A tobacco-specific carcinogen in the fetus

Milunsky, Aubrey; Carmella, Steven G.; Ye, Ming; Hecht, Stephen S.

doi:10.1002/(sici)1097-0223(200004)20:4<307::aid-pd797>3.0.co;2-m

Cited by 47 publications

(20 citation statements)

References 17 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…Of these, N-nitroso compounds are the most likely candidate transplacental liver carcinogens (Anderson et al, 1989;Correa et al, 1990;Beebe et al, 1993;Schuller et al, 1993Schuller et al, , 1994Hecht, 1998). These compounds can cross the human placenta, and their metabolites have been found both in the urine and bound to the fetal haemoglobin of newborns whose mothers smoked cigarettes (Coghlin et al, 1991;Lackmann et al, 1999) and in the fetus in early pregnancy (Milunsky et al, 2000). Cord blood T lymphocytes from newborns has revealed an increased level of mutations (deletions in infants of mothers who smoked (Finette et al, 1997)).…”

Section: Discussionmentioning

confidence: 99%

Parental smoking and childhood cancer: results from the United Kingdom Childhood Cancer Study

2003

View full text Add to dashboard Cite

There are strong a priori reasons for considering parental smoking behaviour as a risk factor for childhood cancer but case -control studies have found relative risks of mostly only just above one. To investigate this further, self-reported smoking habits in parents of 3838 children with cancer and 7629 control children included in the United Kingdom Childhood Cancer Study (UKCCS) were analysed. Separate analyses were performed for four major groups (leukaemia, lymphoma, central nervous system tumours and other solid tumours) and more detailed diagnostic subgroups by logistic regression. In the four major groups, after adjustment for parental age and deprivation there were nonsignificant trends of increasing risk with number of cigarettes smoked for paternal preconception smoking and nonsignificant trends of decreasing risk for maternal preconception smoking (all P-values for trend 40.05). Among the diagnostic subgroups, a statistically significant increased risk of developing hepatoblastoma was found in children whose mothers smoked preconceptionally (OR ¼ 2.68, P ¼ 0.02) and strongest (relative to neither parent smoking) for both parents smoking (OR ¼ 4.74, P ¼ 0.003). This could be a chance result arising from multiple subgroup analysis. Statistically significant negative trends were found for maternal smoking during pregnancy for all diagnoses together (Po0.001) and for most individual groups, but there was evidence of under-reporting of smoking by case mothers. In conclusion, the UKCCS does not provide significant evidence that parental smoking is a risk factor for any of the major groups of childhood cancers. There are strong a priori reasons for considering parental smoking behaviour as a risk factor for childhood cancer. Many proven carcinogens are present in tobacco and tobacco smoke (Hecht, 1999;Hoffmann and Hoffmann, 1997). Tobacco-related compounds have also been detected in human placenta, fetal blood, urine of offspring and in breast milk of smoking mothers (Perlman and Dannenberg, 1942;Everson et al, 1986Everson et al, , 1988Woodward et al, 1986;Hansen et al, 1992;Myers et al, 1996;Pinorini-Godly and Myers, 1996;Arnould et al, 1997;Daube et al, 1997).Previous case -control studies have tended to show weak associations between maternal cigarette smoking during pregnancy and childhood cancers (IARC, 1986;Severson et al, 1993;Tredaniel et al, 1994;Sorahan et al, 1995Sorahan et al, , 1997a Sorahan et al, , b, 2001Klebanoff et al, 1996;Shu et al, 1996). There is somewhat stronger and more consistent evidence for a paternal preconceptional effect, although relative risks in most case -control studies are only just above one (Severson et al, 1993;Shu et al, 1996;Ji et al, 1997;Sorahan et al, 1997b;. This effect has been attributed to germ-cell mutations during spermatogenesis caused by tobacco products (Wyrobeck, 1993;Wyrobek and Adler, 1996;Woodall and Ames, 1997). Relevant studies are reviewed by Thornton and Lee (1998).The United Kingdom Childhood Cancer Study (UKCCS) is a nationwide population-based...

