Argbp2, encoding a negative regulator of abl, is fused to mll in a case of infant m5 acute myeloid leukemia involving 4q35 and 11q23

Access through your institution Buy or subscribe Children with acute myeloid leukemia (AML) in Italy have a probability of event-free survival of 53% at 5 years.1 Acute myeloid leukemia

associated with rearrangements involving the MLL gene (translocations, duplications, inversions, deletions) are frequently found in infants and in patients with secondary leukemias following

treatment with DNA topoisomerase-II inhibitors, and are most often associated with the AML-M5 or -M4 FAB subtypes.2 The MLL gene (also called ALL-1 or HRX), located at 11q23, is involved in

over 60 different translocations leading to gene fusion and over 30 partner genes have so far been cloned and partially characterized.2 The most common translocation is the t(9;11)(p22;q23)

giving rise to the MLL-AF9 fusion gene, while other recurring translocations are the t(11;19)(q23;p13.3) and the t(11;19)(q23;p13.1), producing, respectively, the MLL-ENL and MLL-ELL

oncogenes. Several studies have demonstrated that the transcriptional effector functions of the MLL fusion partners are essential for leukemogenesis; however, there are few common

characteristics among these partner proteins that can clarify their role in leukemogenesis.2 We report the identification of ArgBP2 (Arg-binding-protein-2) as a new partner gene of _MLL_ in

a case of infant AML. A 3-month-old girl was diagnosed as having AML-M5. Her peripheral blood mononuclear cell count was 131 × 106/ml. Peripheral blood and bone marrow smears showed 16 and

30% of blasts, respectively. Immunophenotypic analysis revealed that the leukemic blasts were highly positive (from 42 to 77%) for CD14, CD15, CD33 and C11b. This is a preview of

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* X83604 REFERENCES * Pession A, Rondelli R, Basso G, Rizzari C, Testi AM, Fagioli F _et al_. Treatment and long-term results in children with acute myeloid leukaemia treated according to

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2183–2190. Google Scholar  Download references ACKNOWLEDGEMENTS This work was supported by grants from AIRC (to AP and LLN and a Regional Grant), MURST/FISR, and by the University of Bologna

(funds for selected research topics). LM and SS were supported by AGEOP. AUTHOR INFORMATION AUTHORS AND AFFILIATIONS * Department of Pediatrics, University of Bologna, Bologna, Italy A

Pession, L Montemurro, S Serravalle, R Fazzina & R Tonelli * Center of Pediatric Hematology Oncology, University of Catania, Catania, Italy L Lo Nigro * Division of Pediatrics, Hospital

of Parma, Parma, Italy G Izzi * Department of Pathology and Cancer Center, University of Illinois, Chicago, IL, USA G Nucifora * Department of Genetics, University of Erlangen, Erlangen,

Germany R Slany Authors * A Pession View author publications You can also search for this author inPubMed Google Scholar * L Lo Nigro View author publications You can also search for this

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also search for this author inPubMed Google Scholar * R Tonelli View author publications You can also search for this author inPubMed Google Scholar CORRESPONDING AUTHOR Correspondence to A

Pession. ADDITIONAL INFORMATION Supplementary Information accompanies the paper on the Leukemia website (http://www.nature.com/leu) SUPPLEMENTARY INFORMATION SUPPLEMENTARY MATERIAL (DOC 19

KB) RIGHTS AND PERMISSIONS Reprints and permissions ABOUT THIS ARTICLE CITE THIS ARTICLE Pession, A., Lo Nigro, L., Montemurro, L. _et al._ ArgBP2, encoding a negative regulator of ABL, is

fused to MLL in a case of infant M5 acute myeloid leukemia involving 4q35 and 11q23. _Leukemia_ 20, 1310–1313 (2006). https://doi.org/10.1038/sj.leu.2404222 Download citation * Published: 20

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