Q-omics provides the consensus-scored CRH profile across patient tissues and cancer cell-line models. CRH expression is associated with patient survival in 16 of 34 cancer types, with the highest sampling consensus in KIRC. Among the 18 cancer types available for tumor–normal comparison, CRH is differentially expressed in 6, with the highest sampling consensus in KIRC. Additionally, CRH RNA expression shows 9,257 significant gene co-expression associations, with the highest sampling consensus in TGCT. Together, these results highlight KIRC, and TGCT as cancer lineages where CRH 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 CRH — synthetic lethality, tumor antigen, and pembrolizumab response.
This table summarizes CRH survival associations across molecular data types. CRH RNA expression shows survival associations in the most cancer types (16), followed by mutation status (2) 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 CRH RNA expression–survival associations across cancer types. High CRH expression shows unfavorable associations in KIRC, DLBC, CESC, LUSC and HNSC, but favorable associations in OV. The KIRC Kaplan–Meier curve shows clear separation, with the high-expression group declining faster, consistent with the unfavorable association (log-rank p = .006). Together, the overview and detailed table identify KIRC as the clearest survival context for CRH RNA expression.
This table summarizes CRH tumor–normal expression differences by data type. RNA shows broader differences across cancer types, with a lineage consensus of 6, while mass-spec protein shows differences in 1. The strongest signals are observed in KIRC for RNA and PDAC for protein.
This table ranks reproducible tumor–normal expression differences for CRH. A negative fold-change indicates higher expression in normal tissue than in tumor tissue. CRH shows lower tumor expression in KIRC, LUAD, LUSC and KIRP and higher tumor expression in THCA and KICH. The KIRC box plot shows higher CRH RNA expression in normal versus tumor tissue (log2 FC = −0.201, t-test p < 0.001).
This table shows molecular features associated with CRH in patient tissues and cancer cell lines. In patient samples, CRH 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, CRH 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 SKIN and CNS.
