National Cancer Institute®
Last Modified: May 1, 2002
UI - 11739161
AU - Kawasaki H; Isoyama K; Eguchi M; Hibi S; Kinukawa N; Kosaka Y; Oda T;
TI - Oda M; Nishimura S; Imaizumi M; Okamura T; Hongo T; Okawa H; Mizutani S; Hayashi Y; Tsukimoto I; Kamada N; Ishii E Superior outcome of infant acute myeloid leukemia with intensive chemotherapy: results of the Japan Infant Leukemia Study Group.
SO - Blood 2001 Dec 15;98(13):3589-94
AD - Department of Pediatrics, Mie University, Japan.
This study analyzed data on 35 infants with acute myeloid leukemia (AML) who were treated with intensive chemotherapy between 1995 and 1998 in Japan. The incidence of boys, younger age (< 6 months old), and hyperleukocytosis at onset was high in patients with the M4/M5 subtype (n = 23) in the French-American-British classification, compared with the non-M4/M5 subtype (n = 12). Thirteen (56%) and 16 (70%) patients with the M4/M5 subtype also showed 11q23 translocations and MLL gene rearrangements, respectively, whereas only one patient with the non-M4/M5 subtype had this rearrangement. All 35 patients were treated with the ANLL91 protocol consisting of etoposide, high-dose cytarabine, and anthracyclines. Overall survival and the event-free survival (EFS) rates at 3 years of all patients were 76% (95% confidence interval [CI], 61.3%-90.7%) and 72% (95% CI, 56.4%-87.9%), respectively. EFS showed no significant difference between 2 subgroups divided by age, gender, presence of the MLL gene rearrangements, and white blood cell count at onset; EFS in patients with the M4/M5 subtype tended to be better than those with the non-M4/M5 subtype. Although all 6 patients who underwent allogeneic stem cell transplantation (SCT) have been in complete remission, no benefit of SCT was confirmed. These findings suggest that the intensive chemotherapy with the ANLL91 protocol might have been responsible for the observed good outcome of infant AML, even without SCT. The presence of the MLL gene rearrangements or the age at onset had no impact on the outcome of infant AML.
UI - 11943160
AU - Hamada M; Nishio K; Doe M; Usuki Y; Tanaka T
TI - Farnesylpyridinium, an analog of isoprenoid farnesol, induces apoptosis but suppresses apoptotic body formation in human promyelocytic leukemia cells.
SO - FEBS Lett 2002 Mar 13;514(2-3):250-4
AD - Department of Bio- and Geoscience, Graduate School of Science, Osaka City University, 3-3-138 Sugimoto, Sumiyoshi-ku, Osaka 558-8585, Japan.
1-Farnesylpyridinium (FPy), an analog of isoprenoid farnesol, initially induced morphological changes similar to those of typical apoptosis in human leukemia HL-60 cells but FPy-treated cells were characterized by the absolute absence of final apoptotic events such as fragmentation into apoptotic bodies. FPy-induced cell death was considered to be apoptotic on the basis of the induction of DNA fragmentation and the protection against these events by the coaddition of a pan-caspase inhibitor. The increase in the cytoplasmic cytochrome c level supported the possibility that FPy-treated cells should have the ability to complete the entire apoptotic process ending in cell fragmentation and apoptotic body formation. At concentrations too low to induce apoptosis, FPy could suppress the induction of apoptotic body formation in HL-60 cells by typical inducers of apoptosis such as actinomycin D or anisomycin. FPy exhibited a cytochalasin-like effect on spatial arrangement of actin filament independent of its apoptosis-inducing activity.
UI - 11960341
AU - Ohnishi K; Yoshida H; Shigeno K; Nakamura S; Fujisawa S; Naito K; Shinjo
TI - K; Fujita Y; Matsui H; Sahara N; Takeshita A; Satoh H; Terada H; Ohno R Arsenic trioxide therapy for relapsed or refractory Japanese patients with acute promyelocytic leukemia: need for careful electrocardiogram monitoring.
SO - Leukemia 2002 Apr;16(4):617-22
AD - Department of Medicine III, Hamamatsu University School of Medicine, Handayama, Hamamatsu, Japan.
Recent studies have shown that arsenic trioxide (As(2)O(3)) can induce complete remission in patients with acute promyelocytic leukemia (APL). We tested the efficacy and safety of As(2)O(3) for the treatment of patients with APL who had relapsed from or become refractory to all-trans retinoic acid (ATRA) and conventional chemotherapy in a prospective study. As(2)O(3) at a dose of 0.15 mg/kg was administered until the date of bone marrow remission to a maximum of 60 days. In patients who achieved complete remission (CR), one additional course of As(2)O(3) was administered using the same dose for 25 days. Of 14 patients, 11 (78%) achieved CR. Six of 10 patients who achieved CR showed disappearance of PML-RARalpha transcript by RT-PCR assay. The duration of As(2)O(3)-induced CR ranged from 4 to 22 months (median, 8 months) at a median follow-up of 17 months. Adverse events included 13 electrocardiogram abnormalities (13 QTc prolongation, eight ventricular premature contraction, four nonsustained ventricular tachycardia and two paroxysmal supraventricular tachycardia), seven nausea and vomiting, four pruritus, three peripheral neuropathy, three fluid retention and one APL differentiation syndrome. Four patients received antiarrhythmic agents. Hyperleukocytosis developed in five patients and in three cytotoxic drugs were necessary. Other adverse events were relatively mild. As(2)O(3) treatment is effective and relatively safe in relapsed or refectory patients with APL. Cardiac toxicities in patients with QTc prolongation should be carefully monitored.
