Q-omics provides the consensus-scored TRIM50 profile across patient tissues and cancer cell-line models. TRIM50 expression is associated with patient survival in 24 of 34 cancer types, with the highest sampling consensus in LUAD. Among the 18 cancer types available for tumor–normal comparison, TRIM50 is differentially expressed in 15, with the highest sampling consensus in KIRP. Additionally, TRIM50 RNA expression shows 11,242 significant gene co-expression associations, with the highest sampling consensus in SARC. Together, these results highlight LUAD, KIRP, and SARC as cancer lineages where TRIM50 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 TRIM50 — synthetic lethality, tumor antigen, and pembrolizumab response.
This table summarizes TRIM50 survival associations across molecular data types. TRIM50 RNA expression shows survival associations in the most cancer types (24), followed by mutation status (5). The rightmost column indicates the cancer type with the highest sampling consensus for each molecular layer.
This table ranks reproducible TRIM50 RNA expression–survival associations across cancer types. High TRIM50 expression shows unfavorable associations in STAD and READ, but favorable associations in LUAD, ACC, KIRP and HNSC. The LUAD 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 LUAD as the clearest survival context for TRIM50 RNA expression.
This table summarizes TRIM50 tumor–normal expression differences by data type. RNA shows broader differences across cancer types, with a lineage consensus of 15. The strongest signals are observed in KIRC for RNA.
This table ranks reproducible tumor–normal expression differences for TRIM50. A negative fold-change indicates higher expression in normal tissue than in tumor tissue. TRIM50 shows lower tumor expression in KIRP, KIRC, THCA, LUSC and STAD and higher tumor expression in KICH. The KIRP box plot shows higher TRIM50 RNA expression in normal versus tumor tissue (log2 FC = −2.191, t-test p < 0.001).
This table shows molecular features associated with TRIM50 in patient tissues and cancer cell lines. In patient samples, TRIM50 shows the broadest associations at the RNA and protein expression levels, with SARC recurring as the lineage with the largest associated feature set. In cancer cell lines, TRIM50 RNA and mutation anchors are most strongly linked to RNA-expression features, especially in LUNG_SCLC, while CRISPR and shRNA rows add functional-dependency signals in BONE and CNS.
