Inv(11)(q21q23); KMT2A-MAML2, a Recurrent Genetic Abnormality in T-Cell Therapy–related Acute Lymphoblastic Leukemia

Rachel A. Mariani, Mercedes Silva, Edward Caparelli, Lawrence J. Jennings, Kai Lee Yap, Katrin M. Leuer, Joanna Weinstein, Shunyou Gong*

*Corresponding author for this work

Research output: Contribution to journalArticlepeer-review

2 Scopus citations

Abstract

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.

Original languageEnglish (US)
Pages (from-to)E258-E261
JournalJournal of pediatric hematology/oncology
Volume42
Issue number4
DOIs
StatePublished - May 1 2020

Keywords

  • Inv(11)(q21q23)
  • KMT2A
  • MAML2
  • T-cell ALL
  • Therapy-related acute lymphoblastic leukemia

ASJC Scopus subject areas

  • Pediatrics, Perinatology, and Child Health
  • Hematology
  • Oncology

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