Treatment of Acute Lymphoblastic Leukemia in Children with the BFM Protocol A Cooperative Pilot Study

Boilletot, A; Béhar, C; Benoît, Yves; M, Casteels-Van Daele; J, Chantraine; Mj, Delbeke; Gyselinck, G; Hainaut, H; Lutz, Patrick; Maurus, R

doi:10.1097/00043426-198724000-00008

Cited by 10 publications

(2 citation statements)

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“…Between 1976 and 1981, the EORTC-ALL-58-71 protocol [14] was used, this included a 5-year treatment and an irradiation dose of 2,400 cGy. Between 1981 and 1983 a 3-year protocol was used, EORTC-pilot study BFM 58-81 [15], the irradiation dose depended on a calcu lated risk factor (including the size of liver and spleen and the num ber of lymphoblasts). The high risk group received 2,400 cGy in contrast to 1,800 cGy for the low risk group.…”

Section: Methodsmentioning

confidence: 99%

Factors Contributing to the Impairment of Growth in Children with Acute Lymphoblastic Leukemia

Logghe

Bourguignon²,

Craen

et al. 1988

Horm Res

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Growth was studied in 88 long-term survivors of acute lymphoblastic leukemia who had been treated with three different regimens of therapy. The following time periods were evaluated: (1) during therapy; (2) between the end of therapy and the onset of puberty, and (3) between the onset of puberty and the most recent observation. We found: (1) a reduction of height SDS during therapy, related to the irradiation dose used; no significant effect of the duration of the therapy could be established; (2) a normal growth rate during the second time period studied for the total group, but a further decrease in height SDS for those found to be growth hormone deficient after therapy (47 %), and (3) a further decrease in height SDS during puberty. The timing of puberty in the female patients was normal. We conclude that in patients treated for acute lymphoblastic leukemia, growth impairment has several components, different in timing and mechanism.

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Section: Methodsmentioning

confidence: 99%

Factors Contributing to the Impairment of Growth in Children with Acute Lymphoblastic Leukemia

Logghe

Bourguignon²,

Craen

et al. 1988

Horm Res

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“…Patients were treated according to the EORTC 58881 CLCG trial 18 in the same institution (Debrousse Hospital, Lyon, France). Patients were stratified according to their risk factor.…”

Section: Patientsmentioning

confidence: 99%

Enhanced expression of p16ink4a is associated with a poor prognosis in childhood acute lymphoblastic leukemia

et al. 1999

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The tumor suppressor gene p16 ink4a is homozygously deleted in numerous T as well as in some B lineage acute lymphoblastic leukemia (ALL). We therefore analyzed the clinical and biological implications of this feature by studying p16 ink4a expression in 58 cases of childhood ALL. mRNA and protein were significantly correlated and both appeared more highly expressed in B than in T lineage ALLs: 13 out of the 15 T cell ALLs did not show any p16 ink4a expression. The main result of this study is the strong prognostic value of p16 ink4a expression. When stratifying the patients in three groups according to p16 ink4a expression, we observed in univariate analysis: (1) the shortest disease-free survival for patients presenting a high p16 ink4a level; (2) contrasting with the good prognosis in the group of patients expressing p16 ink4a at low level; (3) while cases without any expression of the inhibitor were associated with a medium course of the disease (P = 0.0165). This prognostic value was confirmed by the multivariate analysis showing therapeutic regimen and p16 ink4a protein expression as the only variables retained in the model. A specific metabolic profile related to cellular survival and proliferation was observed in each of the three p16 ink4a expression groups. Among the cell cycle-related proteins we analyzed, only p21 waf1 bcl-2 and CDK4 were significantly and positively correlated to p16 ink4a . Furthermore, CDK6 was also strongly expressed in the group of cases with high p16 ink4a level. An enhancement of p16 ink4a , p21 waf1 and bcl-2 was previously described in prolonged cellular survival, while aging cells showed a decrease in CDK4 expression. The concomitant high expression of the oncogenic protein CDK4 (and of CDK6), we observed, may amplify the leukemic advantage of prolonged lifespan blast cells by favoring cell progression through G1 phase. These data suggest that at least two mechanisms may be associated in the oncogenesis of very aggressive ALLs, ie deregulation of cell multiplication and prolonged blast lifespan.

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A pilot study of intermediate‐dose methotrexate and cytosine arabinoside, “Spread‐out” or “Up‐front,” in continuation therapy for childhood non‐T, non‐B acute lymphoblastic leukemia a pediatric oncology group study

Krance

Newman

Pinkel

et al. 1991

Cancer

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One hundred six children with newly diagnosed non-T-, non-B-cell acute lymphoblastic leukemia (ALL) were treated in a Pediatric Oncology Group (POG) pilot study in which six courses of intermediate-dose methotrexate (MTX) and cytosine arabinoside (Ara-C) (1 g/m2 each) were added to a "backbone" of standard continuation therapy. The dose and sequence of MTX/Ara-C administration were based on a preclinical model that demonstrated synergism between MTX and Ara-C. Poor-risk patients (n = 49) were assigned to "up-front" therapy, in which the MTX/Ara-C courses were administered during the initial 15 weeks of remission. Standard-risk patients (n = 57) were assigned to "spread-out" therapy, in which the MTX/Ara-C courses were interspersed at 12-week intervals within continuation treatment. Toxicity after intermediate-dose MTX/Ara-C, principally neutropenia and fever, was judged significant but manageable. Unexpectedly, the incidence of fever and neutropenia less than 500/mm3 was greater after "spread-out" therapy (38%) than after "up-front" therapy (6%). At 4 years, the Kaplan-Meier estimate of event-free survival (EFS) is 71% (+/- 7%) for standard-risk patients and 53% (+/- 8%) for poor-risk patients. The results of this pilot study support the use of intermediate-dose MTX/Ara-C in additional studies.

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Treatment of Acute Lymphoblastic Leukemia in Children with the BFM Protocol A Cooperative Pilot Study

Cited by 10 publications

References 0 publications

Factors Contributing to the Impairment of Growth in Children with Acute Lymphoblastic Leukemia

Factors Contributing to the Impairment of Growth in Children with Acute Lymphoblastic Leukemia

Enhanced expression of p16ink4a is associated with a poor prognosis in childhood acute lymphoblastic leukemia

A pilot study of intermediate‐dose methotrexate and cytosine arabinoside, “Spread‐out” or “Up‐front,” in continuation therapy for childhood non‐T, non‐B acute lymphoblastic leukemia a pediatric oncology group study

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