Search

Background:Earlier studies have shown raised risks of leukaemia and non-Hodgkin lymphoma in children, teenagers and young adults resident either at birth or diagnosis in Seascale. Some increases in cancer risk in these age groups have also been noted among those living around Dounreay. We aimed to update previous analyses relating to areas close to these nuclear installations by considering data from an additional 16 years of follow-up.Methods:Cross-sectional analyses compared cancer incidence rates for 1963-2006 among those aged 0-24 years at diagnosis living in geographically specified areas around either Sellafield or Dounreay with general population rates. Cancer incidence for the period 1971-2006 among the cohort of Cumbrian births between 1950 and 2006 was compared to national incidence for 1971-2006 using person-years analysis. Cancer among those born in the postcode sector closest to Dounreay was compared with that among those born in the three adjoining postcode sectors. Analyses considered both cancer overall and ICD-O-3 defined diagnostic subgroups including leukaemia, central nervous system tumours and other malignancies.Results:Apart from previously reported raised risks, no new significantly increased risks for cancer overall or any diagnostic subgroup were found among children or teenagers and young adults living around either nuclear installation. Individuals born close to the installations from 1950 to 2006 were not shown to be at any increased risk of cancer during the period 1971 to date.Conclusions:Analysis of recent data suggests that children, teenagers and young adults currently living close to Sellafield and Dounreay are not at an increased risk of developing cancer. Equally, there is no evidence of any increased cancer risk later in life among those resident in these areas at birth. [ABSTRACT FROM AUTHOR]

Background:We extend our previous study of childhood leukaemia and proximity to high-voltage powerlines by including more recent data and cases and controls from Scotland, by considering 132-kV powerlines as well as 275 and 400 kV and by looking at greater distances from the powerlines.Methods:Case-control study using 53 515 children from the National Registry of Childhood Tumours 1962-2008, matched controls, and calculated distances of mother's address at child's birth to powerlines at 132, 275, and 400 kV in England, Wales and Scotland.Results:Our previous finding of an excess risk for leukaemia at distances out to 600 m declines over time. Relative risk and 95% confidence interval for leukaemia, 0-199 m compared with>1000 m, all voltages: 1960s 4.50 (0.97-20.83), 2000s 0.71 (0.49-1.03), aggregate over whole period 1.12 (0.90-1.38). Increased risk, albeit less strong, may also be present for 132-kV lines. Increased risk does not extend beyond 600 m for lines of any voltage.Conclusions:A risk declining over time is unlikely to arise from any physical effect of the powerlines and is more likely to be the result of changing population characteristics among those living near powerlines. [ABSTRACT FROM AUTHOR]

Background:Concern about the risk of leukaemia in children living near nuclear power plants (NPPs) persists. Previous British analyses have been area based and consequently thought to be less effective than case-control studies.Methods:Cases of childhood leukaemia and non-Hodgkin lymphoma (LNHL) born and diagnosed in Great Britain between 1962 and 2007, with matched cancer-free controls, were analysed by logistic regression to estimate the risk of residential proximity at birth and diagnosis to the nearest NPP, adjusting for relevant variables.Results:For 9821 children with LNHL under the age of 5 years, the estimated extra risk associated with residential proximity to an NPP at birth was negative-interpolated Odds Ratio (OR) at 5 km was 0.86 (0.49-1.52). The comparison of 10 618 children with LNHL under five with 16 760 similarly aged children with other cancers also gave a negative estimate of the extra risk of residential proximity at diagnosis-interpolated OR at 5 km was 0.86 (0.62-1.18).Conclusion:Our results show little evidence of an increase in risk of LNHL to children aged under 5 years from living in the vicinity of an NPP. Risk estimates are incompatible with comparable ones published in a recent German case-control study. [ABSTRACT FROM AUTHOR]

