Q-omics provides the consensus-scored TRIM68 profile across patient tissues and cancer cell-line models. TRIM68 expression is associated with patient survival in 30 of 34 cancer types, with the highest sampling consensus in KIRC. Among the 18 cancer types available for tumor–normal comparison, TRIM68 is differentially expressed in 13, with the highest sampling consensus in KIRC. Additionally, TRIM68 RNA expression shows 20,105 significant gene co-expression associations, with the highest sampling consensus in THYM. Together, these results highlight KIRC, and THYM as cancer lineages where TRIM68 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 TRIM68 — synthetic lethality, tumor antigen, and pembrolizumab response.
This table summarizes TRIM68 survival associations across molecular data types. TRIM68 RNA expression shows survival associations in the most cancer types (30), followed by mutation status (8) and mass-spec protein abundance (5). The rightmost column indicates the cancer type with the highest sampling consensus for each molecular layer.
This table ranks reproducible TRIM68 RNA expression–survival associations across cancer types. High TRIM68 expression shows unfavorable associations in BLCA, but favorable associations in KIRC, HNSC, UCS, SCLC and MESO. The KIRC 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 KIRC as the clearest survival context for TRIM68 RNA expression.
This table summarizes TRIM68 tumor–normal expression differences by data type. RNA shows broader differences across cancer types, with a lineage consensus of 13, while mass-spec protein shows differences in 4. The strongest signals are observed in KIRC for RNA and LSCC for protein.
This table ranks reproducible tumor–normal expression differences for TRIM68. A negative fold-change indicates higher expression in normal tissue than in tumor tissue. TRIM68 shows lower tumor expression in KIRC, THCA and BRCA and higher tumor expression in LIHC, CHOL and COAD. The KIRC box plot shows higher TRIM68 RNA expression in normal versus tumor tissue (log2 FC = −0.727, t-test p < 0.001).
This table shows molecular features associated with TRIM68 in patient tissues and cancer cell lines. In patient samples, TRIM68 shows the broadest associations at the RNA and protein expression levels, with THYM recurring as the lineage with the largest associated feature set. In cancer cell lines, TRIM68 RNA and mutation anchors are most strongly linked to RNA-expression features, especially in KIDNEY, while CRISPR and shRNA rows add functional-dependency signals in BREAST and BLOOD_Leukemia.
