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  • 1
    In: Leukemia, Springer Science and Business Media LLC, Vol. 35, No. 8 ( 2021-08), p. 2332-2345
    Type of Medium: Online Resource
    ISSN: 0887-6924 , 1476-5551
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    Language: English
    Publisher: Springer Science and Business Media LLC
    Publication Date: 2021
    detail.hit.zdb_id: 2008023-2
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  • 2
    In: Blood, American Society of Hematology, Vol. 124, No. 21 ( 2014-12-06), p. 1845-1845
    Abstract: Background: Therapeutic guidelines in essential thrombocytemia (ET) are based on established criteria, ie. age more than 60 years, history of thrombosis, platelets more than 1000-1500 ×109/L and to lesser degree cardio-vascular risk factors. Hydroxyurea and anagrelide are the most commonly used cytoreductive therapy for high risk ET. Despite a proven activity in Ph negative myeloproliferative disorders, generalized use and efficacy of Interferon-alpha (IFN-α) have been hampered by frequent side effects. Nonetheless it is a non leukemogenic therapeutic option for younger patients (pts) and during pregnancy. Two phase II trials using Pegylated (Peg) forms of IFN-α in pts with polycythemia vera (PV) or high risk ET have provided interesting results: i) an improved toxicity profile generally associated with a rapid hematolologic response, ii) a molecular response described in a subset of JAK2V617F positive PV or ET pts treated with PegIFN-α. Aim: To estimate the rationale of PegIFN-α therapy selection in high risk ET patients, efficacy and tolerance. Methods:Cases of high risk ET patients, who started PegIFN-α therapy between 2006 and 2011, were reported by centres of the French Intergroup of Myeloproliferative disorders and included in an observational study. We collected information regarding history of MPN, treatment, hematologic response at different timepoints, toxicities related to PegIFN-α, thrombo-hemorrhagic events and hematologic progression. The current analysis was performed on 103 consecutive pts. Results: Median follow-up from ET diagnosis was 9 years (3-27). 74% of pts were female, median age was 37 years (range 16-67). Previous vascular event was observed in 36% of cases and JAK2V617F mutation was detected in 52% of pts. . Median time from diagnosis to PegIFN-α was 40 months (1-255). PegIFN-α was administered after hydroxyurea and anagrelide in second or third line (56% and 27% respectively). No prior therapy has been used for 16% of pts. Reasons for starting PegIFN-α were lack of hematologic response (21%), toxicity to prior therapies (17%), pregnancy (15%), or medical decision for younger pts (47%). Pts received either PegIFNα-2a (n=91) or PegIFNα-2b (n=12), based on physician decision. According to the 2009 European LeukemiaNet criteria and with a median exposure to PegIFN-α of 29 months (1-92), 81% of pts achieved a complete hematologic response (CHR). Cumulative incidence of CHR were 58 % (95% CI: 49-68), 73% (95% CI: 65-81) and 80% (95% CI: 71-87) at 6, 12 and 24 months respectively. By analysing the response according to JAK2 status, cumulative incidence of CHR was better for the JAK2V617F positive subgroup (p=0.0183, overall). At 36 months estimated CHR rates were 89% (95% CI: 79-95) and 70% (95% CI: 57-82) for JAK2VF positive vs negative subgroup respectively. Median exposure to PegIFN-α was 29 months in both groups. At last follow-up, with a median of 42 months since PegIFN-α initiation, 53% of the pts were still treated with PegIFN-α. Among them, 76% have maintained a CHR. Reasons for discontinuation of PegIFN-α (47% of pts) were consecutive to PegIFN-α toxicity (59%), -mainly chronic moderate non hematologic toxicity-, or hematologic responses were considered insufficient in16%. In addition, PegIFN-α has been stopped in a subset of pts who achieved a durable stable CHR. In Conclusion, This study provides results of PegIFN-α therapy in a cohort of high risk ET pts not included in clinical trials. In this selected population of young pts, a durable efficacy of therapy was observed in half of patients. Characteristics of hematologic response according to molecular status will be presented. These results support the PegIFN-α as an alternative therapy to hydroxyurea and anagrelide in high risk ET, and warrant its investigation in further prospective randomized studies. Disclosures Roy: Merck: Peg-Interferon provided for academic clinical trial in CML Other. Off Label Use: Peg-Interferon in essential thrombocythemia. Gyan:Roche: Research Funding. Nicolini:BMS: Consultancy, Membership on an entity's Board of Directors or advisory committees; Novartis: Consultancy, Membership on an entity's Board of Directors or advisory committees, Research Funding, Speakers Bureau; Ariad: Membership on an entity's Board of Directors or advisory committees, Speakers Bureau. Kiladjian:Roche: Peg-Interferon provided for academic clinical trial in PV Other.
