Q-omics provides the consensus-scored GHSR profile across patient tissues and cancer cell-line models. GHSR expression is associated with patient survival in 12 of 34 cancer types, with the highest sampling consensus in CESC. Among the 18 cancer types available for tumor–normal comparison, GHSR is differentially expressed in 4, with the highest sampling consensus in HNSC. Additionally, GHSR RNA expression shows 6,189 significant pathway-activity associations, with the highest sampling consensus in STAD. Together, these results highlight CESC, HNSC, and STAD as cancer lineages where GHSR 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 GHSR — synthetic lethality, tumor antigen, and pembrolizumab response.
This table summarizes GHSR survival associations across molecular data types. GHSR RNA expression shows survival associations in the most cancer types (12), followed by mutation status (7) and 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 GHSR RNA expression–survival associations across cancer types. High GHSR expression shows unfavorable associations in CESC, KICH, HNSC, KIRP and STAD, but favorable associations in UCS. The CESC Kaplan–Meier curve shows clear separation, with the high-expression group declining faster, consistent with the unfavorable association (log-rank p = .001). Together, the overview and detailed table identify CESC as the clearest survival context for GHSR RNA expression.
This table summarizes GHSR tumor–normal expression differences by data type. RNA shows broader differences across cancer types, with a lineage consensus of 4. The strongest signals are observed in HNSC for RNA.
This table ranks reproducible tumor–normal expression differences for GHSR. A negative fold-change indicates higher expression in normal tissue than in tumor tissue. GHSR shows higher tumor expression in HNSC, LUSC, KIRC and UCEC. The HNSC box plot shows higher GHSR RNA expression in tumor versus normal tissue (log2 FC = +0.032, t-test p = .003).
This table shows molecular features associated with GHSR in patient tissues and cancer cell lines. In patient samples, GHSR shows the broadest associations at the RNA and protein expression levels, with STAD recurring as the lineage with the largest associated feature set. In cancer cell lines, GHSR RNA and mutation anchors are most strongly linked to RNA-expression features, especially in PANCREAS, while CRISPR and shRNA rows add functional-dependency signals in BLOOD_Lymphoma and BLOOD_Leukemia.
