ReviewMolecular biology reports2026
CENP-A in cancer: from centromere identity to genome instability.
Review in Molecular biology reports, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
0 citing papers in PubMed.
No citing paper in PubMed yet.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
2 authors.
Funding
Abstract
Chromatin organization plays a fundamental role in the regulation and preservation of the eukaryotic genome. Histone variants contribute to chromatin dynamics by replacing canonical histones within nucleosomes and conferring specialized structural and regulatory properties. Among these variants, the centromere-specific histone H3 variant CENP-A is essential for establishing and maintaining centromere identity and ensuring accurate chromosome segregation during mitosis. Proper expression, deposition, and maintenance of CENP-A are tightly regulated through dedicated chaperones and mechanisms. Disruption of these regulatory processes can lead to aberrant CENP-A expression or mislocalization, resulting in defective centromere function and chromosome segregation. CENP-A is frequently overexpressed in several human cancers and CENP-A overexpression often correlates with tumor progression, chromosomal instability, and poor prognosis. Ectopic incorporation of CENP-A into non-centromeric chromatin can promote aberrant chromatin states and partial recruitment of kinetochore components. These alterations can disrupt normal kinetochore function and contribute to chromosome missegregation, thereby promoting chromosomal instability (CIN) and tumor evolution. In addition to its role in mitotic fidelity, emerging studies suggest that ectopic CENP-A can interfere with chromatin factors and influence transcriptional regulation. Hence, CENP-A emerges as a potential biomarker for cancer prognosis and therapeutic response. In this review, we summarize current knowledge on the regulation of CENP-A expression and deposition, discuss the functional consequences of its dysregulation in cancer, and highlight emerging clinical and translational implications of targeting centromere chromatin pathways in oncology.
Indexed as
Identifiers
42262626What OpenQuestion holds
Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.