Advanced

t(3;21)(q22;q22) leading to truncation of the RYK gene in atypical chronic myeloid leukemia

Micci, Francesca; Panagopoulos, Ioannis LU ; Haugom, Lisbeth; Andersen, Hege Kilen; Tjonnfjord, Geir E.; Beiske, Klaus and Heim, Sverre (2009) In Cancer Letters 277(2). p.205-211
Abstract
The analysis of a small number of patients with atypical chronic myeloid leukemia showing balanced chromosomal translocations has revealed diverse tyrosine kinase fusion genes, most commonly involving FGFR1, PDGFRA, PDGFRB, JAK2, and ABL. We present a case of aCML with a 3q22;21q22-translocation that led to truncation of the receptor-like tyrosine kinase (RYK) gene and its juxtaposition with sequences from chromosome 21 including the ATP50 gene coding for a mitochondrial ATP synthase. The resulting fusion was not in frame, however, which is why we speculate that an abrogated RYK gene product rather than a chimeric protein might be the leukemogenic result. (c) 2009 Elsevier Ireland Ltd. All rights reserved.
Please use this url to cite or link to this publication:
author
organization
publishing date
type
Contribution to journal
publication status
published
subject
keywords
RYK, Fusion gene, Karyotyping, aCML, ATP50
in
Cancer Letters
volume
277
issue
2
pages
205 - 211
publisher
Elsevier
external identifiers
  • wos:000265475600012
  • scopus:62749090950
ISSN
1872-7980
DOI
10.1016/j.canlet.2008.12.016
language
English
LU publication?
yes
id
633b1ee6-ebf9-4d7f-978d-df658d298025 (old id 1399572)
date added to LUP
2009-06-15 14:59:18
date last changed
2017-06-18 04:16:59
@article{633b1ee6-ebf9-4d7f-978d-df658d298025,
  abstract     = {The analysis of a small number of patients with atypical chronic myeloid leukemia showing balanced chromosomal translocations has revealed diverse tyrosine kinase fusion genes, most commonly involving FGFR1, PDGFRA, PDGFRB, JAK2, and ABL. We present a case of aCML with a 3q22;21q22-translocation that led to truncation of the receptor-like tyrosine kinase (RYK) gene and its juxtaposition with sequences from chromosome 21 including the ATP50 gene coding for a mitochondrial ATP synthase. The resulting fusion was not in frame, however, which is why we speculate that an abrogated RYK gene product rather than a chimeric protein might be the leukemogenic result. (c) 2009 Elsevier Ireland Ltd. All rights reserved.},
  author       = {Micci, Francesca and Panagopoulos, Ioannis and Haugom, Lisbeth and Andersen, Hege Kilen and Tjonnfjord, Geir E. and Beiske, Klaus and Heim, Sverre},
  issn         = {1872-7980},
  keyword      = {RYK,Fusion gene,Karyotyping,aCML,ATP50},
  language     = {eng},
  number       = {2},
  pages        = {205--211},
  publisher    = {Elsevier},
  series       = {Cancer Letters},
  title        = {t(3;21)(q22;q22) leading to truncation of the RYK gene in atypical chronic myeloid leukemia},
  url          = {http://dx.doi.org/10.1016/j.canlet.2008.12.016},
  volume       = {277},
  year         = {2009},
}