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Chromosomal instability (CIN) describes the persistent, elevated rate of gains and losses of chromosomes or chromosomal segments during cell division, resulting in uneven DNA distribution (aneuploidy) and widespread genetic abnormalities. CIN is a hallmark of most cancers, fostering tumor heterogeneity and adaptive resistance to therapies, but is also associated with poor prognosis. Mechanisms underlying CIN include errors in DNA replication, defective spindle assembly checkpoint, centrosome amplification, impaired sister chromatid cohesion, and abnormal chromosome-microtubule attachments. While CIN itself is not a molecular target, many cancer therapies exploit vulnerabilities in CIN-tolerant cells, especially by targeting mitotic regulators or DNA repair pathways. If you seek therapy-relevant molecular targets and pathways involved in CIN (e.g., Aurora kinase A, spindle checkpoint proteins, cohesion factors), those should be specified—otherwise, CIN refers broadly to a cancer-linked phenotype, not a single gene/protein target.
Inhibition of mitotic checkpoint components (e.g., Aurora kinase inhibitors impair chromosome segregation); Modulation of DNA damage response to reduce or increase CIN; Targeting centrosome amplification or chromatid cohesion pathways.
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