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Relapse-incidence and non-relapse mortality (NRM) were 9% (95% CI, 0��5�C17%) and 27% (95% CI, 15�C41%) at day +100 and 50% (95% CI, 34�C65%) and 45% (95% CI, 30�C59%) 3?years after HSCT (Fig?3). Sixteen patients received allogeneic HSCT in first CR. All patients died within 39?months (Fig?2B). The cause of death was relapse in eleven patients (69%) and non-relapse mortality in five patients (31%). Five patients with primary induction failure received haploidentical HSCT. Four of five patients died from non-relapse related complications within http://www.selleckchem.com/products/loxo-101.html 6?months after haploidentical HSCT while one patient relapsed 7?months after haploidentical HSCT. Only two patients were alive and relapse-free after allogeneic HSCT with a follow-up of 32 and 59?months. Abnl(17p) AML was confirmed by FISH in both cases. Both patients had been transplanted http://www.selleckchem.com/products/abc294640.html in aplasia after induction/salvage-therapy and received reduced-intensity conditioning with fludarabine and melphalan. Allogeneic HSCT was tested as a time-dependent covariate in a Cox regression model with age and white blood cell (WBC) count at diagnosis as covariates. The time-dependent covariate allows for a ��group switch�� of transplanted patients at the time of HSCT from the control group (patients treated with chemotherapy only) into the group of transplanted patients in parallel to a Mantel�CByar analysis. In this model, age [HR 1��02 (95% CI, 1��002�C1��05, P?=?0��03)] and WBC count [HR 1��33 for the logarithm of WBC count (��109/l) (95% CI, 1��14�C1��54, P? http://www.selleck.cn/products/ON-01910.html Abnormalities of 17p in AML predict a detrimental outcome when they are part of CK but also when found as a single abnormality (Haferlach et?al, 2008; Nahi et?al, 2008a; Seifert et?al, 2009). In the majority of AML patients with abnl(17p), as shown in other malignancies, the tumour-suppressor effect of the remaining TP53 allele disappears through mutation (Nigro et?al, 1989; Fenaux et?al, 1991; Soenen et?al, 1998; Nahi et?al, 2008a; R��cker et?al, 2012). Current AML chemotherapy is at least partly dependent on the function of TP53 as an apoptosis mediator. This may explain one important finding of this study, namely that consolidation chemotherapy obviously was insufficient to fully eradicate the leukaemic clone, although 36% of our patients achieved CR. Even more astonishing when comparing allogeneic HSCT versus consolidation chemotherapy in patients with abnl(17p) AML in multivariate analysis was that no difference in OS was found (HR 0��97). It is generally accepted that AML patients with adverse risk cytogenetics benefit substantially through allogeneic HSCT (Slovak et?al, 2000; Suciu et?al, 2003; Schlenk et?al, 2010). Our findings indicate that this might not be true for the adverse cytogenetic risk trait abnl(17p) in AML.