UI - 11921023
AU - Bairey O; Kirgner I; Yakobi M; Hamdan A; Ben-Ari Z; Shaklai M
TI - Clinical severe hepatic venoocclusive disease during induction treatment of acute monoblastic leukemia managed with defibrotide.
SO - Am J Hematol 2002 Apr;69(4):281-4
AD - Institute of Hematology, Rabin Medical Center, Beilinson Campus, Petah Tikva and Sackler Faculty of Medicine, Tel Aviv University, Tel Aviv, Israel. firstname.lastname@example.org
Hepatic venoocclusive disease (VOD) is the most common complication of cytoreductive therapy used for stem cell transplantation, but it is rarely encountered during induction treatment of acute leukemia. We describe a patient in whom severe clinical VOD developed shortly after induction treatment for acute monoblastic leukemia. Administration of intravenous defibrotide for 19 days induced complete resolution of the VOD. Further consolidation treatment was resumed including high-dose cytosine arabinoside without further complications. Copyright 2002 Wiley-Liss, Inc.
UI - 11588026
AU - de Witte T; Suciu S; Verhoef G; Labar B; Archimbaud E; Aul C; Selleslag
TI - D; Ferrant A; Wijermans P; Mandelli F; Amadori S; Jehn U; Muus P; Boogaerts M; Zittoun R; Gratwohl A; Zwierzina H; Hagemeijer A; Willemze R Intensive chemotherapy followed by allogeneic or autologous stem cell transplantation for patients with myelodysplastic syndromes (MDSs) and acute myeloid leukemia following MDS.
SO - Blood 2001 Oct 15;98(8):2326-31
AD - University Medical Center St Radboud, Nijmegen, The Netherlands. email@example.com
This study investigated the feasibility of allogeneic (alloSCT) and autologous stem cell transplantation (ASCT) as postconsolidation therapy for patients with myelodysplastic syndromes (MDSs) or acute myeloid leukemia after MDS. Patients with a histocompatible sibling were candidates for alloSCT and the remaining patients for ASCT. Remission-induction therapy consisted of 1 or 2 courses with idarubicin, cytarabine, and etoposide, followed by one intensive consolidation course with cytarabine and mitoxantrone. Initially, bone marrow cells were used for ASCT. Subsequently, mobilized blood stem cells were used in an attempt to shorten posttransplantation hypoplasia. With a median follow-up of 3.6 years the 184 evaluable patients showed a 4-year survival rate of 26% and a median survival of 13 months. The remission-induction chemotherapy induced complete remission (CR) in 100 patients (54%). The 4-year disease-free survival (DFS) rate was 29% and the median DFS was 12 months. Twenty-eight of 39 patients (72%) with a donor were allografted in CR-1, including 2 patients who underwent transplantation in CR-1 without a consolidation course. Thirty-six of 59 patients (61%) without a donor received ASCT in CR-1. The 4-year DFS rates in the group of patients with or without a donor were 31% and 27%, respectively. The 4-year survival rates from CR were 36% and 33%, respectively. This large prospective study shows the feasibility of both alloSCT and ASCT. This treatment approach leads to a relatively high remission rate, and the majority of patients in remission received the SCT in CR-1. The ongoing study investigates whether this approach is better than treatment with chemotherapy only.
UI - 11869960
AU - Hernandez P; Martinez G; Losada R; Machin S; Cayado N; Gramatges A
TI - Cuban experience in the treatment of acute promyelocytic leukemia with ALL transretinoic acid followed by intensive chemotherapy.
SO - Haematologica 2002 Mar;87(3):ELT14
UI - 11952816
AU - Breccia M; Petti MC; D'Elia GM; D'Andrea M; Carmosino I; Alimena G
TI - Cutaneous pleomorphic T-cell lymphoma coexisting with myelodysplastic syndrome transforming into acute myeloid leukemia: successful treatment with a fludarabine-containing regimen.
SO - Eur J Haematol 2002 Jan;68(1):1-3
AD - Department of Cellular Biotechnology and Hematology, University La Sapienza, Via Benevento 6, Rome, Italy. firstname.lastname@example.org
The coexistence of a primary myelodysplastic syndrome (MDS) and a T-cell cutaneous non-Hodgkin's lymphoma is an extremely rare event, which has so far only been reported in a single instance in the literature. We describe herein an additional case in which the lymphoid disease was combined with an MDS at the time of its evolution into acute myeloid leukemia (AML). Both diseases were successfully treated with a regimen containing fludarabine. We discuss possible pathogenetic mechanisms and suggest the use of nonalkylating drugs, such as fludarabine, for the treatment of this rare association of malignancies usually characterized by a very poor response to therapy.