Background:Retinoblastoma is an eye tumour of childhood that occurs in heritable and non-heritable forms. In the heritable form, there is a predisposition to the development of non-ocular subsequent primary tumours (SPTs).Methods:This study included 1927 retinoblastoma patients diagnosed in Britain from 1951 to 2004. Ascertainment was through the (UK) National Registry of Childhood Tumours; cases were followed-up for the occurrence of SPTs. Standardised incidence ratios (SIRs) were calculated.Results:We identified 169 SPTs in 152 patients. The SIR analysis included 145 SPTs with cancer registrations from the years 1971 to 2009. These tumours occurred in 132 patients: 112 of the 781 heritable and 20 of the 1075 (presumed) non-heritable cases under surveillance at the start of this period developed at least one registered SPT. The SIRs for all tumours combined were 13.7 (95% confidence interval 11.3-16.5) in heritable cases and 1.5 (0.9-2.3) in non-heritable cases. The main types of SPT in the heritable cases were leiomyosarcoma, (31 cases; SIR 1018.7 (692.2-1446.0)), osteosarcoma (26 cases; SIR 444.6 (290.4-651.4)), and skin melanoma (12 cases; SIR 18.6 (9.6-32.4)).Conclusion:The risk of SPTs in heritable retinoblastoma is extremely high. This has important implications for the clinical follow-up and counselling of survivors and their families. [ABSTRACT FROM AUTHOR]

Background:Paternal occupational exposures have been proposed as a risk factor for childhood central nervous system (CNS) tumours. This study investigates possible associations between paternal occupational exposure and childhood CNS tumours in Great Britain.Methods:The National Registry of Childhood Tumours provided all cases of childhood CNS tumours born and diagnosed in Great Britain from 1962 to 2006. Controls without cancer were matched on sex, period of birth and birth registration sub-district. Fathers' occupations were assigned to one or more of 33 exposure groups. A measure of social class was also derived from father's occupation at the time of the child's birth.Results:Of 11 119 cases of CNS tumours, 5 722 (51%) were astrocytomas or other gliomas, 2 286 (21%) were embryonal and 985 (9%) were ependymomas. There was an increased risk for CNS tumours overall with exposure to animals, odds ratio (OR) 1.40 (95% confidence intervals (CIs) 1.01, 1.94) and, after adjustment for occupational social class (OSC), with exposure to lead, OR 1.18 (1.01, 1.39). Exposure to metal-working oil mists was associated with reduced risk of CNS tumours, both before and after adjustment for OSC, OR 0.87 (0.75, 0.99).Risk of ependymomas was raised for exposure to solvents, OR 1.73 (1.02,2.92). For astrocytomas and other gliomas, risk was raised with high social contact, although this was only statistically significant before adjustment for OSC, OR 1.15 (1.01,1.31). Exposure to paints and metals appeared to reduce the risk of astrocytomas and embryonal tumours, respectively. However, as these results were the result of a number of statistical tests, it is possible they were generated by chance.Higher social class was a risk factor for all CNS tumours, OR 0.97 (0.95, 0.99). This was driven by increased risk for higher social classes within the major subtype astrocytoma, OR 0.95 (0.91, 0.98).Conclusion:Our results provide little evidence that paternal occupation is a significant risk factor for childhood CNS tumours, either overall or for specific subtypes. However, these analyses suggest that OSC of the father may be associated with risk of some childhood CNS cancers. [ABSTRACT FROM AUTHOR]

Background:Increases in recorded childhood cancer incidence are widely reported, but do not necessarily represent real increases in risk. Time trends might conceal underlying steps caused by changes in diagnosis and registration procedures.Methods:Using records from the National Registry of Childhood Tumours 1966-2005 (N=54 650), the age-sex-standardised rate for residents of Great Britain aged under 15 years was calculated by individual year of diagnosis for each cancer subtype, and the average annual percentage change (trend) was assessed. The timing of assumed step changes in rate was estimated by iterative Poisson regression, and compared graphically with the approximate timing of innovations previously identified from published sources.Results:Estimated timing of underlying steps approximately coincided with the following relevant innovations: biochemical assays, mid-1980s (hepatic and germ-cell cancer); diagnostic imaging, mid-1980s to early 1990s (intracranial/intraspinal tumours, neuroblastoma, soft-tissue sarcoma); revised cancer registration scheme, 1971 (leukaemia, bone and soft-tissue sarcoma); mandatory registration, 1993 (intracranial/intraspinal tumours, retinoblastoma, melanoma/carcinoma); cancer registration improvements, 2001 (leukaemia, renal and hepatic cancer).Conclusion:While the possibility of some real change in risk cannot be excluded, for many cancer subtypes the estimated timing of underlying step changes in rate appeared to correspond with changes in diagnosis or registration procedures. Childhood cancer may have been considerably under-recorded in the past. [ABSTRACT FROM AUTHOR]

