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 ATP5O 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.
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Authors | Francesca Micci, Ioannis Panagopoulos, Lisbeth Haugom, Hege Kilen Andersen, Geir E Tjønnfjord, Klaus Beiske, Sverre Heim |
Journal | Cancer letters
(Cancer Lett)
Vol. 277
Issue 2
Pg. 205-11
(May 18 2009)
ISSN: 1872-7980 [Electronic] Ireland |
PMID | 19168282
(Publication Type: Case Reports, Journal Article, Research Support, Non-U.S. Gov't)
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Chemical References |
- Carrier Proteins
- Membrane Proteins
- RYK protein, human
- Receptor Protein-Tyrosine Kinases
- Adenosine Triphosphatases
- Mitochondrial Proton-Translocating ATPases
- oligomycin sensitivity-conferring protein
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Topics |
- Adenosine Triphosphatases
(genetics)
- Aged
- Carrier Proteins
(genetics)
- Chromosomes, Human, Pair 21
(genetics)
- Humans
- Leukemia, Myeloid, Chronic, Atypical, BCR-ABL Negative
(genetics)
- Male
- Membrane Proteins
(genetics)
- Mitochondrial Proton-Translocating ATPases
- Oncogene Fusion
- Receptor Protein-Tyrosine Kinases
(genetics)
- Translocation, Genetic
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