UI - 11989187
AU - Anderson S; Files J
TI - Tumor lysis syndrome secondary to Gemtuzumab Ozogamicin in a patient with acute myelogenous leukemia.
SO - J Miss State Med Assoc 2002 Apr;43(4):105-6
AD - Department of Medicine, University of Mississippi Medical Center, USA.
UI - 11001891
AU - Tallman MS; Neuberg D; Bennett JM; Francois CJ; Paietta E; Wiernik PH;
TI - Dewald G; Cassileth PA; Oken MM; Rowe JM Acute megakaryocytic leukemia: the Eastern Cooperative Oncology Group experience.
SO - Blood 2000 Oct 1;96(7):2405-11
AD - Northwestern University Medical School, Robert H. Lurie Cancer Center, Chicago IL, USA. email@example.com
Acute megakaryocytic leukemia (AMegL) is a rare subtype of acute myeloid leukemia (AML) evolving from primitive megakaryoblasts. Because of its rarity and the lack of precise diagnostic criteria in the past, few series of adults treated with contemporary therapy have been reported. Twenty among 1649 (1.2%) patients with newly diagnosed AML entered on Eastern Cooperative Oncology Group (ECOG) trials between 1984 and 1997 were found to have AMegL. The median age was 42.5 years (range 18-70). Marrow fibrosis, usually extensive, was present in the bone marrow. Of the 8 patients who had cytogenetic studies performed, abnormalities of chromosome 3 were the most frequent. The most consistent immunophenotypic finding was absence of myeloperoxidase in blast cells from 5 patients. In the most typical 3 cases, the leukemic cells were positive for one to 2 platelet-specific antigens in addition to lacking myeloperoxidase or an antigen consistent with a lymphoid leukemia. Myeloid antigens other than myeloperoxidase and selected T-cell antigens (CD7 and/or CD2) were frequently expressed. Induction therapy included an anthracycline and cytarabine in all cases. Complete remission (CR) was achieved in 10 of 20 patients (50%). Two patients remain alive, one in CR at 160+ months. Resistant disease was the cause of induction failure in all but 3 patients. The median CR duration was 10.6 months (range 1-160+ months). The median survival for all patients was 10.4 months (range 1-160+ months). Although half of the patients achieved CR, the long-term outcome is extremely poor, primarily attributable to resistant disease. New therapeutic strategies are needed.
UI - 11918543
AU - Au WY; Chim CS; Lie AK; Liang R; Kwong YL
TI - Combined arsenic trioxide and all-trans retinoic acid treatment for acute promyelocytic leukaemia recurring from previous relapses successfully treated using arsenic trioxide.
SO - Br J Haematol 2002 Apr;117(1):130-2
AD - University Department of Medicine, University of Hong Kong, Queen Mary Hospital, Hong Kong.
The optimal treatment of acute promyelocytic leukaemia (APL) recurring from relapses successfully treated using arsenic trioxide (As2O3) is undefined. Three APL patients relapsing from As2O3-induced remission were studied. Re-treatment with As2O3 failed in one patient in third relapse, and resulted in morphological but not molecular remission in another patient. Combination therapy with As2O3 and all-trans retinoic acid (ATRA), however, resulted in morphological and molecular remission in all three cases, with a follow-up time ranging from 6 to 16 months. Our results suggest a synergistic therapeutic effect between As2O3 and ATRA in APL in advanced relapse.
UI - 11918536
AU - Salih HR; Starling GC; Brandl SF; Pelka-Fleischer R; Haferlach T;
TI - Hiddemann W; Kiener PA; Nuessler V Differentiation of promyelocytic leukaemia: alterations in Fas (CD95/Apo-1) and Fas ligand (CD178) expression.
SO - Br J Haematol 2002 Apr;117(1):76-85
AD - Department of Immunology, Inflammation and Pulmonary Diseases, Bristol-Myers Squibb Pharmaceutical Research Institute, Princeton, USA. Helmut.Salih@md.uni-tuebingen.de
The survival of leukaemic blasts contributes to the pathological mechanism of acute promyelocytic leukaemia (APL). While treatment of APL using retinoic acid (RA) is a model of differentiation therapy, little is known about possible effects of this treatment on the Fas/FasL system. Investigation of APL cells from patients undergoing differentiation therapy with RA and of promyelocytic HL-60 and monoblastic U-937 cells cultured with RA revealed a reduction of surface expression of both Fas and its ligand. Accordingly, the sensitivity of the cells to anti-Fas-induced apoptosis decreased proportionally and the reduced expression of FasL resulted in a decreased ability of the leukaemic cells to induce apoptosis in T cells. Our findings demonstrate that there are significant changes in Fas and FasL expression during RA treatment of APL, which probably have consequences for the interaction between host immune and leukaemia cells, and thus may be involved in the beneficial effects of differentiation therapy.
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