    Type of Medium: Online Resource
    ISSN: 0006-4971 , 1528-0020
    RVK:
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    Language: English
    Publisher: American Society of Hematology
    Publication Date: 2014
    detail.hit.zdb_id: 1468538-3
    detail.hit.zdb_id: 80069-7
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  • 3
    In: Journal of Infection, Elsevier BV, Vol. 72, No. 2 ( 2016-02), p. 214-222
    Type of Medium: Online Resource
    ISSN: 0163-4453
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    Language: English
    Publisher: Elsevier BV
    Publication Date: 2016
    detail.hit.zdb_id: 2012883-6
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  • 4
    In: Leukemia Research, Elsevier BV, Vol. 56 ( 2017-05), p. 21-28
    Type of Medium: Online Resource
    ISSN: 0145-2126
    Language: English
    Publisher: Elsevier BV
    Publication Date: 2017
    detail.hit.zdb_id: 2008028-1
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  • 5
    In: Bulletin du Cancer, Elsevier BV, Vol. 109, No. 7-8 ( 2022-07), p. 862-872
    Type of Medium: Online Resource
    ISSN: 0007-4551
    Language: French
    Publisher: Elsevier BV
    Publication Date: 2022
    detail.hit.zdb_id: 213270-9
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  • 6
    In: Blood, American Society of Hematology, Vol. 116, No. 21 ( 2010-11-19), p. 2267-2267
    Abstract: Abstract 2267 Prior to the introduction of the tyrosine kinase inhibitors (TKI) into clinical practice, the only curative therapy for chronic myeloid leukaemia (CML) was allogeneic hematopoietic stem cell transplantation (HSCT). HSCT is nowadays recommended for patients in accelerated phase, blastic phase or with the T315I mutation and for patients who experience second-line TKIs (TKI2) failure or intolerance. The impact of TKI2 for CML on the results of subsequent HSCT has not yet been clearly established, although preliminary data does not suggest an increase of non relapse mortality (NRM) in patients previously treated with these agents. To assess whether exposure to TKI2s before HSCT adversely affects outcome, we retrospectively analyzed 31 patients with CML reported to the French registry for HSCT between January 2001 and December 2008 who received a first HSCT for imatinib resistant or intolerant CML subsequently treated with either nilotinib or dasatinib or both. The median age at diagnosis was 39.8 years (range, 19–61). At the start of TKI, 15 (48%) patients were in chronic phase, 12 (39%) patients were in accelerated phase and 4 (13%) patients were in blast crisis. For chronic phase patients, 6 (40%) patients were classified as low Sokal risk, 7 (46%) as intermediate risk, and 2 (14%) as high risk. After imatinib failure (among the 27 patients in chronic or accelerated phase at diagnosis), 21 and 6 patients received dasatinib and nilotinib, respectively. Among these patients, 9 patients received a third line therapy, including 5 sequential therapies with both drugs. The best response to the second and third-line treatments with TKI2 was a complete molecular response in 2 patients, a major molecular response in 2 patients, a complete cytogenetic response (CCR) in 7 patients, a complete hematologic response in 14 patients and no response in 2 patients. 14 patients eventually failed TKI2 treatment because of resistance, whereas 8 were considered as intolerant. Of 14 patients who developed resistance to TKI2, 2 had a mutation identified (T315I in both cases). Median interval from diagnosis to HSCT was 19 months (range, 3–151). At time of transplant, 21 patients were in chronic phase, 10 in accelerated phase and none in blast crisis. 