The flow cytometric detection of aberrant antigen expression is one method proposed for the quantification of minimal residual disease (MRD) in acute leukemias. The present study was designed to investigate the stability of the aberrant antigen expression at relapse or at treatment failure of initial chemotherapy. For this purpose, multiparameter immunophenotyping with a panel of 15 monoclonal antibodies was used at diagnosis as well as at relapse (43 patients with overall 65 aberrations) and at treatment failure (35 patients with overall 66 aberrations). There was a significant decrease in the percentage of the initially described aberrant antigen expression on leukemia blasts at relapse (P = 0.001; n = 65) as well as at treatment failure (P = 0.0001; n = 66) considering all aberrations in the whole leukemia population. Concerning only patients with acute myelogenous leukemia (AML), significant decreases in the aberrant expression could be detected at relapse (P = 0.031; n = 42) and at treatment failure (P = 0.0001; n = 52). The changes in patients with acute lymphoblastic leukemia (ALL) were significant only at relapse (P = 0.006; n = 23). Initially, the most informative aberration was not detectable in four patients at relapse and in seven patients at treatment failure. A decrease of under 50% of the initial value was observed in another 8 patients at relapse and in 10 patients at treatment failure. In further studies assessing the detection of aberrant antigen expression for MRD, quantification of the relapses should be explicitly analyzed regarding the persistence of the initially described aberrant antigen expression. Cytometry (Comm. Clin. Cytometry) 42:247–253, 2000. © 2000 Wiley‐Liss, Inc.
No abstract
Treatment of elderly patients (pts) with AML requires a sensitive balance between efficacy and toxicity. In the AML97 study all pts with AML > 60 years (y) were registered and, according to their clinical status, treated in curative, palliative or supportive intention. From a total of 520 pts enrolled, 375 (72%) pts were allocated to the curative, 112 (22%) to the palliative and 33 (6%) to the supportive part of the protocol. Patient characteristics between the 3 groups differed in respect to age, but not in regard to the distribution de novo and secondary AML. Median age of the pts was 66 y (range 60–80 y), 75 y (range 64–90 y) and 76 y (range 63–97 y) for the curative, palliative and supportive protocol respectively. Curative treatment consisted of one (in case of PR after the first chemotherapy of two) courses of induction therapy (AraC 2 g/m2 iv on day (d) 1,3,5,7 in combination with mitoxantrone 10 mg/m2 iv d 1-3) followed by two consolidation courses (AraC 240 mg/m2 iv d 1-5 combined with mitoxantrone 10 mg/m2 iv d 1-2). Palliative treatment included idarubicin 10 mg po d 1 in combination with thioguanine 40 mg po d 1-5, or AraC 80 mg sc d 1-5 or etoposide 100mg po d 1-5. In the supportive arm transfusions were applied. CR was obtained in 75% (95 CI: 68–82%) of pts with de novo AML and in 61% (95 CI: 50–70%) of pts with secondary AML in the curative arm with an early death rate of 12 % (95CI: 7–17%) and 19% (95 CI: 12–24%) respectively. Cytogenetic risk factors at diagnosis were the most important prognostic factor for CR (p<0,0005, multivariate analysis). Pts with favourable karyotype achieved CR in 93%, with normal in 80 %, with other aberrations in 79% and with unfavourable karyotype in 46%. The overall survival (OS) after 2 years in the curative part of protocol was 0,31 ± 0,03 for all pts. With a median follow up of 283 d (range 33 – 1688) the actual OS was 0,58 ± 0,15, 0,38 ± 0,06, 0,39 ± 0,09 and 0,14 ± 0,05 for pts with favourable, normal, other and unfavourable cytogenetics respectively. Interestingly age was not an important determinant, even if results were analysed in a cohort of 603 pts with AML of any age with a similar induction therapy. CR rates of pts below and above 60 y were identical, if they were stratified by cytogenetic risk factors. Median survival was 54 d and only 12 d for pts treated with palliative chemotherapy and supportive therapy respectively. We conclude, that the curative protocol is able to induce high CR in pts with AML > 60 y with low mortality and CR are not different to those of pts < 60 y, if cytogenetics are taking into account. Despite high CR rate, OS remains low and consolidation therapy need to be improved. Transplant protocols with reduced intensity conditioning are currently tested in these patients. Treatment results in the palliative arm are disappointing and confirm the need to develop novel therapeutic strategies.
No abstract
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