Patterns and temporal trends in the incidence of malignant disease in children: I. Leukaemia and lymphoma.
AffiliationCancer Research Campaign Paediatric and Familial Cancer Research Group, Christie Hospital NHS Trust, Manchester, U.K.
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AbstractPatterns and trends in incidence of leukaemia and lymphoma in children aged under 15 years and resident in the North Western Regional Health Authority area of England at diagnosis, over the 35-year time period 1954-1988, were analysed. The study included 1407 cases registered with the Manchester Children's Tumour Registry, 100% of which had a histologically or cytologically verified diagnosis. Log-linear modelling identified significant linear increases in acute lymphocytic leukaemia (ALL) (average quinquennial increase 4%) and Hodgkin's disease (HD) (10%), but not in acute non-lymphocytic leukaemia nor non-Hodgkin's lymphoma. Additionally, the chi 2 test for trend identified a significant increase in the incidence of chronic myeloid leukaemia. The possibility that the increases seen in ALL and HD are linked to increases in prevalence of unknown infectious agents is discussed.
CitationPatterns and temporal trends in the incidence of malignant disease in children: I. Leukaemia and lymphoma. 1994, 30A (10):1490-8 Eur. J. Cancer
JournalEuropean Journal of Cancer (Oxford, England : 1990)
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Poly (ADP-ribose) metabolism in alkylated mouse L5178Y cells.Boyle, John M (1985-07)Poly ADP-ribosylation of two mouse lymphoma cell lines, L5178Y (LS) and the radiation and alkylating agent resistant derivative AII, was investigated by uptake of [3H]NAD by permeabilised cells into acid-precipitable material that was sensitive to phosphodiesterase but insensitive to DNase and RNase. Basal activities in both lymphoma lines were 3-4-fold greater than in mouse L1210 leukaemia cells. However, total endogenous poly (ADP-R) polymerase activity in both L5178Y cell lines, stimulated by a large excess of DNase in the presence of Triton X-100, was less than half the activity in L1210 cells. Doses of N-methyl-N-nitrosourea (MNU) that produced 20-50% survival of colony-forming units increased poly (ADP-R) in both lymphoma lines by only 25% compared with 377% in L1210 cells when synthesis was measured immediately after a 30-min exposure of MNU. During the first 24 h after MNU AII cells produced a peak of activity that was not seen with LS cells. A second peak was seen in both cell lines between 24 and 48 h following MNU. Concentrations of 3-aminobenzamide (3AB) above 2.5 mM inhibited colony-forming ability of lymphoma cells and equally inhibited uptake of [14C]formate into protein, RNA and DNA indicating that 3AB behaves as a general metabolic poison. Concentrations of 3AB in the toxic range of 3-10 mM inhibited poly (ADP-R) synthesis but no degradation of the polymer was observed. Non-toxic concentrations of 3AB potentiated cell killing by MNU to a similar degree in both lymphoma cell lines. In conclusion, we have found little evidence to support the hypothesis that the differential sensitivity of LS and AII is related to poly ADP-ribosylation. Compared with other mouse cells, L5178Y cells appear deficient in poly (ADP-R) polymerase and poly (ADP-R) glycohydrolase activities.
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Backtracking leukemia to birth: identification of clonotypic gene fusion sequences in neonatal blood spots.Gale, K B; Ford, A M; Repp, R; Borkhardt, A; Keller, C; Eden, Tim O B; Greaves, M F; Leukaemia Research Fund Centre at the Institute of Cancer Research, Chester Beatty Laboratories, 237 Fulham Road, London SW3 6JB, United Kingdom. (1997-12-09)Epidemiological evidence has suggested that some pediatric leukemias may be initiated in utero and, for some pairs of identical twins with concordant leukemia, this possibility has been strongly endorsed by molecular studies of clonality. Direct evidence for a prenatal origin can only be derived by prospective or retrospective detection of leukemia-specific molecular abnormalities in fetal or newborn samples. We report a PCR-based method that has been developed to scrutinize neonatal blood spots (Guthrie cards) for the presence of numerically infrequent leukemic cells at birth in individuals who subsequently developed leukemia. We demonstrate that unique or clonotypic MLL-AF4 genomic fusion sequences are present and detectable in neonatal blood spots from individuals who were diagnosed with acute lymphoblastic leukemia at ages 5 months to 2 years and, therefore, have arisen during fetal hematopoiesis in utero. This result provides unequivocal evidence for a prenatal initiation of acute leukemia in young patients. The method should be applicable to other fusion genes in children with common subtypes of leukemia and will be of value in attempts to unravel the natural history and etiology of this major subtype of pediatric cancer.