Background: Record-based studies have generally reported association of higher childhood leukaemia incidence with higher socioeconomic status (SES), but recent findings are less consistent.Methods: We examined records from the National Registry of Childhood Tumours for evidence of this association in England and Wales during 1976-2005. All eligible leukaemia registrations (N=11940) were grouped by year of diagnosis in decades centred on census years 1981, 1991 and 2001 (N=3748, 3922, 4270, respectively). Using data from the census appropriate to the decade, SES for each case was measured by the child-population-weighted quintile of the Carstairs deprivation index of the census ward containing the address at diagnosis.Results: In each decade, the age-standardised leukaemia rate in the poorest quintile was ∼90% of the rate in the most affluent. Using Poisson regression, the age-adjusted rate ratio per quintile decrease in SES was 0.96 (95% confidence interval 0.94-0.98; P<0.001 for trend) in 1976-1985, 0.97 (0.95-0.99; P=0.008) in 1986-1995 and 0.97 (0.95-0.99; P=0.009) in 1996-2005. Similar association was evident for lymphoid leukaemia, the major subgroup (N=9588 in total), but not for acute myeloid (N=1868) or other/unspecified leukaemia (N=484).Conclusion: Reported childhood leukaemia incidence in England and Wales continues to be higher in relatively affluent communities. Possible explanations include under-diagnosis of leukaemia in children from poorer communities, and/or association of higher SES with hypothesised risk factors, such as population mixing and delayed exposure to infection. [ABSTRACT FROM AUTHOR]

Background: Completeness of ascertainment is a very important aspect of cancer registration. There is no recent published estimate for childhood cancer in Britain.Methods: We estimated completeness of ascertainment by the National Registry of Childhood Tumours for cancer diagnosed under age 15 years in residents of Britain during 2003-04. Stratified two-source capture-recapture was applied to notifications from general cancer registries (CRs) and specialist clinicians. Variation in notification patterns was assessed by logistic regression. Results were verified by cross-checking with Hospital Episode Statistics for leukaemia patients from England born in 1998 and diagnosed before 2005.Results: CRs notified 92-96% of registrations, and specialist clinicians 93%. Notification patterns varied slightly according to registry region, age at diagnosis, diagnostic group, socioeconomic status, and whether the patient had died. Irrespective of stratification by these factors, the overall completeness estimate was 99-100% (assuming independence of sources). Estimated completeness was at least 99% within all subgroups, except for one region (Thames 98-99%) and two small diagnostic groups (germ-cell and gonadal cancer 98-99%, melanoma and non-skin cancer 97-98%).Interpretation: The independence assumption cannot be fully justified, as both sources used records from treatment centres. With this caveat, ascertainment of recently diagnosed childhood cancer in Britain appears to be virtually complete. [ABSTRACT FROM AUTHOR]

Background: Neuroblastoma is the most common malignancy of infancy but little is known about the aetiological factors associated with the development of this tumour. A number of epidemiological studies have previously examined the risk associated with paternal occupational exposures but most have involved small numbers of cases. Here we present results from a large, population-based, case-control study of subjects diagnosed over a period of more than 30 years and recorded in the national registry of childhood tumours in Great Britain.Methods: A case-control study of paternal occupational data for 2920 cases of neuroblastoma, born and diagnosed in Great Britain between 1962 and 1999 and recorded in the National Registry of Childhood Tumours, and 2920 controls from the general population matched on sex, date of birth and birth registration district. Paternal occupations at birth, of the case or control child, were grouped by inferred exposure using an occupational exposure classification scheme. Conditional logistic regression was used to estimate odds ratios (ORs) and 95% confidence intervals (95% CI), for each of the 32 paternal occupational exposure groups.Results: Only paternal occupational exposure to leather was statistically significantly associated with neuroblastoma, OR=5.00 (95% CI 1.07-46.93). However, this association became non-significant on correction for multiple testing.Conclusion: Our findings do not support the hypothesis that paternal occupational exposure is an important aetiological factor for neuroblastoma. [ABSTRACT FROM AUTHOR]