19 patients received a graft from an unrelated donor whereas 12 a match related donor. Stem cell source was peripheral blood, bone marrow or cord blood in 20, 8 and 3 patients, respectively. The conditioning regimen was myeloablative in 21 patients combining either TBI and cyclophosphamide (9 patients) or high dose IV busulfan and cyclophosphamide (12 patients), and a RIC for 10 patients. All patients engrafted successfully: median time to neutrophil and platelet recovery was 18 days and 21 days respectively. Grade 2–4 acute graft-versus-host disease (aGVHD) was observed in 11 (37.9%) patients; grade 3–4 aGVHD occurred in 6 (20.6%) patients. Chronic GVHD was observed in 15 (60%) of 25 patients alive after day 100. The median follow-up after HSCT is 27 months (range, 1.2–50.2). At time of analysis, 11 (35%) patients died, 7 (22.5%) from NRM and 4 (12.5%) from progression of disease. NRM was due to infection (3 patients), GVHD (2 patients), post transplant lymphoma disease (1 patient) and unknown cause (1 patient). The 1-year overall survival (OS) was 79.2% (95% CI, 64,3-94,1%) and the estimated 2-year OS was 55,5% (95% CI, 35,0-75,9%). One-year relapse and NRM rates were respectively 10,3% (95% CI, 2.5–24.6%) and 19.1% (95% CI, 6.7–36.2%). In univariate analysis, no variable had a significant impact on outcome among Sokal score, disease phase at diagnosis, Grathwol score, age at HSCT, time from diagnosis to HSCT, or quality of response before HSCT. In a multivariate analysis, only quality of response (at least better than CCR) was significantly associated with a better outcome in terms of OS (p=0.0459, HR=0.17, 95% CI=0.03-0.97). In conclusion, TKI2 prior to HSCT did not result in an increased risk of NRM. However, our observation that patients in cytogenetic or molecular response at time of HSCT have a significant better outcome underscores the importance of a stringent prospective molecular monitoring under TKI2 therapy and the need for prognostic factors of response under TKI2. Such elements could help to better define after initiating TKI2 treatment patients that could really benefit from HSCT and the best timing of the procedure. Disclosures: No relevant conflicts of interest to declare.
    Type of Medium: Online Resource
    ISSN: 0006-4971 , 1528-0020
    RVK:
    RVK:
    Language: English
    Publisher: American Society of Hematology
    Publication Date: 2010
    detail.hit.zdb_id: 1468538-3
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  • 7
    In: Haematologica, Ferrata Storti Foundation (Haematologica), Vol. 107, No. 12 ( 2022-08-04), p. 2944-2949
    Type of Medium: Online Resource
    ISSN: 1592-8721 , 0390-6078
    Language: Unknown
    Publisher: Ferrata Storti Foundation (Haematologica)
    Publication Date: 2022
    detail.hit.zdb_id: 2186022-1
    detail.hit.zdb_id: 2030158-3
    detail.hit.zdb_id: 2805244-4
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  • 8
    In: Blood, American Society of Hematology, Vol. 132, No. Supplement 1 ( 2018-11-29), p. 5720-5720
    Abstract: Introduction: Graft-versus-host disease (GVHD), and complications of its treatment are the major causes of morbidity and mortality following allogeneic hematopoietic cell transplantation (allo-HCT). With the use of standard GVHD prophylaxis with classical administration of Anti-thymocyte globulin (ATG), calcineurin inhibitors (CNIs) and methotrexate, the incidence of acute and chronic forms of GVHD remains not negligible. Extracorporeal photopheresis (ECP) has shown very promising results as curative strategy for GVHD but also when used prophylactically. The primary objective of this observational study was to perform an exhaustive description concerning patients receiving ECP after steroid resistance for either acute or chronic GVHD following allo-HCT, secondary objectives were to evaluate the efficacy and long-term outcomes. Patients and methods: We included 82 patients who underwent allo-HCT between years 2001 and 2016, 50 (61%) were males, median age at allo-HCT was 52 years (20-67). Major diagnoses were acute leukemias (45%), myelodysplastic syndromes (17%) and multiple myeloma (11%). Before transplantation, 43 (52%) patients were in complete remission or in chronic phase. Donors were identical siblings in 51% of patients, matched unrelated in 24%, mismatched unrelated in 24% and haploidentical in 1%. Hematopoietic Stem Cell source was peripheral blood in 65%, bone marrow in 27% and cord blood in 8%. Conditioning regimens were non myeloablative in 63% cases and myeloablative in 37%. ATG was used during conditioning in 63% of patients. GVHD prophylaxis consisted on cyclosporine A (CsA) alone in 21% of patients, CsA + mycophenolate mofetil in 27%, CsA + methotrexate in 26%, the rest received other combinations. In acute GVHD, first treatment consisted in methyl-prednisolone 2mg/Kg/day in combination with CNIs; and in chronic GVHD, it was methyl-prednisolone 0.5 - 