Q-omics provides the consensus-scored MUL1 profile across patient tissues and cancer cell-line models. MUL1 expression is associated with patient survival in 23 of 34 cancer types, with the highest sampling consensus in HNSC. Among the 18 cancer types available for tumor–normal comparison, MUL1 is differentially expressed in 15, with the highest sampling consensus in COAD. Additionally, MUL1 RNA expression shows 18,315 significant gene co-expression associations, with the highest sampling consensus in ACC. Together, these results highlight HNSC, COAD, and ACC as cancer lineages where MUL1 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 MUL1 — synthetic lethality, tumor antigen, and pembrolizumab response.
This table summarizes MUL1 survival associations across molecular data types. MUL1 RNA expression shows survival associations in the most cancer types (23), followed by mutation status (1) 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 MUL1 RNA expression–survival associations across cancer types. High MUL1 expression shows unfavorable associations in HNSC, LGG, OV, KICH and LUSC, but favorable associations in KIRC. The HNSC 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 HNSC as the clearest survival context for MUL1 RNA expression.
This table summarizes MUL1 tumor–normal expression differences by data type. RNA shows broader differences across cancer types, with a lineage consensus of 15, while mass-spec protein shows differences in 3. The strongest signals are observed in COAD for RNA and HNSC for protein.
This table ranks reproducible tumor–normal expression differences for MUL1. A negative fold-change indicates higher expression in normal tissue than in tumor tissue. MUL1 shows lower tumor expression in COAD, THCA, KIRC and LUAD and higher tumor expression in HNSC and LIHC. The COAD box plot shows higher MUL1 RNA expression in normal versus tumor tissue (log2 FC = −0.838, t-test p < 0.001).
This table shows molecular features associated with MUL1 in patient tissues and cancer cell lines. In patient samples, MUL1 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, MUL1 RNA and mutation anchors are most strongly linked to RNA-expression features, especially in UPPER_AERODIGESTIVE_TRACT, while CRISPR and shRNA rows add functional-dependency signals in SKIN and LARGE_INTESTINE.
