PubMed · 7925723
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H Checkoway, P A Demers. 1994. Occupational case-control studies.. https://doi.org/10.1093/oxfordjournals.epirev.a036140
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BACKGROUND: Most human female cells contain two X chromosomes, only one of which is active. The process of X-chromosome inactivation, which occurs early in development, is usually random, producing tissues with equal mixtures of cells having active X chromosomes of either maternal or paternal origin. However, nonrandom inactivation may occur in a subset of females. If a tumor suppressor gene were located on the X chromosome and if females with a germline mutation in one copy of that suppressor gene experienced nonrandom X-chromosome inactivation, then some or all of the tissues of such women might lack the wild-type suppressor gene function. This scenario could represent a previously unrecognized mechanism for development of hereditary cancers. We investigated whether such a mechanism might contribute to the development of hereditary ovarian cancers. METHODS: Patterns of X-chromosome inactivation were determined by means of polymerase chain reaction amplification of the CAG-nucleotide repeat of the androgen receptor (AR) gene after methylation-sensitive restriction endonuclease digestion of blood mononuclear cell DNA from patients with invasive (n = 213) or borderline (n = 44) ovarian cancer and control subjects without a personal or family history of cancer (n = 50). BRCA1 gene status was determined by means of single-strand conformational polymorphism analysis and DNA sequencing. All statistical tests were two-sided. RESULTS AND CONCLUSIONS: Among individuals informative for the AR locus, nonrandom X-chromosome inactivation was found in the DNA of 53% of those with invasive cancer versus 28% of those with borderline cancer (P = .005) and 33% of healthy control subjects (P = .016). Nonrandom X-chromosome inactivation can be a heritable trait. Nine of 11 AR-informative carriers of germline BRCA1 mutations demonstrated nonrandom X-chromosome inactivation (.0002 < P < .008, for simultaneous occurrence of both). IMPLICATIONS: Nonrandom X-chromosome inactivation may be a predisposing factor for the development of invasive, but not borderline, ovarian cancer.
OBJECTIVE: To assess the possible association between the polymorphisms of CYP1A1 and the susceptibility of lung cancer so as to provide clues for genetic markers of lung cancer. METHODS: CYP1A1 rare genotypes MspI C and VV were detected with the methods of PCR-RFLP and ASA in a case-control study including 59 cases of lung cancer, 59 hospital controls and 73 healthy controls. RESULTS: The frequencies of rare genotypes C and VV of the lung cancer cases were not significantly different from those of the controls, though the frequency of C(25.4%) of the lung cancer cases was higher than that (16.5%) of the controls. However, in the non-smoking group with genotype(C),the risk of lung cancers was 2.43-2.91 times greater than that of the controls. Heterozygote B was overpresented in healthy controls (61.6%),compared to that of lung cancer cases(37.3%), P <0.01,odds ratio 0.37 (95% confidence interval 0.17-0.80). CONCLUSION: Genotype C may be one of the susceptibly genetic markers of lung cancer in the non-smoking population. The risk of lung cancer can be decreased in persons with heterozygote.
BACKGROUND: Between 1990 and 1996, more than 110,000 cases and 2900 deaths from diphtheria were reported in the Russian Federation. In 1994, because disease rates were high among children aged 7-10 years, the age of administration of the second booster dose of diphtheria vaccine was lowered from 9 years to 6 years, the age of school entry. To assess the impact of this policy change, we did a matched case-control study in three Russian cities. METHODS: Children aged 6-8 years who had diphtheria between September, 1994, and December, 1996, were each matched with five to seven children acting as controls who were within 3 months of age of the case and were from the same class at school. We did a matched analysis using conditional logistic regression. FINDINGS: We analysed the immunisation records of 58 cases and 306 controls. All but one case and all controls had received at least three doses of diphtheria-toxoid vaccine. 19 (33%) cases and 144 (47%) controls had received a booster dose of diphtheria toxoid within the previous 2 years. Cases were more likely than were controls to have received only four doses rather than five (odds ratio 2.8 [95% CI 1.2-6.5]) and to have a time since the last dose of diphtheria toxoid of 3-4 years (3.1 [1.1-9.1]) or 5-7 years (15.0 [2.5-89.0]), compared with children for whom it was 2 years or less. On multivariate analysis only a time since the last dose of 5-7 years remained significantly associated with disease (matched odds ratio adjusted for total number of doses 10.9 [1.6-75.1]). CONCLUSION: A booster dose of diphtheria-toxoid vaccine given to children in the Russian Federation at 6-8 years of age reduced the interval since the last dose of diphtheria toxoid and improved protection against diphtheria.