Advanced

Mechanisms underlying neoplasia-associated genomic rearrangements

Fioretos, Thoas LU (2006) In Genomic disorders: The Genomic basis of disease p.327-337
Abstract
Neoplastic disorders are characterized by recurrent somatically acquired chromosomal aberrations that alter the structure and/or expression of a large number of genes. Most “cancer genes” discovered to date in human neoplasms have been identified through isolation of genes at the breakpoints of balanced chromosomal translocations. Although functional studies of such cancer-causing genes have demonstrated their causal role in tumorigenesis, the mechanisms underlying the formation of recurrent chromosomal changes in cancer remain enigmatic. Low-copy repeats (LCRs) are important mediators of erroneous meiotic recombination, resulting in constitutional chromosomal rearrangements. Recently, LCRs have been implicated in the formation of the... (More)
Neoplastic disorders are characterized by recurrent somatically acquired chromosomal aberrations that alter the structure and/or expression of a large number of genes. Most “cancer genes” discovered to date in human neoplasms have been identified through isolation of genes at the breakpoints of balanced chromosomal translocations. Although functional studies of such cancer-causing genes have demonstrated their causal role in tumorigenesis, the mechanisms underlying the formation of recurrent chromosomal changes in cancer remain enigmatic. Low-copy repeats (LCRs) are important mediators of erroneous meiotic recombination, resulting in constitutional chromosomal rearrangements. Recently, LCRs have been implicated in the formation of the frequent and characteristic neoplasia-associated chromosomal aberrations t(9;22)(q34;q1 1) and i(17q), suggesting that similar genome architecture features may play an important role in generating also other somatic chromosomal rearrangements. (Less)
Please use this url to cite or link to this publication:
author
organization
publishing date
type
Chapter in Book/Report/Conference proceeding
publication status
published
subject
in
Genomic disorders: The Genomic basis of disease
editor
Lupski, James R and Stankiewicz, P
pages
327 - 337
publisher
Humana Press
external identifiers
  • Scopus:34548397890
ISBN
978-1-58829-559-0
DOI
10.1007/978-1-59745-039-3_23
language
English
LU publication?
yes
id
d26bf98d-0a74-419a-98e2-42f4c36257e3 (old id 1137397)
date added to LUP
2008-05-22 11:41:00
date last changed
2016-10-13 04:50:34
@misc{d26bf98d-0a74-419a-98e2-42f4c36257e3,
  abstract     = {Neoplastic disorders are characterized by recurrent somatically acquired chromosomal aberrations that alter the structure and/or expression of a large number of genes. Most “cancer genes” discovered to date in human neoplasms have been identified through isolation of genes at the breakpoints of balanced chromosomal translocations. Although functional studies of such cancer-causing genes have demonstrated their causal role in tumorigenesis, the mechanisms underlying the formation of recurrent chromosomal changes in cancer remain enigmatic. Low-copy repeats (LCRs) are important mediators of erroneous meiotic recombination, resulting in constitutional chromosomal rearrangements. Recently, LCRs have been implicated in the formation of the frequent and characteristic neoplasia-associated chromosomal aberrations t(9;22)(q34;q1 1) and i(17q), suggesting that similar genome architecture features may play an important role in generating also other somatic chromosomal rearrangements.},
  author       = {Fioretos, Thoas},
  editor       = {Lupski, James R and Stankiewicz, P},
  isbn         = {978-1-58829-559-0},
  language     = {eng},
  pages        = {327--337},
  publisher    = {ARRAY(0x91d44d0)},
  series       = {Genomic disorders: The Genomic basis of disease},
  title        = {Mechanisms underlying neoplasia-associated genomic rearrangements},
  url          = {http://dx.doi.org/10.1007/978-1-59745-039-3_23},
  year         = {2006},
}