Therapy-Related Acute Myeloid Leukemia 6 Years after Clonal Detection of inv(11)(q21q23) and MLL Gene Rearrangement
Autor: | Kazumi Suzukawa, Yasuhiro Yoda, Toshiro Nagasawa, Yasushi Okoshi, Naoko Takei, Harumi Y. Mukai, Takayoshi Itoh |
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Rok vydání: | 2006 |
Předmět: |
medicine.medical_specialty
Clone (cell biology) Antigens CD34 Bone Marrow Cells Therapy-Related Acute Myeloid Leukemia CD13 Antigens Biology hemic and lymphatic diseases Internal medicine medicine Humans neoplasms Hematology medicine.diagnostic_test Chromosomes Human Pair 11 Myeloid leukemia Neoplasms Second Primary Gene rearrangement Middle Aged medicine.disease Leukemia Myeloid Acute Leukemia medicine.anatomical_structure Chromosome Inversion Immunology Cancer research Female Bone marrow Myeloid-Lymphoid Leukemia Protein Fluorescence in situ hybridization |
Zdroj: | International Journal of Hematology. 83:247-251 |
ISSN: | 0925-5710 |
DOI: | 10.1532/ijh97.05152 |
Popis: | Results of recent studies with animal models suggest that expression of MLL fusion proteins promotes acute leukemogenesis. However, the most potent MLL fusion proteins are not sufficient for the development of acute myeloid leukemia (AML). The clinical data on the pathogenesis of this type of leukemia are limited. We analyzed the case of a patient with therapy-related AML with MLL rearrangement. The patient initially developed AML with t(8;21). Although the patient achieved complete remission with chemotherapy, an abnormal karyotype, inv(11)(q21q23), was detected. After 6-year persistence of a clone with the inversion 11 karyotype in the bone marrow, secondary AML developed. Results of fluorescence in situ hybridization analysis combined with magnet-activated cell sorting analysis showed that MLL rearrangement was detected in CD34+ and CD13+ fractions but not in a CD3+ fraction of the bone marrow. There were 2 important clinical findings. One was that MLL rearrangement was not sufficient for the development of leukemia. The other was that MLL rearrangement targets specific lineages. |
Databáze: | OpenAIRE |
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