Mechanisms underlying neoplasia-associated genomic rearrangements
(2006) 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:
https://lup.lub.lu.se/record/1137397
- author
- Fioretos, Thoas LU
- organization
- publishing date
- 2006
- type
- Chapter in Book/Report/Conference proceeding
- publication status
- published
- subject
- host publication
- 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
- 2016-04-04 12:15:41
- date last changed
- 2022-02-28 21:12:11
@inbook{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}},
booktitle = {{Genomic disorders: The Genomic basis of disease}},
editor = {{Lupski, James R and Stankiewicz, P}},
isbn = {{978-1-58829-559-0}},
language = {{eng}},
pages = {{327--337}},
publisher = {{Humana Press}},
title = {{Mechanisms underlying neoplasia-associated genomic rearrangements}},
url = {{http://dx.doi.org/10.1007/978-1-59745-039-3_23}},
doi = {{10.1007/978-1-59745-039-3_23}},
year = {{2006}},
}