2003
DOI: 10.1046/j.1442-200x.2003.01709.x
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Persistence of TEL‐AML1 transcript in acute lymphoblastic leukemia in long‐term remission

Abstract: Background : It has recently been shown that t (12;21) (p13;q 22) is the most common molecular genetic abnormality in childhood acute lymphoblastic leukemia (ALL). We have analyzed this translocation in an attempt to evaluate its incidence and to monitor minimal residual disease (MRD) with t (12; 21) rearrangement by detection of TEL-AML1 transcript in patients with childhood ALL. Procedure : All cryopreserved bone marrow samples were analyzed using a nested reverse transcriptionpolymerase chain reaction (RT-P… Show more

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Cited by 8 publications
(8 citation statements)
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“…Furthermore, frequent late relapses and similar incidences of the ETV6/RUNX1 transcript in ALLs at diagnosis and relapse have been noted by some (Nakao et al , 1996; Harbott et al , 1997; Seeger et al , 1998, 1999; Tsang et al , 2001) but not by other authors (Loh et al , 1998; Rubnitz et al , 1999; Zuna et al , 1999). The fact that the ETV6/RUNX1 fusion may persist for a long time after cessation of chemotherapy without heralding relapse and that the relapses occasionally are derived from an ETV6/RUNX1 ‐positive clone other than the one present at diagnosis, as evidenced by different ETV6 deletions and IGH/TCR rearrangements at diagnosis and relapse, strongly suggests that some late ‘relapses’ originate in lingering preleukaemic t(12;21)‐positive clones, a finding which may explain why a sustained second remission often can be achieved and which should be taken into account in treatment decisions (Ford et al , 2001; Endo et al , 2003; Konrad et al , 2003; Peham et al , 2004; Zuna et al , 2004; Metzler et al , 2006).…”
mentioning
confidence: 99%
“…Furthermore, frequent late relapses and similar incidences of the ETV6/RUNX1 transcript in ALLs at diagnosis and relapse have been noted by some (Nakao et al , 1996; Harbott et al , 1997; Seeger et al , 1998, 1999; Tsang et al , 2001) but not by other authors (Loh et al , 1998; Rubnitz et al , 1999; Zuna et al , 1999). The fact that the ETV6/RUNX1 fusion may persist for a long time after cessation of chemotherapy without heralding relapse and that the relapses occasionally are derived from an ETV6/RUNX1 ‐positive clone other than the one present at diagnosis, as evidenced by different ETV6 deletions and IGH/TCR rearrangements at diagnosis and relapse, strongly suggests that some late ‘relapses’ originate in lingering preleukaemic t(12;21)‐positive clones, a finding which may explain why a sustained second remission often can be achieved and which should be taken into account in treatment decisions (Ford et al , 2001; Endo et al , 2003; Konrad et al , 2003; Peham et al , 2004; Zuna et al , 2004; Metzler et al , 2006).…”
mentioning
confidence: 99%
“…Hyperdiploidy is reported in up to 50% of children with precursor B-ALL [2] , but it is far less frequent in adult patients. Th e most common chromosomal additions include chromosomes 21 (often multiple copies), 4, 6, 10, 14, 17, 18, 20, X, and duplication of 1q and isochromosome 17q [51,52] . Hyperdiploidy indicates favorable prognosis, particularly in association with trisomy of chromosomes 4, 6, and 10 [2,51,52] .…”
Section: Hyperdiploidymentioning
confidence: 99%
“…It is likely that the observed clinical heterogeneity reflects a diverse pathogenesis of leukemia. The molecular basis of childhood ALL is to a large extent unknown, and it is likely that significant advances in the treatment of this malignancy are dependent on a better understanding of the molecular events that cause the disease (1,2). A number of investigators have attempted to identify groups of genes, termed ʻtranscriptional signaturesʼ whose expression can be directly associated with drug resistance (3).…”
Section: Introductionmentioning
confidence: 99%