Morerio Cristina, Acquila Maura, Rosanda Cristina, Rapella Annamaria, Dufour Carlo, Locatelli Franco, Maserati Emanuela, Pasquali Francesco, Panarello Claudio
Dipartimento di Ematologia ed Oncologia Pediatrica, Istituto di Ricovero e Cura a Carattere Scientifico Istituto G. Gaslini, Genova, Italy.
Cancer Res. 2004 Apr 15;64(8):2649-51. doi: 10.1158/0008-5472.can-03-4026.
PDGFRB, a transmembrane tyrosine kinase receptor for platelet-derived growth factor, is constitutively activated by gene fusion with different partners in myeloproliferative/myelodysplastic disorders with peculiar clinical characteristics. Six alternative partner genes have been described thus far. In this study, we report the molecular cloning of a novel translocation t(5;17)(q33;p11.2) in a case of juvenile myelomonocytic leukemia. The novel partner gene was identified as HCMOGT-1 using 5'-rapid amplification of cDNA ends; fluorescence in situ hybridization and reverse transcriptase-PCR analyses confirmed that the translocation resulted in PDGFRB/HCMOGT-1 fusion. We show that the breakpoint of PDGFRB occurred at the same site of all previously reported PDGFRB translocations.
血小板衍生生长因子受体β(PDGFRB)是一种血小板衍生生长因子的跨膜酪氨酸激酶受体,在具有特殊临床特征的骨髓增殖性/骨髓增生异常性疾病中,它通过与不同伙伴的基因融合而持续激活。迄今为止,已描述了六个替代伙伴基因。在本研究中,我们报告了一例青少年骨髓单核细胞白血病中一种新型易位t(5;17)(q33;p11.2)的分子克隆。使用5'-cDNA末端快速扩增法将新型伙伴基因鉴定为HCMOGT-1;荧光原位杂交和逆转录酶-PCR分析证实该易位导致了PDGFRB/HCMOGT-1融合。我们表明,PDGFRB的断点发生在所有先前报道的PDGFRB易位的相同位点。