Q-omics provides the consensus-scored CEP68 profile across patient tissues and cancer cell-line models. CEP68 expression is associated with patient survival in 24 of 34 cancer types, with the highest sampling consensus in KIRC. Among the 18 cancer types available for tumor–normal comparison, CEP68 is differentially expressed in 12, with the highest sampling consensus in THCA. Additionally, CEP68 protein abundance shows 33,918 significant protein co-abundance associations, with the highest sampling consensus in GBM. Together, these results highlight KIRC, THCA, and GBM as cancer lineages where CEP68 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 CEP68 — synthetic lethality, tumor antigen, and pembrolizumab response.
This table summarizes CEP68 survival associations across molecular data types. CEP68 RNA expression shows survival associations in the most cancer types (24), followed by mutation status (5) and mass-spec protein abundance (6). The rightmost column indicates the cancer type with the highest sampling consensus for each molecular layer.
This table ranks reproducible CEP68 RNA expression–survival associations across cancer types. High CEP68 expression shows unfavorable associations in ACC and LIHC, but favorable associations in KIRC, HNSC, UCS and LGG. 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 CEP68 RNA expression.
This table summarizes CEP68 tumor–normal expression differences by data type. RNA shows broader differences across cancer types, with a lineage consensus of 12, while mass-spec protein shows differences in 7. The strongest signals are observed in THCA for RNA and HNSC for protein.
This table ranks reproducible tumor–normal expression differences for CEP68. A negative fold-change indicates higher expression in normal tissue than in tumor tissue. CEP68 shows lower tumor expression in THCA, BLCA, KICH, UCEC and BRCA and higher tumor expression in LIHC. The THCA box plot shows higher CEP68 RNA expression in normal versus tumor tissue (log2 FC = −1.009, t-test p < 0.001).
This table shows molecular features associated with CEP68 in patient tissues and cancer cell lines. In patient samples, CEP68 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, CEP68 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 KIDNEY and BLOOD_Leukemia.
