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 Blood, 15 March 2004, Vol. 103, No. 6, pp. 2358-2362.
Prepublished online as a Blood First Edition Paper on November 20, 2003; DOI 10.1182/blood-2003-07-2200.

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NEOPLASIA
Brief report

Mutations of the PML tumor suppressor gene in acute promyelocytic leukemia

Carmela Gurrieri, Khedoudja Nafa, Taha Merghoub, Rosa Bernardi, Paola Capodieci, Andrea Biondi, Stephen Nimer, Dan Douer, Carlos Cordon-Cardo, Robert Gallagher, and Pier Paolo Pandolfi

From the Molecular Biology Program, Department of Pathology and Department of Medicine, Memorial Sloan-Kettering Cancer Center, Sloan-Kettering Division, Graduate School of Medical Sciences, Cornell University, New York, NY; Centro Ricerca M. Tettamanti, Clinica Pediatrica Universita' di Milano Bicocca, Monza, Italy; the Division of Hematology, University of Southern California Medical School and Norris Cancer Center, Los Angeles, CA; and the Montefiore Medical Center and Albert Einstein Cancer Center, New York, NY.

The promyelocytic leukemia (PML) tumor suppressor of acute promyelocytic leukemia (APL) is essential for a number of proapoptotic and growth-suppressive pathways as well as for the activity of differentiating agents such as retinoic acid (RA). In human APL, the dose of PML is reduced to heterozygosity given that one allele is involved in the chromosomal translocation while the status of the remaining PML allele is unknown. We have therefore used single-strand conformational polymorphism (SSCP) and sequencing analysis to screen DNA from APL patients for mutations at the PML locus. We identified DNA sequence variations resulting in a truncated PML protein in APL cases that displayed RA resistance and a very poor prognosis. Mutation analysis also led to the identification of aberrant PML sequence variations in other hematopoietic malignancies. Complete functional loss of PML is therefore selected by the APL phenotype and associates with poor prognosis and RA unresponsiveness.


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