title: Acute promyelocytic leukemia: a curable disease.
abstract: The Second International Symposium on Acute Promyelocytic Leukemia (APL) was held in Rome in 12-14 November 1997. Clinical and basic investigators had the opportunity to discuss in this meeting the important advances in the biology and treatment of this disease achieved in the last 4 years, since the First Roman Symposium was held in 1993. The first part of the meeting was dedicated to relevant aspects of laboratory research, and included the following topics: molecular mechanisms of leukemogenesis and of response/resistance to retinoids, biologic and therapeutic effects of new agents such as arsenicals and novel synthetic retinoids; characterization of APL heterogeneity at the morphological, cytogenetic and immunophenotypic level. The updated results of large cooperative clinical trials using variable combinations of all-trans retinoic acid (ATRA) and chemotherapy were presented by the respective group chairmen, and formed the 'core' part of the meeting. These studies, which in most cases integrated the molecular assessment of response to treatment, provided a stimulating framework for an intense debate on the most appropriate frontline treatment options to be adopted in the future. The last day was dedicated to special entities such as APL in the elderly and in the child, as well as the role of bone marrow transplantation. The prognostic value of molecular monitoring studies was also discussed in the final session of the meeting. In this article, we review the major advances and controversial issues in APL biology and treatment discussed in this symposium and emerging from very recent publications. We would like to credit the successful outcome of this meeting to the active and generous input of all invited speakers and to participants from all over the world who provided constructive and fruitful discussions.
authors.affiliation: Department of Cellular Biotechnology and Hematology, University La Sapienza, Rome, Italy.
authors.forename: F
authors.initials: F
authors.lastname: Lo Coco
authors.forename: C
authors.initials: C
authors.lastname: Nervi
authors.forename: G
authors.initials: G
authors.lastname: Avvisati
authors.forename: F
authors.initials: F
authors.lastname: Mandelli
mesh_terms: D000368:Aged; D000970:Antineoplastic Agents / Q000627:therapeutic use*; D000077237:Arsenic Trioxide; D001152:Arsenicals / Q000627:therapeutic use; D002648:Child; D004351:Drug Resistance; D018380:Hematopoietic Stem Cell Transplantation; D006801:Humans; D016130:Immunophenotyping; D007621:Karyotyping; D015473:Leukemia, Promyelocytic, Acute / Q000175:diagnosis / Q000235:genetics / Q000378:metabolism / Q000628:therapy*; D009363:Neoplasm Proteins / Q000378:metabolism; D018365:Neoplasm, Residual; D009687:Nuclear Proteins; D010087:Oxides / Q000627:therapeutic use; D000071156:Promyelocytic Leukemia Protein; D012008:Recurrence; D012106:Research; D012384:Rome; D014157:Transcription Factors / Q000378:metabolism; D014212:Tretinoin / Q000627:therapeutic use*; D025521:Tumor Suppressor Proteins
chemical_list: D000970:Antineoplastic Agents; D001152:Arsenicals; D009363:Neoplasm Proteins; D009687:Nuclear Proteins; D010087:Oxides; D000071156:Promyelocytic Leukemia Protein; D014157:Transcription Factors; D025521:Tumor Suppressor Proteins; C070576:PML protein, human; D014212:Tretinoin; D000077237:Arsenic Trioxide