Q-omics provides the consensus-scored CCNH profile across patient tissues and cancer cell-line models. CCNH expression is associated with patient survival in 27 of 34 cancer types, with the highest sampling consensus in OV. Among the 18 cancer types available for tumor–normal comparison, CCNH is differentially expressed in 11, with the highest sampling consensus in KIRC. Additionally, CCNH protein abundance shows 24,260 significant protein co-abundance associations, with the highest sampling consensus in GBM. Together, these results highlight OV, KIRC, and GBM as cancer lineages where CCNH 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 CCNH — synthetic lethality, tumor antigen, and pembrolizumab response.
This table summarizes CCNH survival associations across molecular data types. CCNH RNA expression shows survival associations in the most cancer types (27), followed by mutation status (5) and mass-spec protein abundance (7). The rightmost column indicates the cancer type with the highest sampling consensus for each molecular layer.
This table ranks reproducible CCNH RNA expression–survival associations across cancer types. High CCNH expression shows unfavorable associations in OV, UVM, KIRP, HNSC and ESCA, but favorable associations in KIRC. The OV Kaplan–Meier curve shows clear separation, with the high-expression group declining faster, consistent with the unfavorable association (log-rank p < 0.001). Together, the overview and detailed table identify OV as the clearest survival context for CCNH RNA expression.
This table summarizes CCNH tumor–normal expression differences by data type. RNA shows broader differences across cancer types, with a lineage consensus of 11, while mass-spec protein shows differences in 6. The strongest signals are observed in KIRC for RNA and HNSC for protein.
This table ranks reproducible tumor–normal expression differences for CCNH. A negative fold-change indicates higher expression in normal tissue than in tumor tissue. CCNH shows lower tumor expression in LUSC, KICH and BRCA and higher tumor expression in KIRC, COAD and READ. The KIRC box plot shows higher CCNH RNA expression in tumor versus normal tissue (log2 FC = +0.233, t-test p < 0.001).
This table shows molecular features associated with CCNH in patient tissues and cancer cell lines. In patient samples, CCNH shows the broadest associations at the RNA and protein expression levels, with GBM recurring as the lineage with the largest associated feature set. In cancer cell lines, CCNH RNA and mutation anchors are most strongly linked to RNA-expression features, especially in LUNG_SCLC, while CRISPR and shRNA rows add functional-dependency signals in UPPER_AERODIGESTIVE_TRACT and LARGE_INTESTINE.
