Q-omics provides the consensus-scored TDRKH profile across patient tissues and cancer cell-line models. TDRKH expression is associated with patient survival in 25 of 34 cancer types, with the highest sampling consensus in KIRP. Among the 18 cancer types available for tumor–normal comparison, TDRKH is differentially expressed in 14, with the highest sampling consensus in LUAD. Additionally, TDRKH RNA expression shows 19,957 significant gene co-expression associations, with the highest sampling consensus in KIRP. Together, these results highlight KIRP, and LUAD as cancer lineages where TDRKH 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 TDRKH — synthetic lethality, tumor antigen, and pembrolizumab response.
This table summarizes TDRKH survival associations across molecular data types. TDRKH RNA expression shows survival associations in the most cancer types (25), followed by mutation status (5) 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 TDRKH RNA expression–survival associations across cancer types. High TDRKH expression shows unfavorable associations in KIRP, ACC, BLCA and LUSC, but favorable associations in LUAD and KIRC. The KIRP Kaplan–Meier curve shows clear separation, with the high-expression group declining faster, consistent with the unfavorable association (log-rank p = .002). Together, the overview and detailed table identify KIRP as the clearest survival context for TDRKH RNA expression.
This table summarizes TDRKH tumor–normal expression differences by data type. RNA shows broader differences across cancer types, with a lineage consensus of 14, while mass-spec protein shows differences in 3. The strongest signals are observed in LUAD for RNA and LUAD for protein.
This table ranks reproducible tumor–normal expression differences for TDRKH. A negative fold-change indicates higher expression in normal tissue than in tumor tissue. TDRKH shows lower tumor expression in KICH and higher tumor expression in LUAD, HNSC, BLCA, COAD and LIHC. The LUAD box plot shows higher TDRKH RNA expression in tumor versus normal tissue (log2 FC = +1.353, t-test p < 0.001).
This table shows molecular features associated with TDRKH in patient tissues and cancer cell lines. In patient samples, TDRKH shows the broadest associations at the RNA and protein expression levels, with KIRP recurring as the lineage with the largest associated feature set. In cancer cell lines, TDRKH 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 SOFT_TISSUE and BLOOD_Leukemia.
