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epipodophyllotoxin/leucèmia

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Common region of ALL-1 gene disrupted in epipodophyllotoxin-related secondary acute myeloid leukemia.

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Translocations at chromosomal band 11q23 characterize most de novo acute lymphoblastic leukemias (ALL) of infants, acute myeloid leukemias (AML) of infants and young children, and secondary AMLs following epipodophyllotoxin exposure. The chromosomal breakpoints at 11q23 have been cloned from

Secondary leukemia or myelodysplastic syndrome after treatment with epipodophyllotoxins.

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OBJECTIVE The incidence of secondary leukemia after epipodophyllotoxin treatment and the relationship between epipodophyllotoxin cumulative dose and risk are not well characterized. The Cancer Therapy Evaluation Program (CTEP) of the National Cancer Institute (NCI) has developed a monitoring plan to

Treatment of children with epipodophyllotoxin-induced secondary acute myeloid leukemia.

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BACKGROUND Secondary acute myeloid leukemia (AML) after treatment with epipodophyllotoxins is being observed with increased frequency. Therapeutic options are limited for patients with secondary AML and the role of bone marrow transplantation is unclear. METHODS The authors report the treatment
OBJECTIVE To estimate the risk of secondary leukemia as a function of the dose of epipodophyllotoxins and anthracyclines. METHODS We conducted a case-control study of the risk of secondary leukemia or myelodysplasia after a solid tumor in childhood within the Société Française d'Oncologie
BACKGROUND Recent reports have documented the occurrence of treatment-related acute myeloid leukemia (AML) following therapy with epipodophyllotoxins. These reports have led to growing concern among oncologists, which could lead to premature abandonment of these agents at a time when the

The epipodophyllotoxin VP16-213 in combination chemotherapy for adults with acute nonlymphoblastic leukaemia.

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A total of 232 previously untreated adults with acute nonlymphoblastic leukaemia were consecutively entered into four successive studies. In the first, complete remission rates and survival were inferior to a group treated on the same regimen in London, suggesting population differences, possibly on

Epipodophyllotoxins, alkylating agents, and radiation and risk of secondary leukaemia after childhood cancer.

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OBJECTIVE To investigate the incidence and aetiology of secondary leukaemia after childhood cancer in Britain. METHODS Cohort study and a case-control study. METHODS Britain and population based National Register of Childhood Tumours. METHODS Cohort of 16,422 one year survivors of childhood cancer

Epipodophyllotoxin-related acute myeloid leukemia: a study of 35 cases.

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To define better the risk of epipodophyllotoxin-related acute myeloid leukemia (AML) after extended follow-up and to assess responses to intensive salvage therapy, all patients who developed this complication after treatment for acute lymphoblastic leukemia (ALL) or non-Hodgkin lymphoma (NHL) in

Acute myeloid leukemia in children treated with epipodophyllotoxins for acute lymphoblastic leukemia.

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METHODS Treatment of cancer with the epipodophyllotoxins (etoposide and teniposide) has been linked to the development of acute myeloid leukemia (AML) in children and adults, but the factors that might influence the risk of this complication of therapy are poorly defined. We therefore assessed the

A comparative analysis of alkylating agent and epipodophyllotoxin-related leukemias.

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This review deals with the differences between leukemias--induced by alkylating agents as opposed to a "new form" of treatment related leukemia due to prior exposure to epipodophyllotoxins the latter having a short treatment--disease onset interval, absence of a MDS phase, a monocytic component and

Myelodysplastic syndrome with t(9;11)(p22;q23) after treatment for B-cell acute lymphoblastic leukemia without epipodophyllotoxins.

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Secondary myelodysplastic syndrome (MDS) with t(9;11)(p22;q23) developed in a child after intensive treatment for B-cell acute lymphoblastic leukemia diagnosed 12 months earlier. His chemotherapy had consisted mainly of cyclophosphamide and methotrexate, but no epipodophyllotoxins. The combination

Epipodophyllotoxin VP 16213 in treatment of acute leukaemias, haematosarcomas, and solid tumours.

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Epipodophyllotoxin VP 16213 (4-demethyl-epipodophyllotoxin-beta-D-ethylidene glucoside), given to 250 patients with various types of malignant disease, induced apparently complete remissions in four out of eight cases of acute monocytoid and acute myelomonocytoid leukaemia but only one complete

Epipodophyllotoxin-related leukemia. Identification of a new subset of secondary leukemia.

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Thirty-seven children and adults who developed acute nonlymphocytic leukemia after the administration of chemotherapy that included etoposide or teniposide for a variety of hematologic and solid malignancies were identified. The secondary leukemia that occurred in these patients could be

Therapy-related acute myeloid leukemia following treatment with epipodophyllotoxins: estimating the risks.

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In the past decade, therapy-related acute myeloid leukemia (t-AML) following treatment with regimens that include inhibitors of topoisomerase-II (TOPO-II) has been reported with increasing frequency. These cases of t-AML generally have a shorter latency period than t-AML following alkylator therapy,

Secondary acute myeloblastic leukemia in a child with acute lymphoblastic leukemia treated with epipodophyllotoxins.

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Etoposide is a semi-synthetic, topoisomerase active podophyllotoxin derivative which frequently causes deletions and rearrangements on chromosomes 11q23 and 11q22. It can cause therapy-related, acute myeloblastic leukemia in patients receiving the drug in a schedule-dependent manner. Here we present
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