Molecular Monitoring of the myl/Retinoic Acid Receptor-α Fusion Gene in Acute Promyelocytic Leukemia by Polymerase Chain Reaction

The acute promyelocytic leukemia (APL) t(15;17) translocation generates a myl/retinoic acid receptor-alpha (RAR-alpha) chimeric gene that is transcribed as a fusion myl/RAR-alpha messenger RNA. Using primer sets derived from RAR-alpha and myl cDNAs, we were able to amplify the breakpoint sites of th...

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Bibliographic Details
Published in:	Blood Vol. 80; no. 2; pp. 492 - 497
Main Authors:	Biondi, Andrea, Rambaldi, Alessandro, Pandolfi, Pier Paolo, Rossi, Vincenzo, Giudici, Giovanni, Alcalay, Myriam, Coco, Francesco Lo, Diverio, Daniela, Pogliani, Enrico M., Lanzi, Eraldo M., Mandelli, Franco, Masera, Giuseppe, Barbui, Tiziano, Pelicci, Pier Giuseppe
Format:	Journal Article
Language:	English
Published:	Washington, DC Elsevier Inc 15-07-1992 The Americain Society of Hematology
Subjects:	Adolescent Adult Antineoplastic Combined Chemotherapy Protocols Base Sequence Biological and medical sciences Bone Marrow - pathology Bone Marrow Transplantation Carrier Proteins - genetics Child Child, Preschool Chromosome Mapping Chromosomes, Human, Pair 15 Chromosomes, Human, Pair 17 Cloning, Molecular DNA, Neoplasm - genetics Exons Female Follow-Up Studies Hematologic and hematopoietic diseases Humans Introns Leukemia, Promyelocytic, Acute - blood Leukemia, Promyelocytic, Acute - genetics Leukemia, Promyelocytic, Acute - pathology Leukemias. Malignant lymphomas. Malignant reticulosis. Myelofibrosis Male Medical sciences Molecular Sequence Data Oligodeoxyribonucleotides Oncogenes Polymerase Chain Reaction - methods Receptors, Retinoic Acid Translocation, Genetic Tretinoin - metabolism Chromosomal aberration Human Promyelocytic leukemia Polymerase chain reaction Abnormal chromosome Exploration Malignant hemopathy Molecular biology Retinoic acid Chromosome translocation
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Summary:	The acute promyelocytic leukemia (APL) t(15;17) translocation generates a myl/retinoic acid receptor-alpha (RAR-alpha) chimeric gene that is transcribed as a fusion myl/RAR-alpha messenger RNA. Using primer sets derived from RAR-alpha and myl cDNAs, we were able to amplify the breakpoint sites of the fusion transcripts of all 35 APL RNA samples by reverse polymerase chain reaction (PCR) and nested primer approach of two rounds of amplification. DNA fragments of different size were obtained according to the chromosome 15 breakpoints (intron 3-bcr 3; exon 6-bcr 2; and intron 6-bcr 1). bcr 1 and bcr 3 represent the regions of the myl locus most frequently involved among APL (48.5 and 34.2 of cases, respectively); bcr 3 constitutes 62.5% of cases among M3V as compared with 25.9% of M3 cases. The feasibility of monitoring the APL clone by PCR analysis in five APL patients who received different treatment (chemotherapy, all-trans-retinoic acid or bone marrow transplantation) was evaluated. In five of nine bone marrow samples of patients in complete remission, t(15;17)-positive cells could be detected by PCR analysis. We conclude that PCR amplification of the myl/RAR-alpha junctions represents the easiest and rapid method for diagnosis and monitoring of the APL clone.
ISSN:	0006-4971 1528-0020
DOI:	10.1182/blood.V80.2.492.492