10th anniversary articleInversions and tandem translocations involving chromosome 14q11 and 14q32 in T-prolymphocytic leukemia and T-cell leukemias in patients with ataxia telangiectasia☆
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Cited by (106)
From the archives of MD Anderson Cancer Center: Aleukemic T-prolymphocytic leukemia, a rare presentation and review of the literature
2023, Annals of Diagnostic PathologyCitation Excerpt :Abnormalities of chromosome 8, including t(8;8)(p11–12;q12), trisomy 8q and isochromosome 8q, are frequent, seen in 60–80 % of T-PLL. Deletions of 12p13 and 11q22, (locus for the ataxia telangiectasia mutated [ATM]) (70 % of cases) and deletions of TP53 (30 % of cases) are also common [1,4,5]. Molecular studies show frequent loss-of-function mutations of the tumor suppressor ATM gene (80 % of patients) that result in impaired DNA double-strand break repair.
Current understandings on T-cell prolymphocytic leukemia and its association with TCL1 proto-oncogene
2020, Biomedicine and PharmacotherapyImpact of alemtuzumab therapy and route of administration in T-prolymphocytic leukemia: A single-center experience
2015, Clinical Lymphoma, Myeloma and LeukemiaPathobiology of Peripheral T-Cell Lymphomas
2014, Pathobiology of Human Disease: A Dynamic Encyclopedia of Disease MechanismsATM and DNA-PKcs make a complementary couple in DNA double strand break repair
2012, Mutation Research - Reviews in Mutation ResearchCitation Excerpt :According to this model, ATM-mediated phosphorylation of KAP-1 (a core component of heterochromatin) would be a crucial step for relaxing heterochromatin regions that otherwise would be inaccessible, thus facilitating its repair [74]. Curiously, no cytogenetic studies published to date with human AT cells from affected individuals have reported increased frequency of residual chromosome breaks or chromosome rearrangements involving breakpoints corresponding to defined heterochromatic regions, such as those regions in chromosomes 1, 9 and 16 or pericentromeric regions of human chromosomes [75–79], suggesting that ATM roles in DSB repair are heterogeneous and keep on demanding continuous research. In this regard, evidence suggests that this kinase is indeed involved in the resolution of breaks located in more accessible regions, for example those arising during V(D)J or CSR.
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This work was supported in part by a grant from the Medical Research Council.