across cancer types. High MSL3 expression shows unfavorable associations in LGG, LIHC and KIRP, but favorable associations in BLCA, SKCM and UCS. The BLCA Kaplan–Meier curve shows clear separation, with the low-expression group declining faster, consistent with the favorable association (log-rank p = .001). Together, the overview and detailed table identify BLCA as the clearest survival context for MSL3 RNA expression.
This table summarizes MSL3 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 5. The strongest signals are observed in KIRC for RNA and LSCC for protein.
This table ranks reproducible tumor–normal expression differences for MSL3. A negative fold-change indicates higher expression in normal tissue than in tumor tissue. MSL3 shows lower tumor expression in KICH and higher tumor expression in KIRC, COAD, LIHC, STAD and HNSC. The KIRC box plot shows higher MSL3 RNA expression in tumor versus normal tissue (log2 FC = +0.490, t-test p < 0.001).
This table shows molecular features associated with MSL3 in patient tissues and cancer cell lines. In patient samples, MSL3 shows the broadest associations at the RNA and protein expression levels, with KIRP recurring as the lineage with the largest associated feature set. In cancer cell lines, MSL3 RNA and mutation anchors are most strongly linked to RNA-expression features, especially in LIVER, while CRISPR and shRNA rows add functional-dependency signals in CNS and UPPER_AERODIGESTIVE_TRACT.