In 2008, the German Childhood Cancer Registry published the results of the Kinderkrebs in der Umgebung von Kernkraftwerken (KiKK) study of childhood cancer and leukaemia around German nuclear power stations. The positive findings appeared to conflict with the results of a recent British analysis carried out by the Committee on Medical Aspects of Radiation in the Environment (COMARE), published in 2005. The present paper first describes the COMARE study, which was based on data from the National Registry of Children's Tumours (NRCT); in particular, the methodology used in this study is described. Although the results of the COMARE study were negative for childhood leukaemia, this apparent discrepancy could be accounted for by a number of differences in approach, especially those relating to the distances from the power stations and the ages of the children studied. The present study was designed to match the KiKK study as far as possible. The incidence observed (18 cases within 5 km against 14.58 expected, p = 0.21) was not significantly raised. The risk estimate for proximity in the regression fitted was actually negative, though the confidence intervals involved are so wide that the difference from that reported in the KiKK study is only marginally statistically significant (p = 0.063). [ABSTRACT FROM AUTHOR]

Background: Weak associations between total and LDL cholesterol and ischaemic stroke compared with coronary heart disease (CHD) are at odds with the similar effectiveness of statin drugs in preventing ischaemic stroke and CHD, suggesting that other lipid sub-fractions that are affected by statins might be better predictors of ischaemic stroke. Apolipoprotein B levels are reduced by statins and are a stronger predictor of CHD than total and LDL cholesterol in patients both on and off statins. However, there are very few published data on apolipoproteins and stroke risk and no studies in patients with previous transient ischaemic attack (TIA). Methods: We performed a prospective cohort study of the associations of baseline total cholesterol, LDL, HDL, apolipoproteins A1 and B (apo A1; apo B) and risk of ischaemic stroke in 261 patients with previous TIA. Cox proportional hazards models were used to determine crude and multivariate-adjusted hazard ratios (HR) above versus below median values at 10-years follow-up. Results: The apo B/apo A1 ratio was the strongest independent predictor of ischaemic stroke (HR = 2.94, 95% CI 1.43–5.88, p = 0.003) followed by apo B (HR = 2.26, 95% CI 1.16–4.38, p = 0.02). The associations between total cholesterol, LDL, HDL, LDL/HDL ratio and apo A1 and ischaemic stroke risk did not reach statistical significance. Conclusions: Apo B and the apo B/apo A1 ratio are predictive of ischaemic stroke in patients with previous TIA. Further studies are required to determine whether the prognostic value of apolipoprotein levels is maintained in patients on statins. Copyright © 2006 S. Karger AG, Basel [ABSTRACT FROM AUTHOR]

In a registry-based case-control study, we compared the site-specific occurrence of nonmelanoma (keratinocytic) skin cancers among patients with cutaneous melanoma cases (cases, n = 3774) and solid tumours (controls, n = 349,923), respectively. Overall, patients with melanoma were almost five-fold more likely to develop keratinocytic cancers compared with solid tumour controls (adjusted OR 4.7, 95% CI 4.1-5.3), but the risks varied depending upon the site of melanoma. Whereas patients with melanoma of the head and neck had similarly increased risks of keratinocytic cancers across all body sites, patients with melanoma of the trunk were significantly more likely to develop keratinocyte cancer diagnosed on the trunk (adjusted OR 12.5, 95% CI 7.2-20.2) than on the head and neck (adjusted OR 3.0, 95% CI 2.2-4.3). Similar colocalisation of skin tumours was observed for patients with melanomas of the lower limb. These findings provide support for the hypothesis that skin cancers at different anatomical sites may arise through different causal pathways. [ABSTRACT FROM AUTHOR]

