Q-omics provides the consensus-scored GHR profile across patient tissues and cancer cell-line models. GHR expression is associated with patient survival in 27 of 34 cancer types, with the highest sampling consensus in KIRC. Among the 18 cancer types available for tumor–normal comparison, GHR is differentially expressed in 16, with the highest sampling consensus in THCA. Additionally, GHR RNA expression shows 19,121 significant gene co-expression associations, with the highest sampling consensus in THYM. Together, these results highlight KIRC, THCA, and THYM as cancer lineages where GHR 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 GHR — synthetic lethality, tumor antigen, and pembrolizumab response.
This table summarizes GHR survival associations across molecular data types. GHR RNA expression shows survival associations in the most cancer types (27), followed by mutation status (3). The rightmost column indicates the cancer type with the highest sampling consensus for each molecular layer.
This table ranks reproducible GHR RNA expression–survival associations across cancer types. High GHR expression shows unfavorable associations in BLCA, HNSC and THCA, but favorable associations in KIRC, MESO and LIHC. 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 GHR RNA expression.
This table summarizes GHR tumor–normal expression differences by data type. RNA shows broader differences across cancer types, with a lineage consensus of 16. The strongest signals are observed in THCA for RNA.
This table ranks reproducible tumor–normal expression differences for GHR. A negative fold-change indicates higher expression in normal tissue than in tumor tissue. GHR shows lower tumor expression in THCA, KIRP, LUAD, COAD, LIHC and STAD. The THCA box plot shows higher GHR RNA expression in normal versus tumor tissue (log2 FC = −2.270, t-test p < 0.001).
This table shows molecular features associated with GHR in patient tissues and cancer cell lines. In patient samples, GHR shows the broadest associations at the RNA and protein expression levels, with THYM recurring as the lineage with the largest associated feature set. In cancer cell lines, GHR RNA and mutation anchors are most strongly linked to RNA-expression features, especially in LIVER, while CRISPR and shRNA rows add functional-dependency signals in LARGE_INTESTINE and BONE.