Q-omics provides the consensus-scored CCT6B profile across patient tissues and cancer cell-line models. CCT6B expression is associated with patient survival in 25 of 34 cancer types, with the highest sampling consensus in COAD. Among the 18 cancer types available for tumor–normal comparison, CCT6B is differentially expressed in 10, with the highest sampling consensus in KICH. Additionally, CCT6B protein abundance shows 24,743 significant protein co-abundance associations, with the highest sampling consensus in CCRCC. Together, these results highlight COAD, KICH, and CCRCC as cancer lineages where CCT6B 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 CCT6B — synthetic lethality, tumor antigen, and pembrolizumab response.
This table summarizes CCT6B survival associations across molecular data types. CCT6B RNA expression shows survival associations in the most cancer types (25), followed by mutation status (2) and mass-spec protein abundance (9). The rightmost column indicates the cancer type with the highest sampling consensus for each molecular layer.
This table ranks reproducible CCT6B RNA expression–survival associations across cancer types. High CCT6B expression shows unfavorable associations in THCA, but favorable associations in COAD, KIRC, LIHC, READ and UCS. The COAD 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 COAD as the clearest survival context for CCT6B RNA expression.
This table summarizes CCT6B 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 10. The strongest signals are observed in KICH for RNA and CCRCC for protein.
This table ranks reproducible tumor–normal expression differences for CCT6B. A negative fold-change indicates higher expression in normal tissue than in tumor tissue. CCT6B shows lower tumor expression in KICH, THCA, KIRC, HNSC and KIRP and higher tumor expression in COAD. The KICH box plot shows higher CCT6B RNA expression in normal versus tumor tissue (log2 FC = −1.197, t-test p < 0.001).
This table shows molecular features associated with CCT6B in patient tissues and cancer cell lines. In patient samples, CCT6B shows the broadest associations at the RNA and protein expression levels, with CCRCC recurring as the lineage with the largest associated feature set. In cancer cell lines, CCT6B RNA and mutation anchors are most strongly linked to RNA-expression features, especially in URINARY_TRACT, while CRISPR and shRNA rows add functional-dependency signals in OESOPHAGUS and CNS.