Dopaminergic transmission in the central nervous system is thought to underlie addictive behaviours, including smoking. One effective smoking cessation drug, bupropion, enhances dopaminergic transmission; conversely, antipsychotic drugs, which are dopamine antagonists, are associated with increased smoking. Thus we hypothesized that subfertile women treated with the potent dopamine agonist bromocriptine might smoke less as a consequence of their treatment. Among 4608 subfertile women those conceiving on bromocriptine were half as likely to smoke as those taking other drugs or those conceiving without medication (p < 0.0001). This observation supports the role of dopamine in nicotine addiction, and suggests that bromocriptine-like drugs could be used effectively by pregnant women to aid cessation. [ABSTRACT FROM AUTHOR]

This study investigates the extent to which the distinctive cross-sectional marital status picture of risk for cancer of the uterine cervix (single, married, widowed, divorced in ascending order of risk) has persisted in post-war Britain. Incidence and mortality due to invasive cervical cancer amongst single women now exceeds that of the married, and for both has become much closer to that of the widowed and divorced. A dramatic increase in carcinoma in situ in Scotland, seen particularly in the single since 1982, must partly reflect changes in screening and diagnostic classification, but is also consistent with the later occurrence of the sexual revolution in Scotland. Overall in Britain, the distribution of screening and hysterectomy cannot account for the present day pattern of the disease. Available data on patterns of smoking and oral contraceptive use are broadly consistent with a role for them in determining the current disease pattern associated with marital status but their possible involvement cannot be disentangled from the more likely effect of changing levels of sexual activity increasing the risk of sexually transmitted disease. As marital status becomes a less important social indicator of sexual behaviour, it has also become a much less reliable marker of cervical cancer risk. [ABSTRACT FROM AUTHOR]

A response by the authors to a letter to the editor about their article "Childhood leukaemia near British nuclear installations: methodological issues and recent results," published in a previous issue is presented.

In a meta-analysis of testicular cancer in twins, twins had a 30% increased risk (estimate 1.31, 95% CI 1.1–1.6), providing indirect support for the hypothesis that in utero hormone variations influence risk of testicular cancer. The summary-estimate for dizygotic twins was 1.3 (1.0–1.7) and for monozygotic or same sex twins 1.4 (1.2–1.8).British Journal of Cancer (2008) 98, 171–173. doi:10.1038/sj.bjc.6604136 www.bjcancer.com Published online 11 December 2007 [ABSTRACT FROM AUTHOR]

We studied childhood cancer incidence in a population-based twin cohort using record linkage to the National Registry of Childhood Tumours. After correcting for mortality, an incidence deficit was observed (Standardized Incidence Ratio (SIR) 79; 95% Confidence Interval (CI) 39-120). Pooled analysis with data from published cohort studies indicates a similar significant incidence reduction (SIR 81, 95% CI 67-96). Further studies are warranted. [ABSTRACT FROM AUTHOR]

To test the hypothesis that in utero exposure to high levels of oestrogen increases the risk of male breast cancer, we followed 115 235 male twins for more than 3.5 million person-years at risk. We observed 11 cases of male breast cancer versus 16.16 expected based on national rates (standardized rate ratio 0.68, 95% confidence interval 0.34-1.22) and conclude that any adverse influence of in utero oestrogen exposure is likely to be small. [ABSTRACT FROM AUTHOR]

A response by M.E. Kroll and colleagues to a letter to the editor about their article "Childhood leukaemia and socioeconomic status in England and Wales 1976-2005: evidence of higher incidence in relatively affluent communities persists over time," in the June 12, 2012 issue is presented.

A response from the authors of the article "Updated investigations of cancer excesses in individuals born or resident in the vicinity of Sellafield and Dounreay" in the 2014 issue is presented.

A response by M.E. Kroll and colleagues to a letter to the editor about their article "Childhood leukaemia and socioeconomic status in England and Wales 1976-2005: evidence of higher incidence in relatively affluent communities persists over time," in the June 12, 2012 issue is presented.

We report further analyses from an epidemiological study of childhood cancer and residence at birth near high-voltage power lines in the UK. These results suggest that the elevated risks for childhood leukaemia that we previously found for overhead power lines may be higher for older age at diagnosis and for myeloid rather than lymphoid leukaemia. There are differences across regions of birth but not forming any obvious pattern. Our results suggest the decline in risk we previously reported from the 1960s to the 2000s is linked to calendar year of birth or of cancer occurrence rather than the age of the power lines concerned. Finally, we update our previous analysis of magnetic fields to include later subjects.

