Q-omics provides the consensus-scored TSFM profile across patient tissues and cancer cell-line models. TSFM expression is associated with patient survival in 21 of 34 cancer types, with the highest sampling consensus in UVM. Among the 18 cancer types available for tumor–normal comparison, TSFM is differentially expressed in 15, with the highest sampling consensus in HNSC. Additionally, TSFM protein abundance shows 25,977 significant protein co-abundance associations, with the highest sampling consensus in LSCC. Together, these results highlight UVM, HNSC, and LSCC as cancer lineages where TSFM 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 TSFM — synthetic lethality, tumor antigen, and pembrolizumab response.
This table summarizes TSFM survival associations across molecular data types. TSFM RNA expression shows survival associations in the most cancer types (21), followed by mutation status (2) and mass-spec protein abundance (9). The rightmost column indicates the cancer type with the highest sampling consensus for each molecular layer.
This table ranks reproducible TSFM RNA expression–survival associations across cancer types. High TSFM expression shows unfavorable associations in UVM, LIHC, LUAD, HNSC, UCS and SKCM. The UVM 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 UVM as the clearest survival context for TSFM RNA expression.
This table summarizes TSFM 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 8. The strongest signals are observed in HNSC for RNA and CCRCC for protein.
This table ranks reproducible tumor–normal expression differences for TSFM. A negative fold-change indicates higher expression in normal tissue than in tumor tissue. TSFM shows higher tumor expression in HNSC, STAD, LUAD, BLCA, LUSC and COAD. The HNSC box plot shows higher TSFM RNA expression in tumor versus normal tissue (log2 FC = +0.561, t-test p < 0.001).
This table shows molecular features associated with TSFM in patient tissues and cancer cell lines. In patient samples, TSFM 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, TSFM RNA and mutation anchors are most strongly linked to RNA-expression features, especially in LARGE_INTESTINE, while CRISPR and shRNA rows add functional-dependency signals in PANCREAS and BLOOD_Lymphoma.