1 mg/Kg/day + CNIs. ECP was performed using peripheral venous access. ECP was initiated after transplantation either for acute GVHD [N=28 (34%), 9 grade II, 3 grade III and 16 grade IV] affecting skin alone (N=5), gut alone (N=14), gut + liver (N=8); or for chronic GVHD [N=54 (66%), 19 (35%) limited and 35 (65%) extensive] . A total of 3300 ECP sessions were performed, majority were twice a week; the median number of sessions/patient was 21 (min: 2, max: 131) for a median duration of 4.2 months (range: 0.5-73). ECP response evaluation was assessed after 4 weeks of treatment, patients were considered responding to ECP if more than 50% resolution of clinical GVHD manifestation of the organ involved was registered. Results: Among the 28 patients treated for acute GHVD, one was not evaluable because of disease progression and early death, 11/27 (41%) were responders to ECP and 16/27 (59%) were not responders and died later from GVHD associated to other complications. Among the 54 patients with chronic GVHD, 32/54 (59%) were responders. Of note, in both forms of acute and chronic GVHD, responding patients had more skin forms whereas non-responding patients has more organ-involved forms especially liver and gut. After a median follow-up of 26 months, 32 (39%) patients are alive and 50 (61%) died, 43 from TRM causes (17 in the aGVHD group and 26 in the cGVHD group). Patients with acute GVHD had a median OS of 6 months with a survival probability at 2 years of 31% [95%CI: 14-56], those with chronic GVHD had a median OS of 36 months with a survival probability at 2 years of 55% [95%CI: 40-78] . Patients with chronic GVHD had better PFS probability at 2 years with 55% (95% CI: 43-70) versus 27% (95% CI: 14-51) for those with acute GVHD, p=0.007. In stepwise multivariate analysis, acute GVHD grade III-IV, significantly impacted on OS (HR=7.77, 95%CI: 1.7-34), p=0.007, while ATG and also aGVHD grade III-IV, negatively impacted PFS, HR=2, 95%CI: 1.02-4.12, p=0.04, and HR=5.88, 95%CI: 1.7-20, p=0.005 respectively. Conclusion: We confirm that ECP is an effective treatment for GVHD in a good proportion of patients with overall response rate of 59%. Interestingly, we observed a better PFS in patients receiving ECP for longer time as in the case of chronic GVHD, which could be related to the GVL effect itself but also a possible involvement of the ECP. As patients with advanced phase of GVHD were poor responders, we suggest that an early use of ECP in the acute phase of the inflammation before organ damage, could lead to optimal results. Disclosures Michallet: Novartis: Research Funding; Octapharma: Membership on an entity's Board of Directors or advisory committees; Chugai: Consultancy. Nicolini:Incyte: Consultancy, Honoraria, Speakers Bureau; Sun Pharma: Consultancy; Bristol-Myers Squibb: Consultancy, Honoraria, Speakers Bureau.
    Type of Medium: Online Resource
    ISSN: 0006-4971 , 1528-0020
    RVK:
    RVK:
    Language: English
    Publisher: American Society of Hematology
    Publication Date: 2018
    detail.hit.zdb_id: 1468538-3
    detail.hit.zdb_id: 80069-7
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  • 9
    In: Blood, American Society of Hematology, Vol. 114, No. 22 ( 2009-11-20), p. 3286-3286
    Abstract: Abstract 3286 Poster Board III-1 Introduction: Nilotinib, a potent and highly selective BCR-ABL kinase inhibitor, is approved for the treatment of patients (pts) with Philadelphia chromosome-positive chronic myelogeneous leukemia (Ph+ CML) in chronic phase (CML-CP) and accelerated phase (CML-AP) who are resistant or intolerant to prior therapy including imatinib. The ENACT study is a Phase IIIb, open-label, multicenter study that evaluated the efficacy and safety of nilotinib in adult pts with imatinib-resistant or intolerant CML in a clinical practice setting outside of a registration program. It is the largest single source of efficacy and safety information of any available tyrosine kinase inhibitor (TKI) in CML, particularly among the elderly. Methods: The present is a sub-analysis of the ENACT study on the efficacy and safety of 400 mg twice daily nilotinib in elderly (aged =60 years) pts initiating treatment in CML-CP who were resistant and/or intolerant to imatinib. Results: Of the 1,422 CML-CP pts enrolled in the ENACT study