Epidemiological evidence of increased risks for childhood leukaemia from magnetic fields has implicated, as one source of such fields, high-voltage overhead lines. Magnetic fields are not the only factor that varies in their vicinity, complicating interpretation of any associations. Underground cables (UGCs), however, produce magnetic fields but have no other discernible effects in their vicinity. We report here the largest ever epidemiological study of high voltage UGCs, based on 52,525 cases occurring from 1962-2008, with matched birth controls. We calculated the distance of the mother's address at child's birth to the closest 275 or 400 kV ac or high-voltage dc UGC in England and Wales and the resulting magnetic fields. Few people are exposed to magnetic fields from UGCs limiting the statistical power. We found no indications of an association of risk with distance or of trend in risk with increasing magnetic field for leukaemia, and no convincing pattern of risks for any other cancer. Trend estimates for leukaemia as shown by the odds ratio (and 95% confidence interval) per unit increase in exposure were: reciprocal of distance 0.99 (0.95-1.03), magnetic field 1.01 (0.76-1.33). The absence of risk detected in relation to UGCs tends to add to the argument that any risks from overhead lines may not be caused by magnetic fields.

We previously reported an association between childhood leukaemia in Britain and proximity of the child's address at birth to high-voltage power lines that declines from the 1960s to the 2000s. We test here whether a 'corona-ion hypothesis' could explain these results. This hypothesis proposes that corona ions, atmospheric ions produced by power lines and blown away from them by the wind, increase the retention of airborne pollutants in the airways when breathed in and hence cause disease. We develop an improved model for calculating exposure to corona ions, using data on winds from meteorological stations and considering the whole length of power line within 600 m of each subject's address. Corona-ion exposure is highly correlated with proximity to power lines, and hence the results parallel the elevations in leukaemia risk seen with distance analyses. But our model explains the observed pattern of leukaemia rates around power lines less well than straightforward distance measurements, and ecological considerations also argue against the hypothesis. This does not disprove the corona-ion hypothesis as the explanation for our previous results, but nor does it provide support for it, or, by extension, any other hypothesis dependent on wind direction.

Background: Paternal occupational exposures have been proposed as a risk factor for childhood leukaemia. This study investigates possible associations between paternal occupational exposure and childhood leukaemia in Great Britain., Methods: The National Registry of Childhood Tumours provided all cases of childhood leukaemia born and diagnosed in Great Britain between 1962 and 2006. Controls were matched on sex, period of birth and birth registration subdistrict. Fathers' occupations were assigned to 1 or more of 33 exposure groups. Social class was derived from father's occupation at the time of the child's birth., Results: A total of 16 764 cases of childhood leukaemia were ascertained. One exposure group, paternal social contact, was associated with total childhood leukaemia (odds ratio 1.14, 1.05-1.23); this association remained significant when adjusted for social class. The subtypes lymphoid leukaemia (LL) and acute myeloid leukaemia showed increased risk with paternal exposure to social contact before adjustment for social class. Risk of other leukaemias was significantly increased by exposure to electromagnetic fields, persisting after adjustment for social class. For total leukaemia, the risks for exposure to lead and exhaust fumes were significantly <1. Occupationally derived social class was associated with risk of LL, with the risk being increased in the higher social classes., Conclusion: Our results showed some support for a positive association between childhood leukaemia risk and paternal occupation involving social contact. Additionally, LL risk increased with higher paternal occupational social class.

Background: Wilms tumour is an embryonal malignant tumour that accounts for 90% of childhood kidney cancers. Parental occupational exposure has been hypothesised to be a cause of childhood Wilms tumour, in particular exposure to pesticides. However, the findings are inconsistent., Procedure: We have examined the association between paternal occupational exposures and Wilms tumour using birth registration data for cases (n = 2568) from the National Registry of Childhood Tumours (NRCT) and matched controls (n = 2,568) drawn from the general population of Great Britain. Paternal occupation, as recorded at the time of birth, was used to infer "occupational exposure" using a previously defined occupational exposure classification scheme. Odds ratios and 95% confidence intervals were generated using conditional logistic regression with exact methods to estimate the association between each paternal occupational exposure group and childhood Wilms tumour., Results: All odds ratios were close to 1.00 and no statistically significant associations were observed., Conclusion: The results of this study failed to support any of the previously identified associations between paternal occupation and childhood Wilms tumour., (Copyright 2009 Wiley-Liss, Inc.)

