Journal
CANCER CELL
Volume 4, Issue 2, Pages 89-94Publisher
CELL PRESS
DOI: 10.1016/S1535-6108(03)00195-8
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Funding
- NIGMS NIH HHS [GM51994] Funding Source: Medline
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The role of intragenic point mutations in human cancer is well established. However, the contribution of massive genomic changes collectively known as aneuploidly is less certain. Recent experimental work suggests that aneuploidy is required for sporadic carcinogenesis in mice and that it may collaborate with intragenic mutations during tumorigenesis. The genomic plasticity afforded by aneuploidly could facilitate emergence of protumorigenic gene dosage changes and accelerate accumulation of oncogenes; and loss of tumor suppressor genes. These new findings force us to rethink the pathogenesis of carcinoma in ways that have significant implications for diagnosis and therapy.
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