Q-omics provides the consensus-scored MYL5 profile across patient tissues and cancer cell-line models. MYL5 expression is associated with patient survival in 24 of 34 cancer types, with the highest sampling consensus in COAD. Among the 18 cancer types available for tumor–normal comparison, MYL5 is differentially expressed in 10, with the highest sampling consensus in KIRC. Additionally, MYL5 RNA expression shows 17,166 significant gene co-expression associations, with the highest sampling consensus in THYM. Together, these results highlight COAD, KIRC, and THYM as cancer lineages where MYL5 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 MYL5 — synthetic lethality, tumor antigen, and pembrolizumab response.
This table summarizes MYL5 survival associations across molecular data types. MYL5 RNA expression shows survival associations in the most cancer types (24), followed by mutation status (3) 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 MYL5 RNA expression–survival associations across cancer types. High MYL5 expression shows unfavorable associations in COAD, UVM, ACC and LGG, but favorable associations in SKCM and BRCA. The COAD 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 COAD as the clearest survival context for MYL5 RNA expression.
This table summarizes MYL5 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 1. The strongest signals are observed in KIRC for RNA and HNSC for protein.
This table ranks reproducible tumor–normal expression differences for MYL5. A negative fold-change indicates higher expression in normal tissue than in tumor tissue. MYL5 shows lower tumor expression in HNSC, KICH and THCA and higher tumor expression in KIRC, LIHC and KIRP. The KIRC box plot shows higher MYL5 RNA expression in tumor versus normal tissue (log2 FC = +0.841, t-test p < 0.001).
This table shows molecular features associated with MYL5 in patient tissues and cancer cell lines. In patient samples, MYL5 shows the broadest associations at the RNA and protein expression levels, with THYM recurring as the lineage with the largest associated feature set. In cancer cell lines, MYL5 RNA and mutation anchors are most strongly linked to RNA-expression features, especially in PANCREAS, while CRISPR and shRNA rows add functional-dependency signals in BREAST and UPPER_AERODIGESTIVE_TRACT.
