Inv(11)(q21q23); KMT2A-MAML2, a Recurrent Genetic Abnormality in T-Cell Therapy-related Acute Lymphoblastic Leukemia.
Child, Preschool
Chromosome Inversion
Chromosomes, Human, Pair 11
Histone-Lysine N-Methyltransferase
/ genetics
Humans
Male
Myeloid-Lymphoid Leukemia Protein
/ genetics
Neoplasms, Second Primary
/ genetics
Oncogene Proteins, Fusion
/ genetics
Precursor B-Cell Lymphoblastic Leukemia-Lymphoma
/ genetics
Trans-Activators
/ genetics
Journal
Journal of pediatric hematology/oncology
ISSN: 1536-3678
Titre abrégé: J Pediatr Hematol Oncol
Pays: United States
ID NLM: 9505928
Informations de publication
Date de publication:
05 2020
05 2020
Historique:
pubmed:
26
7
2019
medline:
4
11
2020
entrez:
26
7
2019
Statut:
ppublish
Résumé
T-cell therapy-related acute lymphoblastic leukemia (T-t-ALL) is a rare condition associated with previous cytotoxic therapy for another disease. Here we report T-t-ALL with inv(11)(q21q23), which involves KMT2A and MAML2, a transcriptional coactivator of NOTCH proteins, that occurred after chemotherapy for Philadelphia chromosome-positive B-cell acute lymphoblastic leukemia. This case describes the youngest patient with T-t-ALL harboring inv(11)(q21q23) and is the first independent report following an initial series also occurring in children. Our results lend further support to the observation that the KMT2A-MAML2 fusion gene resulting from inv(11)(q21q23) is likely a recurrent cytogenetic abnormality in T-t-ALL and appears to be associated with pediatric cases.
Identifiants
pubmed: 31343482
doi: 10.1097/MPH.0000000000001572
pii: 00043426-202005000-00037
doi:
Substances chimiques
KMT2A protein, human
0
MAML2 protein, human
0
Oncogene Proteins, Fusion
0
Trans-Activators
0
Myeloid-Lymphoid Leukemia Protein
149025-06-9
Histone-Lysine N-Methyltransferase
EC 2.1.1.43
Types de publication
Case Reports
Journal Article
Langues
eng
Sous-ensembles de citation
IM
Pagination
e258-e261Références
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