between January 2006 and October 2008, 452 (32%) were elderly (=60 years) at study initiation and 165 (37%) of these pts were =70 years [10 (2%) were =80 years]. Countries that enrolled =20 elderly pts include France, Italy, USA, Germany, UK, Spain, Canada, and Brazil. At study initiation, elderly pts had longer median durations of CML ( 〈 60: 51.1 months; =60: 69.3; =70: 66.6) and higher proportions with CML duration 〉 5 years ( 〈 60: 43%; =60: 56%; =70: 52%). Besides imatinib, prior CML treatments received by elderly pts included dasatinib (=60: 20%; =70: 19%), cytarabine (=60: 23%; =70: 19%), busulfan (=60: 10%; =70: 7%), and interferons (=60: 50%; =70: 42%). Elderly pts were previously treated with imatinib for longer median durations ( 〈 60: 27.4 months; =60: 32.7; =70: 29.9), with higher proportions treated for 〉 5 years ( 〈 60: 12%; =60: 19%; =70: 18%). The proportion of imatinib-intolerant to resistant elderly pts was about 1:1, which was higher than the proportion among 〈 60 pts at about 0.6:1, such that relatively few elderly pts had prior highest imatinib dose 〉 800 mg ( 〈 60: 34%; =60: 26%; =70: 21%). While response rates to prior imatinib were similar, among pts who required therapy after failing imatinib, elderly pts had lower cytogenetic response rates ( 〈 60: 22%; =60: 17%; =70: 19%) to prior dasatinib. During ENACT, less than 50% of elderly pts experienced nilotinib dose interruptions (=60: 46%; =70: 41%) and reductions (=60: 7%; =70: 6%) lasting 〉 5 days, which was consistent with the overall ENACT dataset. The median duration of dose interruptions and reductions was 15 (=70: also 15) and 41 (=70: 32) days, respectively. The main reason for dose interruptions and reductions was adverse events (AEs). The median duration of nilotinib exposure was 227 days (=70: 219) and the median dose intensity was 749 mg/day (=70: 775). Efficacy was similar among elderly pts, with 39% (=70: 35%) of pts achieving complete hematologic response (CHR), 41% (=70: 39%) achieving major cytogenetic response (MCyR) and 31% (=70: 33%) achieving complete cytogenetic response (CCyR). MCyR rate was also similar among elderly hematologic responders (=60: 64%; =70: 65%). Among elderly pts requiring nilotinib therapy after both imatinib and dasatinib, and therefore have more resistant CML, CHR rate was 39% (=70: 32%), MCyR rate was 28% (=70: 29%) and CCyR rate was 20% (=70: 16%). Safety was likewise similar among elderly pts, with grade 3/4 study drug-related AEs occurring in 56% of pts (=70: 53%). The most frequent of these AEs were thrombocytopenia (=60: 24%; =70: 21%) and neutropenia (=60: 14%; =70: 11%). The most common method of managing these AEs was brief dose interruptions and/or reductions [thrombocytopenia (=60:86/108 pts; =70: 30/35), neutropenia (=60: 42/62 pts; =70: 9/18)]. Among elderly pts with prior dasatinib, 53% (=70: 58%) experienced grade 3/4 study drug-related AEs, while 7 out of 8 pts with pleural effusion on dasatinib no longer had it on nilotinib. Conclusions: In ENACT, pts aged =60 years at study initiation appear to have longer durations of CML, be more heavily pre-treated and more intolerant to imatinib than the younger cohort. Nonetheless, nilotinib induced comparable clinical responses in CML-CP pts regardless of age. Importantly, the safety profile of nilotinib is maintained in elderly pts. Disclosures: le Coutre: Novartis: Honoraria, Research Funding; BMS: Honoraria. Turkina:Novartis Pharmaceuticals: Honoraria. Kim:Bristol-Myers Squibb: Honoraria, Membership on an entity's Board of Directors or advisory committees, Research Funding; Novartis: Honoraria, Membership on an entity's Board of Directors or advisory committees, Research Funding; Wyeth: Research Funding. Ceglarek:Novartis Pharmaceuticals: Honoraria. Shen:Novartis Pharmaceuticals: Honoraria. Smith:Novartis Pharmaceuticals: Honoraria. Rizzieri:Novartis Pharma: Honoraria, Research Funding, Speakers Bureau. Szczudlo:Novartis: Employment. Berton:Novartis Pharmaceuticals: Employment. Wang:Novartis Pharmaceuticals: Employment. Wang:Novartis Pharmaceuticals: Research Funding. Nicolini:Novartis Pharma: Consultancy, Honoraria, Research Funding, Speakers Bureau; Bristol Myers Squibb: Consultancy, Honoraria, Research Funding, Speakers Bureau; Chemgenex: Honoraria, Speakers Bureau.
