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Correspondence
Fatal acute monocytic leukaemia with t(6;11) (q27;q23) translocation and KRAS mutation
  1. Sai-Ching Jim Yeung1,2,
  2. Ahmed Elsayem1,
  3. Gregory N Fuller3,
  4. Gary Lu4,
  5. M James You4
  1. 1Department of Emergency Medicine, The University of Texas MD Anderson Cancer Center, Houston, Texas, USA
  2. 2Department of Endocrine Neoplasia and Hormonal Disorders, The University of Texas MD Anderson Cancer Center, Houston, Texas, USA
  3. 3Department of Pathology, The University of Texas MD Anderson Cancer Center, Houston, Texas, USA
  4. 4Department of Hematopathology, The University of Texas MD Anderson Cancer Center, Houston, Texas, USA
  1. Correspondence to Dr Sai-Ching Jim Yeung, Department of Emergency Medicine, The University of Texas MD Anderson Cancer Center, 1515 Holcombe Blvd., Unit 1468, Houston, TX 77030, USA; syeung{at}mdanderson.org

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Introduction

Acute myeloid leukaemia (AML) with t(6;11)(q27;q23), resulting in a chimeric MLL/AF6 gene, is rare (≤0.6% of adult cases),1 ,2 and is associated with poor prognosis.2 ,3 The majority of these cases are acute myelomonocytic leukaemia, or acute monoblastic/monocytic leukaemia,1 and they have increased risk for hyperleukocytosis requiring leukapheresis.4 The RAS association domain (RA1) at the N-terminus of AF6 is sufficient for MLL-AF6 to mediate leukemogenesis.5 Although an activated KRAS mutation accelerates MLL/AF4-driven leukemogenesis in transgenic mice,6 whether it will do the same with MLL/AF6 is unknown. Here, we report a rare and aggressive case of acute monocytic leukaemia with both MLL/AF6 and KRAS G12D.

Case report

A middle-aged man in his 40s had sore throat, chills, night sweats and swelling in the neck for four days prior to presentation to a local emergency centre. Concurrently, non-pruritic purple skin lesions appeared on his body. A complete blood count showed a white blood cell (WBC) count of 3 25 000/mm3, a platelet count of 60 000/mm3, and 92% monocytes in the blood smear. He was given 6 g of hydroxyurea orally and transferred to a tertiary cancer centre for emergent treatment of hyperleukocytosis. His past medical history, social history and family history were non-contributory.

Upon arrival at the cancer centre, he became dyspneic. His vital signs were: blood pressure 107/53 mm Hg; heart rate …

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