Fragile sites in cancer: more than meets the eye

This Opinion article discusses recent studies that have provided new insights into the mechanisms of common fragile site instability and the resulting genomic effects, which include the generation of focal copy number alterations that affect the genomic landscape of many cancers. Ever since initial...

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Published inNature reviews. Cancer Vol. 17; no. 8; pp. 489 - 501
Main Authors Glover, Thomas W., Wilson, Thomas E., Arlt, Martin F.
Format Journal Article
LanguageEnglish
Published London Nature Publishing Group UK 01.08.2017
Nature Publishing Group
Subjects
631/208/737/211
631/337/1427/2566
631/337/151
631/337/641/2187
631/67/68
631/67/69
631/80/641/151/2356
631/80/641/151/2357
Analysis
Anaphase
Animals
Biomedicine
Cancer
Cancer Research
Chromosomal Instability
Chromosome Breakage
Chromosome Fragile Sites
Chromosome rearrangements
Chromosome translocations
Chromosomes
Copy number
DNA Breaks, Double-Stranded
DNA Copy Number Variations
DNA Replication
Fragile sites
Gene Rearrangement
Genomes
Genomic instability
Humans
Ionizing radiation
Metaphase
Neoplasms - genetics
Oncogenes - genetics
opinion-2
Online AccessGet full text
ISSN1474-175X
1474-1768
1474-1768
DOI10.1038/nrc.2017.52

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Abstract This Opinion article discusses recent studies that have provided new insights into the mechanisms of common fragile site instability and the resulting genomic effects, which include the generation of focal copy number alterations that affect the genomic landscape of many cancers. Ever since initial suggestions that instability at common fragile sites (CFSs) could be responsible for chromosome rearrangements in cancers, CFSs and associated genes have been the subject of numerous studies, leading to questions and controversies about their role and importance in cancer. It is now clear that CFSs are not frequently involved in translocations or other cancer-associated recurrent gross chromosome rearrangements. However, recent studies have provided new insights into the mechanisms of CFS instability, their effect on genome instability, and their role in generating focal copy number alterations that affect the genomic landscape of many cancers.
AbstractList Ever since early suggestions that instability at common fragile sites (CFSs) could be responsible for chromosome rearrangements in cancers, CFSs and associated genes have been the subject of numerous studies, leading to questions and controversies about their role and importance in cancer. It is now clear that CFSs are not frequently involved in translocations or other cancer-associated recurrent gross chromosome rearrangements. However, recent studies have provided new insights into the mechanisms of CFS instability, their impact on genome instability, and their role in generating focal copy number alterations that affect the genomic landscape of many cancers.
Ever since initial suggestions that instability at common fragile sites (CFSs) could be responsible for chromosome rearrangements in cancers, CFSs and associated genes have been the subject of numerous studies, leading to questions and controversies about their role and importance in cancer. It is now clear that CFSs are not frequently involved in translocations or other cancer-associated recurrent gross chromosome rearrangements. However, recent studies have provided new insights into the mechanisms of CFS instability, their effect on genome instability, and their role in generating focal copy number alterations that affect the genomic landscape of many cancers.
Ever since initial suggestions that instability at common fragile sites (CFSs) could be responsible for chromosome rearrangements in cancers, CFSs and associated genes have been the subject of numerous studies, leading to questions and controversies about their role and importance in cancer. It is now clear that CFSs are not frequently involved in translocations or other cancer-associated recurrent gross chromosome rearrangements. However, recent studies have provided new insights into the mechanisms of CFS instability, their effect on genome instability, and their role in generating focal copy number alterations that affect the genomic landscape of many cancers.Ever since initial suggestions that instability at common fragile sites (CFSs) could be responsible for chromosome rearrangements in cancers, CFSs and associated genes have been the subject of numerous studies, leading to questions and controversies about their role and importance in cancer. It is now clear that CFSs are not frequently involved in translocations or other cancer-associated recurrent gross chromosome rearrangements. However, recent studies have provided new insights into the mechanisms of CFS instability, their effect on genome instability, and their role in generating focal copy number alterations that affect the genomic landscape of many cancers.
This Opinion article discusses recent studies that have provided new insights into the mechanisms of common fragile site instability and the resulting genomic effects, which include the generation of focal copy number alterations that affect the genomic landscape of many cancers. Ever since initial suggestions that instability at common fragile sites (CFSs) could be responsible for chromosome rearrangements in cancers, CFSs and associated genes have been the subject of numerous studies, leading to questions and controversies about their role and importance in cancer. It is now clear that CFSs are not frequently involved in translocations or other cancer-associated recurrent gross chromosome rearrangements. However, recent studies have provided new insights into the mechanisms of CFS instability, their effect on genome instability, and their role in generating focal copy number alterations that affect the genomic landscape of many cancers.
Audience Academic
Author Wilson, Thomas E.
Arlt, Martin F.
Glover, Thomas W.
Author_xml – sequence: 1
  givenname: Thomas W.
  surname: Glover
  fullname: Glover, Thomas W.
  email: glover@umich.edu
  organization: Thomas W. Glover is at the Department of Human Genetics; the Department of Pathology; and the Department of Pediatrics and Communicable Diseases, University of Michigan Medical School, Ann Arbor, Michigan 48109, USA, the Department of Pathology
– sequence: 2
  givenname: Thomas E.
  surname: Wilson
  fullname: Wilson, Thomas E.
  organization: Thomas E. Wilson is at the Department of Human Genetics; and the Department of Pathology, University of Michigan Medical School, Ann Arbor, Michigan 48109, USA., and the Department of Pathology, University of Michigan Medical School, Ann Arbor, Michigan 48109, USA
– sequence: 3
  givenname: Martin F.
  surname: Arlt
  fullname: Arlt, Martin F.
  organization: Martin F. Arlt is at the Department of Human Genetics, University of Michigan Medical School, Ann Arbor, Michigan 48109, USA
BackLink https://www.ncbi.nlm.nih.gov/pubmed/28740117$$D View this record in MEDLINE/PubMed
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SecondaryResourceType review_article
Snippet This Opinion article discusses recent studies that have provided new insights into the mechanisms of common fragile site instability and the resulting genomic...
Ever since initial suggestions that instability at common fragile sites (CFSs) could be responsible for chromosome rearrangements in cancers, CFSs and...
Ever since early suggestions that instability at common fragile sites (CFSs) could be responsible for chromosome rearrangements in cancers, CFSs and associated...
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SubjectTerms 631/208/737/211
631/337/1427/2566
631/337/151
631/337/641/2187
631/67/68
631/67/69
631/80/641/151/2356
631/80/641/151/2357
Analysis
Anaphase
Animals
Biomedicine
Cancer
Cancer Research
Chromosomal Instability
Chromosome Breakage
Chromosome Fragile Sites
Chromosome rearrangements
Chromosome translocations
Chromosomes
Copy number
DNA Breaks, Double-Stranded
DNA Copy Number Variations
DNA Replication
Fragile sites
Gene Rearrangement
Genomes
Genomic instability
Humans
Ionizing radiation
Metaphase
Neoplasms - genetics
Oncogenes - genetics
opinion-2
Title Fragile sites in cancer: more than meets the eye
URI https://link.springer.com/article/10.1038/nrc.2017.52
https://www.ncbi.nlm.nih.gov/pubmed/28740117
https://www.proquest.com/docview/1946507671
https://www.proquest.com/docview/1923115573
https://pubmed.ncbi.nlm.nih.gov/PMC5546318
Volume 17
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