Q-omics provides the consensus-scored TUFM profile across patient tissues and cancer cell-line models. TUFM expression is associated with patient survival in 26 of 34 cancer types, with the highest sampling consensus in SKCM. Among the 18 cancer types available for tumor–normal comparison, TUFM is differentially expressed in 15, with the highest sampling consensus in BLCA. Additionally, TUFM protein abundance shows 19,851 significant protein co-abundance associations, with the highest sampling consensus in LSCC. Together, these results highlight SKCM, BLCA, and LSCC as cancer lineages where TUFM 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 TUFM — synthetic lethality, tumor antigen, and pembrolizumab response.
This table summarizes TUFM survival associations across molecular data types. TUFM RNA expression shows survival associations in the most cancer types (26), 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 TUFM RNA expression–survival associations across cancer types. High TUFM expression shows unfavorable associations in SKCM, UVM, LGG, UCS and ACC, but favorable associations in BRCA. The SKCM 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 SKCM as the clearest survival context for TUFM RNA expression.
This table summarizes TUFM 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 6. The strongest signals are observed in BLCA for RNA and CCRCC for protein.
This table ranks reproducible tumor–normal expression differences for TUFM. A negative fold-change indicates higher expression in normal tissue than in tumor tissue. TUFM shows higher tumor expression in BLCA, COAD, STAD, LIHC, LUAD and KIRP. The BLCA box plot shows higher TUFM RNA expression in tumor versus normal tissue (log2 FC = +1.005, t-test p < 0.001).
This table shows molecular features associated with TUFM in patient tissues and cancer cell lines. In patient samples, TUFM 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, TUFM RNA and mutation anchors are most strongly linked to RNA-expression features, especially in OVARY, while CRISPR and shRNA rows add functional-dependency signals in LARGE_INTESTINE and UPPER_AERODIGESTIVE_TRACT.
