centromere protein MGenealiases: C22orf18 · CENP-M · PANE1
Q-omics provides the consensus-scored CENPM profile across patient tissues and cancer cell-line models. CENPM expression is associated with patient survival in 30 of 34 cancer types, with the highest sampling consensus in ACC. Among the 18 cancer types available for tumor–normal comparison, CENPM is differentially expressed in 16, with the highest sampling consensus in KIRC. Additionally, CENPM protein abundance shows 26,560 significant protein co-abundance associations, with the highest sampling consensus in LSCC. Together, these results highlight ACC, KIRC, and LSCC as cancer lineages where CENPM 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 CENPM — synthetic lethality, tumor antigen, and pembrolizumab response.
This table summarizes CENPM survival associations across molecular data types. CENPM RNA expression shows survival associations in the most cancer types (30), followed by mutation status (1) and mass-spec protein abundance (10). The rightmost column indicates the cancer type with the highest sampling consensus for each molecular layer.
This table ranks reproducible CENPM RNA expression–survival associations across cancer types. High CENPM expression shows unfavorable associations in ACC, KIRC, MESO, KICH, KIRP and UVM. The ACC 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 ACC as the clearest survival context for CENPM RNA expression.
This table summarizes CENPM tumor–normal expression differences by data type. RNA shows broader differences across cancer types, with a lineage consensus of 16, while mass-spec protein shows differences in 10. The strongest signals are observed in KIRC for RNA and LSCC for protein.
This table ranks reproducible tumor–normal expression differences for CENPM. A negative fold-change indicates higher expression in normal tissue than in tumor tissue. CENPM shows higher tumor expression in KIRC, BLCA, LUAD, KIRP, THCA and KICH. The KIRC box plot shows higher CENPM RNA expression in tumor versus normal tissue (log2 FC = +1.528, t-test p < 0.001).
This table shows molecular features associated with CENPM in patient tissues and cancer cell lines. In patient samples, CENPM 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, CENPM RNA and mutation anchors are most strongly linked to RNA-expression features, especially in BLOOD_Myeloma, while CRISPR and shRNA rows add functional-dependency signals in BREAST and BLOOD_Lymphoma.
