Chromosomal instability as a source of genomic plasticity

Duaa H Al-Rawi; Samuel F Bakhoum

doi:10.1016/j.gde.2022.101913

Chromosomal instability as a source of genomic plasticity

Curr Opin Genet Dev. 2022 Jun:74:101913. doi: 10.1016/j.gde.2022.101913. Epub 2022 May 5.

Authors

Duaa H Al-Rawi¹, Samuel F Bakhoum²

Affiliations

¹ Human Oncology and Pathogenesis Program, Memorial Sloan Kettering Cancer Center, New York, NY, USA; Department of Medicine, Memorial Sloan Kettering Cancer Center, New York, NY, USA. Electronic address: duaa.h.alrawi@gmail.com.
² Human Oncology and Pathogenesis Program, Memorial Sloan Kettering Cancer Center, New York, NY, USA; Department of Radiation Oncology, Memorial Sloan Kettering Cancer Center, New York, NY, USA. Electronic address: samuel.bakhoum@gmail.com.

Abstract

Chromosomal instability (CIN) is a hallmark of the most aggressive malignancies. Features of these tumors include complex genomic rearrangements, the presence of mis-segregated chromosomes in micronuclei, and extrachromosomal DNA (ecDNA) formation. Here, we review the development of CIN, and examine CIN in the context of cancer evolution, tumor genomic evolution, and therapeutic resistance. We also discuss the role of whole-genome duplications, breakage-fusion-bridge cycles, ecDNA or double minutes in gene amplification promoting tumor evolution.

Keywords: Cancer Evolution; Chromosomal Instability; Micronuclei; ecDNA.

Publication types

Review
Research Support, Non-U.S. Gov't
Research Support, N.I.H., Extramural

MeSH terms

Chromosomal Instability* / genetics
Gene Amplification
Genomic Instability
Genomics
Humans
Neoplasms* / pathology
Oncogenes

Abstract

Publication types

MeSH terms

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