2012
DOI: 10.1159/000338769
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Rearrangement of the Myeloid/Lymphoid Leukemia Gene in Therapy-Related Myelodysplastic Syndrome in Patients Previously Treated with Agents Targeting DNA Topoisomerase II

Abstract: <b><i>Background:</i></b> Therapy-related acute myeloid leukemias (t-AML), with balanced translocations affecting the 11q23 point in the myeloid/lymphoid leukemia (MLL) gene, are one of the most serious complications of treatments with topoisomerase II inhibitors. However, only a few reports of t-AML exist. We aimed to study if these translocations are cumulative-dose-dependent, their frequency in therapy-related myelodysplastic syndrome and the relationship between their presence, the … Show more

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Cited by 8 publications
(4 citation statements)
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“…of patients/No. screened Clinical phenotype Primary mutation/associated with other abnormalities Consanguinity Reference RPL with birth deformities Egypt Rec † Rec † Rec † t(3;8)(p25;p11) t(4;6)(p24;q25) t(7;21)(p11;p11) De novo - - 30y/M 22y/F 22y/F 1/- 1/- 1/- Repeated abortions, stillbirth, fetal malformation, and birth of mentally handicapped children - - Gaboon et al 2015 ) RPL Rec Rec Rec Rec t(1;15)(p35;q15) t(3;15)(p23;q26.2) t(3;7)(p26;p15) t(4;6)(q25;q26) Fam 23-50y/ 7F, 5 M 12/224 Recurrent abortions and the birth of dysmorphic/mentally handicapped infants Primary Consanguineous couple involving translocation in chromosomes 11 and 12 Elhady et al 2020 ) Therapy-related acute myeloid leukemias Rec t(v;11q23) De novo Median: 37y/ 46 M, 28F 6/120 Poor topoisomerase II inhibitor treatment outcome Primary - Mosad et al 2012 ) Down syndrome Rec t(4;21)(q25;q22) Mat 8y/F 1/1 Severe growth retardation, microcephaly, hearing impairment, and specific facies Associated with partial trisomy 4q25-qter and 21(pter-q22) - El-Ruby et al 2007 ) ...…”
Section: Resultsmentioning
confidence: 99%
“…of patients/No. screened Clinical phenotype Primary mutation/associated with other abnormalities Consanguinity Reference RPL with birth deformities Egypt Rec † Rec † Rec † t(3;8)(p25;p11) t(4;6)(p24;q25) t(7;21)(p11;p11) De novo - - 30y/M 22y/F 22y/F 1/- 1/- 1/- Repeated abortions, stillbirth, fetal malformation, and birth of mentally handicapped children - - Gaboon et al 2015 ) RPL Rec Rec Rec Rec t(1;15)(p35;q15) t(3;15)(p23;q26.2) t(3;7)(p26;p15) t(4;6)(q25;q26) Fam 23-50y/ 7F, 5 M 12/224 Recurrent abortions and the birth of dysmorphic/mentally handicapped infants Primary Consanguineous couple involving translocation in chromosomes 11 and 12 Elhady et al 2020 ) Therapy-related acute myeloid leukemias Rec t(v;11q23) De novo Median: 37y/ 46 M, 28F 6/120 Poor topoisomerase II inhibitor treatment outcome Primary - Mosad et al 2012 ) Down syndrome Rec t(4;21)(q25;q22) Mat 8y/F 1/1 Severe growth retardation, microcephaly, hearing impairment, and specific facies Associated with partial trisomy 4q25-qter and 21(pter-q22) - El-Ruby et al 2007 ) ...…”
Section: Resultsmentioning
confidence: 99%
“…Further molecular studies analysing the chromosome breakpoints are required to determine the plausible mechanisms responsible for generating KMT2A translocations in mature B‐NHL. Acute leukemia and MDS associated KMT2A translocations arise due to inhibition of the enzyme DNA topoisomerase II by chemotherapeutic drugs . Our patients had no history of exposure to topoisomerase II inhibitors, as well as alkylating agents or radiation, which have also been implicated in the genesis of KMT2A translocations.…”
Section: Discussionmentioning
confidence: 99%
“…While t‐AML is a known complication of Ewing sarcoma therapy (in our patient, presumably due to topoisomerase II inhibitor exposure given the timing and underlying KMT2A rearrangement), 3 treatment of two concurrent malignancies in a single patient is a significant challenge. To the greatest extent possible, we overlapped agents useful for treating both AML and Ewing sarcoma.…”
Section: Figurementioning
confidence: 97%