Q-omics provides the consensus-scored TRIQK profile across patient tissues and cancer cell-line models. TRIQK expression is associated with patient survival in 26 of 34 cancer types, with the highest sampling consensus in KIRC. Among the 18 cancer types available for tumor–normal comparison, TRIQK is differentially expressed in 13, with the highest sampling consensus in HNSC. Additionally, TRIQK RNA expression shows 19,819 significant gene co-expression associations, with the highest sampling consensus in UVM. Together, these results highlight KIRC, HNSC, and UVM as cancer lineages where TRIQK 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 TRIQK — synthetic lethality, tumor antigen, and pembrolizumab response.
This table summarizes TRIQK survival associations across molecular data types. TRIQK RNA expression shows survival associations in the most cancer types (26), followed by mass-spec protein abundance (1). The rightmost column indicates the cancer type with the highest sampling consensus for each molecular layer.
This table ranks reproducible TRIQK RNA expression–survival associations across cancer types. High TRIQK expression shows unfavorable associations in LUSC, UVM, KIRP and STAD, but favorable associations in KIRC 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 TRIQK RNA expression.
This table summarizes TRIQK 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 1. The strongest signals are observed in HNSC for RNA and LSCC for protein.
This table ranks reproducible tumor–normal expression differences for TRIQK. A negative fold-change indicates higher expression in normal tissue than in tumor tissue. TRIQK shows lower tumor expression in THCA, KICH and LUSC and higher tumor expression in HNSC, KIRP and KIRC. The HNSC box plot shows higher TRIQK RNA expression in tumor versus normal tissue (log2 FC = +0.820, t-test p < 0.001).
This table shows molecular features associated with TRIQK in patient tissues and cancer cell lines. In patient samples, TRIQK 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, TRIQK RNA and mutation anchors are most strongly linked to RNA-expression features, especially in URINARY_TRACT, while CRISPR and shRNA rows add functional-dependency signals in UPPER_AERODIGESTIVE_TRACT and BLOOD_Leukemia.