show abstract

Section: Discussionmentioning

confidence: 99%

Parental smoking and childhood cancer: results from the United Kingdom Childhood Cancer Study

2003

View full text Add to dashboard Cite

show abstract

“…30 In addition, mutagenic chemicals from maternal smoking cross the placenta enhancing the plausibility of an effect of parental smoking on pediatric leukemia risk. 31 Our analysis showed a significant association between paternal smoking and hyperdiploid leukemia, in the inverse direction, when compared to other leukemia subtypes (see Results). Because parental smoking was not significantly associated with RAS mutation-positive leukemia overall (Table 1), this suggests that another molecular subtype of leukemia may be positively associated with paternal smoking.…”

Section: 23mentioning

confidence: 99%

RAS mutation is associated with hyperdiploidy and parental characteristics in pediatric acute lymphoblastic leukemia

et al. 2005

View full text Add to dashboard Cite

We explored the relationship of RAS gene mutations with epidemiologic and cytogenetic factors in a case series of children with leukemia. Diagnostic bone marrow samples from 191 incident leukemia cases from the Northern California Childhood Leukemia Study were typed for NRAS and KRAS codon 12 and 13 mutations. A total of 38 cases (20%) harbored RAS mutations. Among the 142 B-cell acute lymphoblastic leukemia (ALL) cases, RAS mutations were more common among Hispanic children (P ¼ 0.11) or children born to mothers o30 years (P ¼ 0.007). Those with hyperdiploidy at diagnosis (450 chromosomes) had the highest rates of RAS mutation (P ¼ 0.02). A multivariable model confirmed the significant associations between RAS mutation and both maternal age and hyperdiploidy. Interestingly, smoking of the father in the 3 months prior to pregnancy was reported less frequently among hyperdiploid leukemia patients than among those without hyperdiploidy (P ¼ 0.02). The data suggest that RAS and high hyperdiploidy may be cooperative genetic events to produce the leukemia subtype; and furthermore, that maternal age and paternal preconception smoking or other factors associated with these parameters are critical in the etiology of subtypes of childhood leukemia.

show abstract

“…Further, tobacco smoke contains 40 known carcinogens, which permeate the placenta and are passed to the fetus (Florek et al, 2011;Milunsky, Carmella, Ye, & Hecht, 2000). For example, one of the N-nitrosamines in tobacco smoke, nicotine-derived nitrosamine ketone (NNK), is a cause of lung cancer.…”

mentioning

confidence: 99%

“…For example, one of the N-nitrosamines in tobacco smoke, nicotine-derived nitrosamine ketone (NNK), is a cause of lung cancer. NNAL (4-(methylnitrosamino)-1-(3-pyridyl)-1-butanol), a metabolite of NNK, has been found at elevated levels in newborns of mothers who smoke and also in newborns of nonsmoking mothers exposed to SHS (Milunsky et al, 2000). Florek et al (2011) reported that more than 50% of infants with nonsmoking mothers who reported exposure to SHS during pregnancy had detectable levels of NNAL in their urine at birth.…”

mentioning

confidence: 99%

Families at Risk: Home and Car Smoking Among Pregnant Women Attending a Low-Income, Urban Prenatal Clinic

Stotts

Northrup

Hutchinson

et al. 2014

Nicotine &Amp; Tobacco Research

View full text Add to dashboard Cite

show abstract

A tobacco-specific carcinogen in the fetus

Cited by 47 publications

References 17 publications

Parental smoking and childhood cancer: results from the United Kingdom Childhood Cancer Study

Parental smoking and childhood cancer: results from the United Kingdom Childhood Cancer Study

RAS mutation is associated with hyperdiploidy and parental characteristics in pediatric acute lymphoblastic leukemia

Families at Risk: Home and Car Smoking Among Pregnant Women Attending a Low-Income, Urban Prenatal Clinic

Contact Info

Product

Resources

About