Originally published as JCO Early Release 10.1200/JCO.2005.04.531 on April 4 2005
Journal of Clinical Oncology, Vol 23, No 15 (May 20), 2005: pp. 3433-3438
© 2005 American Society of Clinical Oncology.
Allogeneic Stem-Cell Transplantation May Overcome the Adverse Prognosis of Unmutated VH Gene in Patients With Chronic Lymphocytic Leukemia
Carol Moreno,
Neus Villamor,
Dolors Colomer,
Jordi Esteve,
Rodrigo Martino,
Josep Nomdedéu,
Francesc Bosch,
Armando López-Guillermo,
Elías Campo,
Jorge Sierra,
Emili Montserrat
From the Department of Hematology and the Hematopathology Unit, Institute of Hematology and Oncology, Hospital Clínic, Institut d'Investigacions Biomèdiques August Pi i Sunyer; and Department of Hematology, Hospital de Sant Pau, Barcelona, Spain
Address reprint requests to Emili Montserrat, MD, Department of Hematology, Hospital Clínic, Villarroel, 170, 08036 Barcelona, Spain; e-mail: emontse{at}clinic.ub.es
PURPOSE: To investigate whether allogeneic stem-cell transplantation (allo-SCT) may overcome the negative impact of unmutated VH genes in the outcome of patients with chronic lymphocytic leukemia (CLL).
PATIENTS AND METHODS: We analyzed the outcome of patients who underwent SCT according to their VH mutational status.
RESULTS: Thirty-four patients (14 allo-SCT and 20 autologous SCT [auto-SCT]) presented unmutated VH genes and 16 patients presented mutated VH genes (nine allo-SCT and seven auto-SCT). Tumoral burden pre-SCT was significantly higher in the allo-SCT patients independent of the VH mutational status. The risk of relapse was significantly higher after auto-SCT (5-year risk, 61%; 95% CI, 44% to 84%) than after allo-SCT (5-year risk 12%, 95% CI, 3% to 44%; P < .05). In the unmutated group, 13 of 20 auto-SCT and two of 14 allo-SCT patients experienced disease progression, with a risk of relapse at 5 years of 66% (95% CI, 48% to 93%) v 17% (95% CI, 5% to 60%), respectively (P = .01).
CONCLUSION: These results show that allo-SCT may overcome the unfavorable effect of unmutated VH genes in patients with CLL.
Supported by grant No. 01/1581, Red de Genómica de Cáncer grant No. 03/10, and Red Estudio de Neoplasias linfoides grant No. 03/179, Instituto Nacional de Salud Carlos III-Ministerio de Sanidad from Fondo de Investigaciones Sanitarias (Spain) and the José Carreras International Leukemia Foundation grant Nos. EM-04; CR-04. C.M. is a recipient of a grant from the Fundación Española de Hematología y Hemoterapia.
Presented at the 45th meeting of the American Society of Hematology, San Diego, CA, December 6–9, 2003.
Authors' disclosures of potential conflicts of interest are found at the end of this article.
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