Therapy-related acute myeloid leukemia with t(2;11)(q37;q23) after treatment for osteosarcoma

Bella Bielorai*, Claus Meyer, Luba Trakhtenbrot, Hana Golan, Esther Rozner, Ninette Amariglio, Shai Izraeli, Rolf Marschalek, Amos Toren

*Corresponding author for this work

Research output: Contribution to journalArticlepeer-review


The survival rate for children with osteosarcoma (OS) has improved dramatically with the introduction of multiagent chemotherapy. As the number of pediatric cancer survivors increases, there is a concern about the development of secondary malignant neoplasms. Secondary acute myeloid leukemia (AML) has been rarely reported after treatment for OS. We describe a 14-year-old boy with OS of the left ileum who developed secondary AML 15 months after completion of treatment. Cytogenetic analysis of the leukemic cells demonstrated deletion 11q23, whereas fluorescence in situ hybridization revealed rearrangement of the MLL gene. Only the addition of the long-distance inverse polymerase chain reaction technique identified the SEPT2 as the MLL fusion partner resulting in t(2;11)(q37;q23) that was reported in a very few secondary AML cases. Because of the cryptic nature of MLL translocations that cannot be detected by conventional cytogenetics or may misinterpreted as deletion, additional molecular techniques are required to identify the precise translocation partner. Because long-distance inverse polymerase chain reaction is not available in most molecular laboratories, the true incidence of t(2;11)(q37;q23) and the involvement of SEPT2 as the MLL translocation partner could be more prevalent in secondary AML.

Original languageEnglish
Pages (from-to)288-291
Number of pages4
JournalCancer Genetics and Cytogenetics
Issue number2
StatePublished - Dec 2010


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