Q-omics provides the consensus-scored TMIE profile across patient tissues and cancer cell-line models. TMIE expression is associated with patient survival in 25 of 34 cancer types, with the highest sampling consensus in KIRC. Among the 18 cancer types available for tumor–normal comparison, TMIE is differentially expressed in 14, with the highest sampling consensus in KIRP. Additionally, TMIE RNA expression shows 12,867 significant gene co-expression associations, with the highest sampling consensus in THYM. Together, these results highlight KIRC, KIRP, and THYM as cancer lineages where TMIE 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 TMIE — synthetic lethality, tumor antigen, and pembrolizumab response.
This table summarizes TMIE survival associations across molecular data types. TMIE RNA expression shows survival associations in the most cancer types (25), followed by mutation status (1) 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 TMIE RNA expression–survival associations across cancer types. High TMIE expression shows unfavorable associations in KIRC, MESO and UCEC, but favorable associations in SARC, UCS and STAD. The KIRC Kaplan–Meier curve shows clear separation, with the high-expression group declining faster, consistent with the unfavorable association (log-rank p = .003). Together, the overview and detailed table identify KIRC as the clearest survival context for TMIE RNA expression.
This table summarizes TMIE tumor–normal expression differences by data type. RNA shows broader differences across cancer types, with a lineage consensus of 14. The strongest signals are observed in HNSC for RNA.
This table ranks reproducible tumor–normal expression differences for TMIE. A negative fold-change indicates higher expression in normal tissue than in tumor tissue. TMIE shows lower tumor expression in KIRP, HNSC, LUAD, KIRC and BRCA and higher tumor expression in LIHC. The KIRP box plot shows higher TMIE RNA expression in normal versus tumor tissue (log2 FC = −0.719, t-test p < 0.001).
This table shows molecular features associated with TMIE in patient tissues and cancer cell lines. In patient samples, TMIE 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, TMIE 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 BLOOD_Lymphoma and LARGE_INTESTINE.
