Q-omics provides the consensus-scored MYO1A profile across patient tissues and cancer cell-line models. MYO1A expression is associated with patient survival in 24 of 34 cancer types, with the highest sampling consensus in SKCM. Among the 18 cancer types available for tumor–normal comparison, MYO1A is differentially expressed in 13, with the highest sampling consensus in KIRC. Additionally, MYO1A RNA expression shows 14,217 significant gene co-expression associations, with the highest sampling consensus in ESCA. Together, these results highlight SKCM, KIRC, and ESCA as cancer lineages where MYO1A 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 MYO1A — synthetic lethality, tumor antigen, and pembrolizumab response.
This table summarizes MYO1A survival associations across molecular data types. MYO1A RNA expression shows survival associations in the most cancer types (24), followed by mutation status (7) and mass-spec protein abundance (4). The rightmost column indicates the cancer type with the highest sampling consensus for each molecular layer.
This table ranks reproducible MYO1A RNA expression–survival associations across cancer types. High MYO1A expression shows unfavorable associations in ACC, GBM and LUAD, but favorable associations in SKCM, CESC and OV. The SKCM 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 SKCM as the clearest survival context for MYO1A RNA expression.
This table summarizes MYO1A tumor–normal expression differences by data type. RNA shows broader differences across cancer types, with a lineage consensus of 13, while mass-spec protein shows differences in 3. The strongest signals are observed in KIRC for RNA and COAD for protein.
This table ranks reproducible tumor–normal expression differences for MYO1A. A negative fold-change indicates higher expression in normal tissue than in tumor tissue. MYO1A shows lower tumor expression in COAD and LUSC and higher tumor expression in KIRC, THCA, KIRP and LIHC. The KIRC box plot shows higher MYO1A RNA expression in tumor versus normal tissue (log2 FC = +0.337, t-test p < 0.001).
This table shows molecular features associated with MYO1A in patient tissues and cancer cell lines. In patient samples, MYO1A shows the broadest associations at the RNA and protein expression levels, with ESCA recurring as the lineage with the largest associated feature set. In cancer cell lines, MYO1A RNA and mutation anchors are most strongly linked to RNA-expression features, especially in OESOPHAGUS, while CRISPR and shRNA rows add functional-dependency signals in CNS and LARGE_INTESTINE.
