Juvenile myelomonocytic leukemia with t(7;11)(p15;p15) and NUP98-HOXA11 fusion.

Abstract

The t(7;11)(p15;p15) translocation has been reported as a rare and recurrent chromosomal abnormality in acute myeloid leukemia (AML) patients. The NUP98-HOXA9 fusion gene with t(7;11)(p15;p15) was identified and revealed to be essential for leukemogenesis and myeloproliferative disease. To date, t(7;11)(p15;p15) with NUP98-HOXA11 fusion has been reported only in one case of ph-negative chronic myeloid leukemia (CML). Here, we report a case of a 3-year-old girl with juvenile myelomonocytic leukemia (JMML) carrying t(7;11)(p15;p15) abnormality with NUP98-HOXA11 fusion. AML chemotherapy followed by bone marrow transplantation (BMT) was found to be effective in treating this disorder, and she remains in complete remission for 3 years after BMT. We suggest the possibility that AML chemotherapy might be effective for treating JMML with t(7;11)(p15;p15) abnormality and NUP98-HOXA11 fusion.

• Authors: Yoko Mizoguchi, Naoto Fujita, Tomohiko Taki, Yasuhide Hayashi, Kazuko Hamamoto
• Journal: American journal of hematology (Am J Hematol) Vol. 84 Issue 5 Pg. 295-7 (May 2009) ISSN: 1096-8652 [Electronic] United States
• PMID: 19338047 (Publication Type: Case Reports, Journal Article)

Chemical References

• Antineoplastic Agents
• Homeodomain Proteins
• NUP98-HOXA11 fusion protein, human
• Nuclear Pore Complex Proteins
• Oncogene Proteins, Fusion

Topics

• Antineoplastic Agents (therapeutic use)
• Bone Marrow Transplantation
• Child, Preschool
• Chromosomes, Human, Pair 11
• Chromosomes, Human, Pair 7
• Combined Modality Therapy
• Female
• Homeodomain Proteins (genetics)
• Humans
• Leukemia, Myelomonocytic, Juvenile (genetics, physiopathology, therapy)
• Nuclear Pore Complex Proteins (genetics)
• Oncogene Proteins, Fusion (genetics)
• Remission Induction
• Translocation, Genetic