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• W1600194035 abstract "Children with leukaemia that is refractory to chemotherapy prior to stem cell transplantation (SCT), or that relapses early following SCT, have a poor prognosis (Mehta & Davies, 2009). Establishing a graft-versus-leukaemia (GVL) effect may improve the cure rate, but can be associated with significant toxicity (Mehta et al, 1997; Vettenranta et al, 2003). We hypothesized that the addition of alpha interferon (IFNα) to SCT or to donor lymphocyte infusion (DLI) might induce or augment GVL in a more controllable manner (Nagafuji et al, 1998; Steegmann et al, 1999). Seventeen children received IFNα therapy with initial SCT (n = 4) or following relapse and together with second SCT (n = 7) or DLI (n = 6). Initial diagnoses included: chronic myeloid leukaemia (CML) (n = 3, one in blast crisis), Philadelphia-positive acute lymphoblastic leukaemia (Ph+ ALL; n = 6), common ALL (n = 1), myeloproliferative disease/myelodysplasia/acute myeloid leukaemia (AML) (n = 3), AML refractory to or relapsed during first line chemotherapy (n = 2), bilineage leukaemia refractory to chemotherapy (n = 2). IFNα was started at a dose of 3 megaunits/m2 subcutaneously 3 d per week and escalated to 3 megaunits/m2 5 d per week then 5 megaunits/m2 5 d per week at 2 weekly intervals as tolerated and continued in the absence of graft-versus-host disease (GVHD) for up to 1 year. Three patients (CML) received concomitant therapy with Glivec® for a period of time – all are now off therapy. Patient outcomes are shown in Table I. Ten patients (59%) developed acute GVHD (aGVHD); grade I (n = 1), grade II (n = 5) and grade III (n = 4), 2 weeks to 14 months from starting IFNα. aGVHD responded to stopping IFNα and use of topical steroids in three patients; seven received high dose steroids, two received antibody therapy (inflixamab and dacluzimab). Seven patients developed chronic GVHD (cGVHD): four limited, three extensive. Three received ciclosporin (CSA), two received methotrexate. One patient died from lung GVHD. Two patients have residual impaired lung damage, one is awaiting lung transplant. Three patients have on-going cGVHD [sclerodermous skin (n = 2); skin and mouth (n = 1)] requiring minimal immunosuppression 36–72 months from starting IFNα. Ten patients (59%) remain well and in remission, at a median of 56 months (range 14–136 months) from therapy, four of who have not developed GVHD. Four (24%) died from relapse, at a median of 15 months (range 8–27 months), one despite grade III skin and gut GVHD. Three died from transplant-related complications: lung GVHD (n = 1), idiopathic pneumonitis (n = 1) and aspergillus infection (n = 1). Overall, this data shows promising results for the use of IFNα to augment GVL responses in patients with high-risk leukaemia not cured with standard transplant procedures. Control of disease was better in those who developed GVHD, however, mortality was higher, resulting in a similar overall survival (Fig 1). Kaplan Meier survival curve following IFNαtherapy depending on whether or not patients developed graft-versus-host disease (GVHD). There was no survival advantage for either group (P = 0·92). This early data warrants a formal study of IFNα+/− DLI post-SCT. Early use of IFNα prompted by detection of minimal residual disease prior to overt leukaemic relapse, coupled with rapid cessation of IFNα at onset of GVHD, may augment the GVL response and reduce mortality from GVHD in this high-risk group of children (Slavin et al, 1990; Arnold et al, 1993; Singhal et al, 1999). Nichola Cooper and Paul Veys performed the analysis and wrote the paper, Kanchan Rao, Nick Goulden and Persis Amrolia were involved in the design of the study, in managing the patients and in the collection of data. All authors contributed to the writing of the paper. No author has a relevant conflict of interest." @default.
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• W1600194035 date "2011-10-08" @default.
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• W1600194035 title "Alpha interferon augments the graft-versus-leukaemia effect of second stem cell transplants and donor lymphocyte infusions in high-risk paediatric leukaemias" @default.
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• W1600194035 doi "https://doi.org/10.1111/j.1365-2141.2011.08889.x" @default.
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