Q-omics provides the consensus-scored MYO1G profile across patient tissues and cancer cell-line models. MYO1G expression is associated with patient survival in 24 of 34 cancer types, with the highest sampling consensus in HNSC. Among the 18 cancer types available for tumor–normal comparison, MYO1G is differentially expressed in 12, with the highest sampling consensus in KIRC. Additionally, MYO1G protein abundance shows 28,342 significant protein co-abundance associations, with the highest sampling consensus in LSCC. Together, these results highlight HNSC, KIRC, and LSCC as cancer lineages where MYO1G 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 MYO1G — synthetic lethality, tumor antigen, and pembrolizumab response.
This table summarizes MYO1G survival associations across molecular data types. MYO1G RNA expression shows survival associations in the most cancer types (24), followed by mutation status (4) 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 MYO1G RNA expression–survival associations across cancer types. High MYO1G expression shows unfavorable associations in UVM and LUSC, but favorable associations in HNSC, SKCM, UCEC and CESC. The HNSC 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 HNSC as the clearest survival context for MYO1G RNA expression.
This table summarizes MYO1G tumor–normal expression differences by data type. RNA shows broader differences across cancer types, with a lineage consensus of 12, while mass-spec protein shows differences in 5. The strongest signals are observed in KIRC for RNA and CCRCC for protein.
This table ranks reproducible tumor–normal expression differences for MYO1G. A negative fold-change indicates higher expression in normal tissue than in tumor tissue. MYO1G shows lower tumor expression in LUSC and higher tumor expression in KIRC, HNSC, THCA, KIRP and STAD. The KIRC box plot shows higher MYO1G RNA expression in tumor versus normal tissue (log2 FC = +2.209, t-test p < 0.001).
This table shows molecular features associated with MYO1G in patient tissues and cancer cell lines. In patient samples, MYO1G shows the broadest associations at the RNA and protein expression levels, with LSCC recurring as the lineage with the largest associated feature set. In cancer cell lines, MYO1G 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 BREAST and BLOOD_Lymphoma.
