Q-omics provides the consensus-scored TRIM67 profile across patient tissues and cancer cell-line models. TRIM67 expression is associated with patient survival in 24 of 34 cancer types, with the highest sampling consensus in UVM. Among the 18 cancer types available for tumor–normal comparison, TRIM67 is differentially expressed in 11, with the highest sampling consensus in HNSC. Additionally, TRIM67 RNA expression shows 16,638 significant gene co-expression associations, with the highest sampling consensus in UVM. Together, these results highlight UVM, and HNSC as cancer lineages where TRIM67 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 TRIM67 — synthetic lethality, tumor antigen, and pembrolizumab response.
This table summarizes TRIM67 survival associations across molecular data types. TRIM67 RNA expression shows survival associations in the most cancer types (24), followed by mutation status (5) and mass-spec protein abundance (2). The rightmost column indicates the cancer type with the highest sampling consensus for each molecular layer.
This table ranks reproducible TRIM67 RNA expression–survival associations across cancer types. High TRIM67 expression shows unfavorable associations in UVM, KICH, COAD and BRCA, but favorable associations in PAAD and LGG. 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 TRIM67 RNA expression.
This table summarizes TRIM67 tumor–normal expression differences by data type. RNA shows broader differences across cancer types, with a lineage consensus of 11, while mass-spec protein shows differences in 2. The strongest signals are observed in HNSC for RNA and COAD for protein.
This table ranks reproducible tumor–normal expression differences for TRIM67. A negative fold-change indicates higher expression in normal tissue than in tumor tissue. TRIM67 shows lower tumor expression in COAD and higher tumor expression in HNSC, LUAD, LIHC, BRCA and LUSC. The HNSC box plot shows higher TRIM67 RNA expression in tumor versus normal tissue (log2 FC = +0.040, t-test p < 0.001).
This table shows molecular features associated with TRIM67 in patient tissues and cancer cell lines. In patient samples, TRIM67 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, TRIM67 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 LARGE_INTESTINE and BLOOD_Leukemia.