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 Blood, 1 December 2007, Vol. 110, No. 12, pp. 4073-4076.
Prepublished online as a Blood First Edition Paper on August 21, 2007; DOI 10.1182/blood-2007-06-095554.

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NEOPLASIA

Brief Report

The PRKAR1A gene is fused to RARA in a new variant acute promyelocytic leukemia

Alberto Catalano1, Mark A. Dawson2, Karthiga Somana3, Stephen Opat2, Anthony Schwarer2, Lynda J. Campbell3, and Harry Iland1

1 Institute of Haematology, Royal Prince Alfred Hospital, Sydney; 2 Clinical Haematology and Bone Marrow Transplant Unit, the Alfred Hospital, Melbourne; and 3 Victorian Cancer Cytogenetics Service, St Vincent's Hospital, Melbourne, Australia

We report the molecular and cytogenetic characterization of a novel variant of acute promyelocytic leukemia (APL). The bone marrow showed 88% hypergranular promyelocytes, and the karyotype was 47,XY,+22 [5]/46,XY[30]. Fluorescence in situ hybridization (FISH) indicated disruption and deletion of the 5'-end of the RARA gene. Treatment with all-trans retinoic acid, idarubicin, and arsenic trioxide induced cytogenetic complete remission without morphologic evidence of residual leukemia. The diagnostic marrow was negative for PML-RARA transcripts by reverse transcription–polymerase chain reaction (RT-PCR), but an atypical product was observed. Sequencing showed partial homology to the PRKAR1A gene, encoding the regulatory subunit type I-{alpha} of cyclic adenosine monophosphate–dependent protein kinase. RT-PCR using specific primers for PRKAR1A and RARA amplified 2 transcript splice variants of a PRKAR1A-RARA fusion gene, and PRKAR1A and RARA FISH probes confirmed the fusion. This novel PRKAR1A-RARA gene rearrangement is the fifth variant APL in which the RARA partner gene has been identified and the second known rearrangement of PRKAR1A in a malignant disease. This trial was registered at www.actr.org.au with the Australian Clinical Trials Registry as number 12605000070639.


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