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Alteration of SMRT Tumor Suppressor Function in Transformed Non-Hodgkin Lymphomas

Departments of ¹ Medicine and ² Pathology, Cardinal Bernardin Cancer Center, Loyola University Medical Center, Maywood, Illinois; ³ Department of Cancer Genetics, Roswell Park Cancer Institute, Buffalo, New York; ⁴ Haematology Department, Royal Free Hospital; ⁵ Royal Marsden Hospital/Institute of Cancer Research, London, United Kingdom; ⁶ Illinois Mathematics and Science Academy, Aurora, Illinois; ⁷ Metabolism Branch, National Cancer Institute, Bethesda, Maryland; ⁸ Institut National de la Sante et de la Recherche Medicale, Lille, France; and ⁹ Department of Pathology, University of Arizona, Tucson, Arizona

Requests for reprints: Lionel J. Coignet, Department of Cancer Genetics, Roswell Park Cancer Institute, Cell and Virus Building, Room 323, Elm and Carlton Streets, Buffalo, NY 14263. Phone: 716-8451242; Fax: 716-8451698; E-mail: lionel.coignet{at}roswellpark.org.

Indolent non-Hodgkin lymphomas are characterized by a prolonged phase that is typically followed by a clinical progression associated with an accelerated clinical course and short survival time. Previous studies have not identified a consistent cytogenetic or molecular abnormality associated with transformation. The development of a transformed phenotype, evolving from the original low-grade component, most likely depends on multiple genetic events, including the activation of synergistic dominant oncogenes and a loss of tumor suppressor gene functions. Complex karyotypes and relatively bad chromosome morphology are typical of transformed non-Hodgkin lymphomas, rendering complete cytogenetic analysis difficult. Here, we report the use of transformed non-Hodgkin lymphoma cell lines and primary samples to identify the involvement of the silencing mediator of retinoic acid and thyroid hormone receptor (SMRT) gene that maps at chromosome 12q24 in transformed non-Hodgkin lymphomas. We also show that down-regulation of SMRT in the immortalized "Weinberg's model" cell lines induces transformation of the cells. Assessment of cDNA array profiles should further help us to design a working model for SMRT involvement in non-Hodgkin lymphoma transformation as a novel, nonclassical tumor suppressor.

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