LACK OF TEL AML1 FUSION IN PEDIATRIC AML - FURTHER EVIDENCE FOR LINEAGE SPECIFICITY OF TEL/AML1/

Citation
Ml. Loh et al., LACK OF TEL AML1 FUSION IN PEDIATRIC AML - FURTHER EVIDENCE FOR LINEAGE SPECIFICITY OF TEL/AML1/, Leukemia research, 22(5), 1998, pp. 461-464
Citations number
21
Categorie Soggetti
Oncology,Hematology
Journal title
ISSN journal
01452126
Volume
22
Issue
5
Year of publication
1998
Pages
461 - 464
Database
ISI
SICI code
0145-2126(1998)22:5<461:LOTAFI>2.0.ZU;2-2
Abstract
Background: the TEL/AML1 fusion associated with t(12;21)(p13;q22) is t he most common gene rearrangement in childhood malignancy, occurring i n approximately 25% of pediatric acute lymphoblastic leukemia. The TEL /AML1 rearrangement is cryptic at the cytogenetic level but confers a favorable prognosis. The AML1 gene was first identified by virtue of i ts involvement in adult and pediatric acute myeloid malignancies assoc iated with t(8;21) and t(3;21)(q26;q22.1). We have therefore determine d the frequency of the TEL/AML1 fusion in pediatric myeloid leukemias by RT-PCR analysis. Methods: total RNA was isolated from cryopreserved bone marrow samples of 38 pediatric patients with AML. RNA quality wa s controlled for by amplification of the TEL gene. An RT-PCR assay was then used to test for the presence of the TEL/AML1 fusion. Results: 2 9 patients had adequate RNA for analysis. Zero out of 29 pediatric AML patients had evidence for the :TEL/AML1 fusion by RT-PCR. Conclusions : the TEL/AML1 fusion does not occur in children with AML and suggests that the TEL/AML1 rearrangement is restricted in pediatric hematologi c malignancy to B lineage ALL. (C) 1998 Elsevier Science Ltd. All righ ts reserved.