Background: Several small studies combined have suggested that twins develop fewer childhood cancers than singletons. The national Swedish Family-Cancer Database contains information on a large population of multiple births providing an unbiased dataset for the estimation of cancer risk in twins. Lifelong cancer incidence in these twins has already been reported as similar to that in singleton births. In contrast, the present paper presents robust estimates of a significantly reduced childhood cancer risk in twins to age 15., Methods: Standardised incidence ratios (SIR) were used to measure cancer risk for twins, taking the corresponding rates for singletons as reference. Rates were adjusted for age, sex, period of birth, and residential area. Follow up data cover the period 1958-2002., Results: Overall childhood cancer risk was significantly reduced in all twins (SIR 0.81 [95% CI: 0.69-0.94]) as was the risk for Wilms tumour (SIR 0.34 [95% CI: 0.09-0.88]). These significant reductions in risk were both driven by effects in same sex twins (overall cancer SIR 0.77 [95% CI: 0.64-0.93], Wilms tumour 0.12 [95% CI: 0.00-0.71]). Leukaemia risk was also significantly reduced for same sex twins (SIR 0.69 [95% CI: 0.47-0.97])., Conclusions: Our study provides the evidence that twins experience less childhood cancer than singletons. The risk reduction is most marked for Wilms tumour but may, to a varying extent, be true for a number of childhood neoplasms., ((c) 2008 Wiley-Liss, Inc.)

We explored the influence of maternal smoking during late pregnancy on the likelihood of smoking among offspring in adolescence and adulthood, using birth cohort data collected in the United Kingdom as part of the 1958 National Child Development Study. Longitudinal analysis indicated that maternal smoking during late pregnancy was associated with an increased likelihood of being a non-smoker at 16-year, 23-year and 33-year follow-up. This association differed between male and female offspring, with women showing no significant association and men showing an increased likelihood of being a non-smoker. There did not appear to be any association between maternal smoking during late pregnancy and cigarette consumption among offspring who reported smoking for either sex. These results are inconsistent with some previous reports that maternal smoking during pregnancy increases the likelihood of smoking among female offspring, although the observation of a moderating effect of sex on smoking behaviour is consistent with several previous reports. We discuss possible mechanisms for this association, and suggest factors that may account for the observed sex differences in this association, and the discrepancy between our results and some previous reports.

Objective: To summarize, in a systematic review, the evidence for the effect of stopping smoking on recurrence, cancer-specific and all cause-mortality among smokers with newly diagnosed bladder cancer., Materials and Methods: Two electronic databases and the reference lists of identified primary studies and reviews were searched. Studies were included if a hazard ratio and its confidence intervals could be extracted. A predefined set of study characteristics was extracted which defined whether studies were giving valid prognostic data on the effects of smoking in reasonably homogenous cohorts. The results of studies were synthesized qualitatively., Results: Fifteen relevant studies were identified; former and current smokers were combined in many studies. Many studies produced information on prognosis that was confounded by the mixing of incident and prevalent cases. Only three studies examined the influence of smoking on prognosis in only incident cases, most of whom had superficial disease. Of these, only one was of high quality. These three studies and the other 12 showed suggestive evidence that continued smoking or a lifetime of smoking constitutes a moderate risk factor for recurrence and death, and that stopping smoking could favourably change this. However, the evidence base for this is weak because of the methodological shortcomings and because most studies' results were not statistically significant. A life-table model showed that if stopping smoking altered the prognosis, the size of the benefit would be clinically worthwhile., Conclusion: There is suggestive evidence that stopping smoking might favourably alter the course of bladder cancer, but this is insufficient for clinicians to inform patients that doing so will improve their prognosis, and for providing specialized services to assist in stopping smoking to patients with bladder cancer.