Impact of allogeneic haematopoietic stem cell transplantation in patients with abnl(17p) acute myeloid leukaemia
Brigitte Mohr, Johannes Schetelig, Kerstin Schäfer-Eckart, Norbert Schmitz, Mathias Hänel, Wolf Rösler, Norbert Frickhofen, Hartmut Link, Andreas Neubauer, Ulrich Schuler, Uwe Platzbecker, Jan M Middeke, Gerhard Ehninger, Martin Bornhäuser, Markus Schaich, Friedrich Stölzel, Study Alliance Leukaemia (SAL), Brigitte Mohr, Johannes Schetelig, Kerstin Schäfer-Eckart, Norbert Schmitz, Mathias Hänel, Wolf Rösler, Norbert Frickhofen, Hartmut Link, Andreas Neubauer, Ulrich Schuler, Uwe Platzbecker, Jan M Middeke, Gerhard Ehninger, Martin Bornhäuser, Markus Schaich, Friedrich Stölzel, Study Alliance Leukaemia (SAL)
Abstract
The role of allogeneic stem cell transplantation (HSCT) as compared to chemotherapy in acute myeloid leukaemia (AML) patients with abnormalities of chromosome 17p [abnl(17p)] has not yet been defined. Therefore, we analysed 3530 AML patients treated in three randomized, prospective, controlled clinical trials and compared post-remission therapies using a multivariate Cox regression analysis to determine whether allogeneic HSCT is superior than chemotherapy in overcoming the detrimental impact of patients with abnl(17p) AML. One hundred and forty-three patients (4%) were identified with abnl(17p) AML. All patients had received intensive induction chemotherapy. Forty-seven patients with a median age of 54 years (18-69 years) proceeded to allogeneic HSCT in first or second remission. The 3-year overall survival (OS) rate for the entire cohort of patients was 4% [95% confidence interval (CI), 1-7%]. OS and event-free survival at 3 years, calculated from the day of HSCT, was 11% (95% CI, 2-20%) and 6% (95% CI, 0-13%), respectively. Multivariate Cox regression analysis showed no benefit of allogeneic HSCT compared to chemotherapy (Hazard Ratio 0·97, 95% CI 0·56-1·67, P = 0·9). In conclusion, allogeneic HSCT does not improve survival in patients with abnl(17p) AML as compared to other adverse cytogenetic risk abnormalities.
© 2013 Blackwell Publishing Ltd.
Source: PubMed