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What could explain the clustering of leukaemia cases?
- Wendy J Jones (10 June 2005)
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Childhood leukaemia clusters
- Douglas J Holdstock (28 June 2005)
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The causes of childhood leukaemia:No more mystery!?
- Petar I. Ivanovski, Verica J. Ivanovski (7 October 2005)
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Wendy J Jones, staff grade cancer genetics Singleton hospital ,Swansea
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Spatial clustering of cases of childhood leukaemia has been demonstated[1,2,3]leading to speculation of an infectious agent responsible at least in part as an aetiology. Knox also delineated the clustering as " a group of long standing focal environmental hazards, most effective within a few hundred yards of the source but detectable as far as 3km. Population mixing is also thought to be a contributory factor.Along with people are their animals and the FeLV cat leukaemia virus did seem a good candidate agent, but there has been no evidence from immunological studies that this is the case[4]. What remains interesting is that radiotransmitter studies of roaming cats show a similar spatial range of territories. Distances vary as to sex of the cat and whether urban or rural, but roaming areas cover on average between 0.5-2.0 ha for urban cats and up to 50 ha for rural males.[5]Taken as a circle these areas work out to be radii of 39-79m to 398m. . Maybe this should be revisted,after all we had to think outside the box to discover that pasteurella pestis was spread by the rat but carried by the fleas. 1.Alexander F E, Chan L C ,et al British Journal of Cancer 75(3):457- 63,1997. 2.Petridou E ,Revinthi K,et al British Journal of Cancer 73 (10) 1278-83, 1996 May 3.Knox E G , Gilman E A, Journal of Epidemiology and Public Health50(3) 313-9, 1996 Jun 4.N Nowotny, A Uthman et al Letter to the Lancet1995 vol 346 July 22 "Is it possible to catch leukaemia from a cat?" 5.Fromont E .PhD Thesis 1997 http://biomserv.univ-lyon1.fr/txtdoc/THESES/FROMONT/TheseEnFROE.pdf Competing interests: None declared |
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Douglas J Holdstock, Editor, Medicine, Conflict & Survival Medact, The Grayston Centre, 28 Charles Square, London N1 6HT
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EDITOR - The Committee on Medical Aspects of Radiation in the Environment (COMARE) has once again confirmed the existence of small but significant clusters of childhood leukaemia around the nuclear reprocessing plants at Sellafield and Dounreay and the Atomic Weapons Establishnent at Burghfield (1). COMARE is still unable to suggest a cause, as on standard models of radiation protection radiation exposures are too small. I suggest, though, that an explanation is implied in Dickinson's editorial (2). Dickinson notes that an unusual pattern of exposure to infection may increase the risk of childhood leukaemia, and refers to Greaves' proposal that two events are needed, one damage to DNA before birth and the second a challenge from infection (3). Even tiny doses of alpha-irradiation from exposures to plutonium could induce genomic instability, either in parental germ cells or in the foetus by crossing the placental barrier. The risk from these is not known but could be appreciably higher than currently accepted (4), and sufficient to constitute Greaves' first event. While the number of cases in the clusters is small, childhood leukaemia, even though now treatable in many cases, is still devastating for the child and its family. But these cases might be prevented by ending both nuclear reprocessing at Sellafield (which may result in any case from the recent radiation leak there) and the UK's nuclear weapons programme. [229 words] 1. Committee on Medical Aspects of Radiation in the Environment. The incidence of childhood cancer around nuclear installations in Great Britain. 10th report. Didcot: National Radiological Protection Board, 2005. 2. Dickinson HO. The causes of childhood leukaemia. BMJ 2005; 330: 1279- 80. (4 June). 3. Greaves MF, Wiemels J. Origin of chromosome translocations in childhood leukaemia. Nat Rev Cancer 2003; 3: 639-49. 4. Report of the Committee Examining Radiation Risks of Internal Emitters (CERRIE). Didcot: National Radiological Protection Board, 2004. Competing interests: None declared |
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Petar I. Ivanovski, Paediatrician, Assistant Professor of Paediatrics 11000 Belgrade, Verica J. Ivanovski
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Editor - Dickinson made a very concise review on the causes of childhood leukaemia (1). But we are still at the very beginning. Let me put some more light on this matter. Mostly owing to Greaves et al nowadays we know that there is no leukaemia without leukaemogenic genetics, which is prenatal for most childhood leukaemias(2). One percent of the newborns have TEL-AML1 (2). These newborns constitute a population at risk (N), from which leukaemic cases are recruited under the influence of an unknown event (U), giving a known incidence (I) of childhood leukaemia that has been almost unchangeable for many decades. But, not every child with this prenatal leukaemogenic genetics will develop leukaemia, because humans possess a very complicated cancer protection system (P). So, for example, for TEL-AML1 leukaemia P = 100 (and probably for many other cancers) (2). This means that only 1 of 100 newborns with TEL-AML1 will later develop leukaemia. All this could be summarized in the following equation: N x U / P = I. Now it is an easy thing to calculate the incidence of TEL-AML1 leukaemia. Let us put in this equation the known facts: 1% of newborns x U / 100 = 1 case of TEL-AML1 ALL in 10000 newborns (1%xU/100=0,01xU:100=1xU:10000)(2). The predictive value of U does not exceed 100% = 1(rate of population influenced by U). According to the literature, U first significantly appeared around 1940 in Great Britain (3). Because TEL-AML1 is located in precursor B cells, U must be a strong immunoantigen to cause a proliferative stress on these cells, must be regularly repetitive to cause additional postnatal mutations for overt leukaemia (to cause deletions of normal allelic TEL) (4), to have unselective influence in early life of all children (with and without leukaemogenic genetics) and to occur every year. Only systematic vaccination against diphtheria fulfills all the above. It seems that U is not an unknown event!? Draper et al concluded that electromagnetic fields could be responsable for some leukaemias(5). It is not known how electromagnetic force can cause a proliferation of B cells! But, DNA damage (read leukaemogenic genetics or TEL-AML1) could be the result of the electromagnetic field influence of high voltage power lines or it could be a natural consequence of the earth’s magnetic field, which affects all of us all the time(1). Altogether, vaccination of the transgenic TEL-AML1 mice is inevitable! After that, the possibility of leukaemia prevention may not just be a wishful thinking. References: 1. Dickinson HO. The causes of childhood leukaemia. BMJ 2005; 330: 1279-1280. 2. Mori H, Colman SM, Xiao Z, Ford AM, Healy LE, Donaldson C, Hows JM, Navarrete C, Greaves M. Chromosome translocations and covert leukaemic clones are generated during normal fetal development. PNAS, 2002; 99: 8242 -8247. 3. Court Brown WM, Doll R. Leukemia in childhood and young adult life. Trends in mortality in relation to etiology. BMJ, 1961 April 8; 5231: 981- 989. 4. Raynaud S, Cave H, Breans M, Bastard C, Cacheux V, Grosgeorge J, Guidal -Giroux C, Guo C, Vilmer E, Narynen P, Grandchamp B. The 12;21 translocation involving TEL and deletion of the other TEL allele: two frequently associated alterations found in childhood acute lymphoblastic leukaemia. Blood, 1996 Apr 1;87 (7): 2891-2899. 5. Draper G, Vincent T, Kroll ME, Swanson J. Childhood cancer in relation to distance from high voltage power lines in England and Wales: case control study. BMJ 2005; 330: 1290-1293. Competing interests: None declared |
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