Q-omics provides the consensus-scored GHDC profile across patient tissues and cancer cell-line models. GHDC 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, GHDC is differentially expressed in 13, with the highest sampling consensus in KIRC. Additionally, GHDC protein abundance shows 22,160 significant protein co-abundance associations, with the highest sampling consensus in LUAD. Together, these results highlight KIRC, and LUAD as cancer lineages where GHDC 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 GHDC — synthetic lethality, tumor antigen, and pembrolizumab response.
This table summarizes GHDC survival associations across molecular data types. GHDC RNA expression shows survival associations in the most cancer types (26), followed by mutation status (4) and mass-spec protein abundance (4). The rightmost column indicates the cancer type with the highest sampling consensus for each molecular layer.
This table ranks reproducible GHDC RNA expression–survival associations across cancer types. High GHDC expression shows unfavorable associations in LIHC and UVM, but favorable associations in KIRC, READ, MESO and BRCA. 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 GHDC RNA expression.
This table summarizes GHDC 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 5. The strongest signals are observed in KIRC for RNA and LSCC for protein.
This table ranks reproducible tumor–normal expression differences for GHDC. A negative fold-change indicates higher expression in normal tissue than in tumor tissue. GHDC shows lower tumor expression in KICH and LUSC and higher tumor expression in KIRC, COAD, LIHC and CHOL. The KIRC box plot shows higher GHDC RNA expression in tumor versus normal tissue (log2 FC = +0.645, t-test p < 0.001).
This table shows molecular features associated with GHDC in patient tissues and cancer cell lines. In patient samples, GHDC shows the broadest associations at the RNA and protein expression levels, with LUAD recurring as the lineage with the largest associated feature set. In cancer cell lines, GHDC 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 LUNG_NSCLC_LUAD and UPPER_AERODIGESTIVE_TRACT.
