Q-omics provides the consensus-scored GHRL profile across patient tissues and cancer cell-line models. GHRL expression is associated with patient survival in 27 of 34 cancer types, with the highest sampling consensus in HNSC. Among the 18 cancer types available for tumor–normal comparison, GHRL is differentially expressed in 10, with the highest sampling consensus in LUSC. Additionally, GHRL RNA expression shows 14,840 significant gene co-expression associations, with the highest sampling consensus in TGCT. Together, these results highlight HNSC, LUSC, and TGCT as cancer lineages where GHRL 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 GHRL — synthetic lethality, tumor antigen, and pembrolizumab response.
This table summarizes GHRL survival associations across molecular data types. GHRL RNA expression shows survival associations in the most cancer types (27), 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 GHRL RNA expression–survival associations across cancer types. High GHRL expression shows favorable associations in HNSC, LUAD, UVM, BLCA, UCS and SKCM. The HNSC 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 HNSC as the clearest survival context for GHRL RNA expression.
This table summarizes GHRL tumor–normal expression differences by data type. RNA shows broader differences across cancer types, with a lineage consensus of 10, while mass-spec protein shows differences in 2. The strongest signals are observed in LUSC for RNA and PDAC for protein.
This table ranks reproducible tumor–normal expression differences for GHRL. A negative fold-change indicates higher expression in normal tissue than in tumor tissue. GHRL shows lower tumor expression in LUSC, KICH, THCA, LUAD and STAD and higher tumor expression in KIRC. The LUSC box plot shows higher GHRL RNA expression in normal versus tumor tissue (log2 FC = −0.772, t-test p < 0.001).
This table shows molecular features associated with GHRL in patient tissues and cancer cell lines. In patient samples, GHRL shows the broadest associations at the RNA and protein expression levels, with TGCT recurring as the lineage with the largest associated feature set. In cancer cell lines, GHRL RNA and mutation anchors are most strongly linked to RNA-expression features, especially in BLOOD_Leukemia, while CRISPR and shRNA rows add functional-dependency signals in SOFT_TISSUE and LIVER.
