Q-omics provides the consensus-scored CENPF profile across patient tissues and cancer cell-line models. CENPF expression is associated with patient survival in 29 of 34 cancer types, with the highest sampling consensus in KIRP. Among the 18 cancer types available for tumor–normal comparison, CENPF is differentially expressed in 17, with the highest sampling consensus in BLCA. Additionally, CENPF protein abundance shows 35,437 significant protein co-abundance associations, with the highest sampling consensus in LSCC. Together, these results highlight KIRP, BLCA, and LSCC as cancer lineages where CENPF 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 CENPF — synthetic lethality, tumor antigen, and pembrolizumab response.
This table summarizes CENPF survival associations across molecular data types. CENPF RNA expression shows survival associations in the most cancer types (29), followed by mutation status (7) and mass-spec protein abundance (11). The rightmost column indicates the cancer type with the highest sampling consensus for each molecular layer.
This table ranks reproducible CENPF RNA expression–survival associations across cancer types. High CENPF expression shows unfavorable associations in KIRP, ACC, MESO, LIHC, KIRC and KICH. The KIRP 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 KIRP as the clearest survival context for CENPF RNA expression.
This table summarizes CENPF tumor–normal expression differences by data type. RNA shows broader differences across cancer types, with a lineage consensus of 17, while mass-spec protein shows differences in 10. The strongest signals are observed in KIRC for RNA and CCRCC for protein.
This table ranks reproducible tumor–normal expression differences for CENPF. A negative fold-change indicates higher expression in normal tissue than in tumor tissue. CENPF shows higher tumor expression in BLCA, HNSC, KIRC, KIRP, STAD and LUSC. The BLCA box plot shows higher CENPF RNA expression in tumor versus normal tissue (log2 FC = +3.452, t-test p < 0.001).
This table shows molecular features associated with CENPF in patient tissues and cancer cell lines. In patient samples, CENPF shows the broadest associations at the RNA and protein expression levels, with LSCC recurring as the lineage with the largest associated feature set. In cancer cell lines, CENPF RNA and mutation anchors are most strongly linked to RNA-expression features, especially in BONE, while CRISPR and shRNA rows add functional-dependency signals in OVARY and BLOOD_Leukemia.
