Q-omics provides the consensus-scored TRHDE profile across patient tissues and cancer cell-line models. TRHDE 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, TRHDE is differentially expressed in 13, with the highest sampling consensus in COAD. Additionally, TRHDE RNA expression shows 20,053 significant protein co-abundance associations, with the highest sampling consensus in GBM. Together, these results highlight KIRC, COAD, and GBM as cancer lineages where TRHDE 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 TRHDE — synthetic lethality, tumor antigen, and pembrolizumab response.
This table summarizes TRHDE survival associations across molecular data types. TRHDE RNA expression shows survival associations in the most cancer types (26), followed by mutation status (8) 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 TRHDE RNA expression–survival associations across cancer types. High TRHDE expression shows unfavorable associations in UCEC, UVM, LUSC, MESO and DLBC, but favorable associations in KIRC. 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 TRHDE RNA expression.
This table summarizes TRHDE 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 2. The strongest signals are observed in COAD for RNA and CCRCC for protein.
This table ranks reproducible tumor–normal expression differences for TRHDE. A negative fold-change indicates higher expression in normal tissue than in tumor tissue. TRHDE shows lower tumor expression in COAD, LUAD, BRCA, LUSC, THCA and UCEC. The COAD box plot shows higher TRHDE RNA expression in normal versus tumor tissue (log2 FC = −1.259, t-test p < 0.001).
This table shows molecular features associated with TRHDE in patient tissues and cancer cell lines. In patient samples, TRHDE shows the broadest associations at the RNA and protein expression levels, with GBM recurring as the lineage with the largest associated feature set. In cancer cell lines, TRHDE RNA and mutation anchors are most strongly linked to RNA-expression features, especially in OVARY, while CRISPR and shRNA rows add functional-dependency signals in LARGE_INTESTINE and SOFT_TISSUE.
