Hereditary ATM gene mutations cause ataxia-telangiectasia, a pleiotropic disorder associated with a high incidence of lymphoid malignancies. Acquired ATM alterations have been described in sporadic lymphoproliferative disorder suggesting that the ATM gene contributes to lymphomagenesis. To assess th
ATM gene alterations in childhood acute lymphoblastic leukemias
✍ Scribed by Fabienne Gumy Pause; Pierre Wacker; Philippe Maillet; David Betts; André-Pascal Sappino
- Publisher
- John Wiley and Sons
- Year
- 2003
- Tongue
- English
- Weight
- 48 KB
- Volume
- 22
- Category
- Article
- ISSN
- 1059-7794
No coin nor oath required. For personal study only.
✦ Synopsis
The original article to which this Erratum refers was published in Human Mutation 21:554
In the online version of this article, Dr. Gumy Pause's last name was incorrectly coded as ''Pause.'' Please find the author's name properly coded here, as last name ''Gumy Pause.'' The publisher apologizes for this error.
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## Background: Loss of heterozygosity (loh) at the atm gene (mutated in ataxia telangiectasia [at] patients) and atm protein deficiency occur in 14% and 34%, respectively, of patients with chronic lymphocytic leukemia (cll). atm protein deficiency also is associated with aggressive disease and wors
## Abstract High hyperdiploidy (51–67 chromosomes) is the most common cytogenetic abnormality pattern in childhood B‐cell precursor acute lymphoblastic leukemia (ALL), occurring in 25–30% of such cases. High hyperdiploid ALL is characterized cytogenetically by a nonrandom gain of chromosomes X, 4,
## Abstract A major feature of ataxia‐telangiectasia (A‐T) is an increased risk of cancer, particularly of lymphoid malignancies. We studied __ATM__ gene involvement in leukemic cells derived from 39 pediatric T‐cell acute lymphoblastic leukemias (ALLs). Two types of sequence changes—truncating and
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