    Type of Medium: Online Resource
    ISSN: 0006-4971 , 1528-0020
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    Language: English
    Publisher: American Society of Hematology
    Publication Date: 2009
    detail.hit.zdb_id: 1468538-3
    detail.hit.zdb_id: 80069-7
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  • 10
    In: Blood, American Society of Hematology, Vol. 114, No. 22 ( 2009-11-20), p. 1109-1109
    Abstract: Abstract 1109 Poster Board I-131 The main objective of the CML-Registry of the European Treatment and Outcome Study (EUTOS) is to collect diagnostic, treatment and outcome data of CML-patients in Europe in order to allow for the analysis of prognostic factors, the evaluation of the quality of care and the comparative assessment of outcomes. Methods Eligibility criteria were: diagnosis of chronic phase Ph+ or bcr/abl positive CML between 2002 and 2006, age ≥ 18 years, and start with any kind of imatinib-based treatment in a prospective study within six months after first diagnosis. For hematologic (HR), cytogenetic (CgR), and molecular (MR) remission the ELN criteria were used. Competing risk estimations and Landmark analyses were applied when indicated. Patients from the FI-LMC-group in France (n=526), Germany (n=644), Italy (n=513), The Netherlands (n=119), the Nordic Countries (Denmark, Finland, Norway, Sweden, n=140)) and Switzerland (n=13) were included (date: 07/11/2009), for an overall n of 1955 patients. Results Median age was 52.5 years and 45% were female. The Euro prognostic score profile was for 38% of the patients low, for 51% intermediate and for 11% high risk. Imatinib 400 mg was allocated to 41%, Imatinib 600 mg to 8%, Imatinib 800 mg to 17%, and Imatinib-based combinations with IFN or Ara C to 34% of the patients. Median observation time was 24 months (range: 1-81). Complete hematologic remission (CHR) was finally achieved by 97%, complete cytogenetic remission (CCgR) by 94%, and major molecular remission (MMR) after 18 months by 62%. Overall survival (OS) after 60 months was 92%. Euro score clearly separated high risk vs. non high risk patients with regard to CHR (p=.0002), CCgR (p=.0023), but not for MMR, whereas Sokal score did so for CCgR (p 〈 .0001). Deletion 9q did not show any impact on CHR, CCgR or MMR. Using Landmark-analysis with those 1012 patients who provided complete data for CHR, CCgR and MMR, CHR within 6 months from day 1 of imatinib treatment showed an impact on the chance to achieve CCgR (96.1% vs. 87.5% p=.0003) and MMR at 18 month (56.1% vs. 48.5%, p=.087). CHR within 3 months did not show a relevant impact on CCgR and MMR. Partial CgR (Ph+ 〈 35%, n=725)) within 6 months was associated with a higher chance to achieve MMR at 18 month (62.8% vs. 51.4% p=.0003). Patients who did not achieve CCgR within 3 (93%), 6 (70%), 12 (29%) or 18 (18%) months experienced an increasing risk for disease progression of 6%, 7%, 11% and 14% respectively but still showed a chance to eventually achieve CCgR of 87%, 83%, 60%, and 36%. Conclusions: This combined analysis of multinational European data showed very good response data regarding CHR, CCgR, MMR, and OS. Current prognostic CML scores seem to not separate prognosis of CML-patients sufficiently well. Early response markers like CHR and CgR after 6 months allow to differentiate the prognosis with regard to MMR but their clinical relevance may be questioned. Patients without CCgR within 6 months have a higher risk for disease progression and thus a closer follow up is indicated. With accumulating observation time the European CML Registry will allow to answer many clinically relevant questions about the prognostic value of early response markers. Disclosures Hasford: Novartis Pharma: Research Funding. Rosti:Novartis Pharma, Bristol Myers Squibb: Consultancy, Speakers Bureau. Baccarani:Novartis Pharma, Bristol Myers Squibb, Merck Sharp & Dome, Pfizer: Consultancy, Speakers Bureau. Montrucchio:Novartis Pharma : Employment. Rancati:Novartis Pharma: Employment. Simonsson:Novartis, BMS, Schering-Plough: Consultancy, Honoraria, Research Funding. Ossenkoppele:Novartis Pharma, BMS: Consultancy. Hehlmann:Novartis Pharma: Research Funding.
    Type of Medium: Online Resource
    ISSN: 0006-4971 , 1528-0020
    RVK:
    RVK:
    Language: English
    Publisher: American Society of Hematology
    Publication Date: 2009
    detail.hit.zdb_id: 1468538-3
    detail.hit.zdb_id: 80069-7
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