Q-omics provides the consensus-scored TCAF2 profile across patient tissues and cancer cell-line models. TCAF2 expression is associated with patient survival in 25 of 34 cancer types, with the highest sampling consensus in SKCM. Among the 18 cancer types available for tumor–normal comparison, TCAF2 is differentially expressed in 7, with the highest sampling consensus in KIRC. Additionally, TCAF2 RNA expression shows 18,574 significant gene co-expression associations, with the highest sampling consensus in UVM. Together, these results highlight SKCM, KIRC, and UVM as cancer lineages where TCAF2 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 TCAF2 — synthetic lethality, tumor antigen, and pembrolizumab response.
This table summarizes TCAF2 survival associations across molecular data types. TCAF2 RNA expression shows survival associations in the most cancer types (25), 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 TCAF2 RNA expression–survival associations across cancer types. High TCAF2 expression shows unfavorable associations in KIRP and LGG, but favorable associations in SKCM, ESCA, LUAD and LUSC. The SKCM 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 SKCM as the clearest survival context for TCAF2 RNA expression.
This table summarizes TCAF2 tumor–normal expression differences by data type. RNA shows broader differences across cancer types, with a lineage consensus of 7, while mass-spec protein shows differences in 2. The strongest signals are observed in KIRC for RNA and CCRCC for protein.
This table ranks reproducible tumor–normal expression differences for TCAF2. A negative fold-change indicates higher expression in normal tissue than in tumor tissue. TCAF2 shows lower tumor expression in UCEC, KICH and THCA and higher tumor expression in KIRC, HNSC and BLCA. The KIRC box plot shows higher TCAF2 RNA expression in tumor versus normal tissue (log2 FC = +1.442, t-test p < 0.001).
This table shows molecular features associated with TCAF2 in patient tissues and cancer cell lines. In patient samples, TCAF2 shows the broadest associations at the RNA and protein expression levels, with UVM recurring as the lineage with the largest associated feature set. In cancer cell lines, TCAF2 RNA and mutation anchors are most strongly linked to RNA-expression features, especially in LIVER, while CRISPR and shRNA rows add functional-dependency signals in LARGE_INTESTINE and BLOOD_Lymphoma.
