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Träfflista för sökning "WFRF:(Adami Hans Olov) srt2:(1995-1999);pers:(Ekbom A)"

Sökning: WFRF:(Adami Hans Olov) > (1995-1999) > Ekbom A

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1.
  • Adami, Hans-Olov, et al. (författare)
  • The aetiology and pathogenesis of human breast cancer
  • 1995
  • Ingår i: Mutation research. - 0027-5107 .- 1873-135X. ; 333:1-2, s. 29-35
  • Tidskriftsartikel (refereegranskat)abstract
    • Whilst investigators have clearly shown that non-hereditary factors dominate the aetiology of human breast cancer, they have failed to identify quantitatively important causes, and prospects for prevention remain indeed limited. However, progress in epidemiological and basic research has taken place during the last few years. Current evidence suggests that breast cancer may be affected by the intra-uterine environment, that exposures during adolescence are particularly important, and that pregnancy has a dual effect on breast cancer risk: an early increase followed by long-term protection. Great variation exists in the structural development of the breast ductal system already in the newborn--and by inference in utero--and a pregnancy induces permanent structural changes in the mammary gland. We suggest that these observations fit into an aetiological model with the following key components: (1) breast cancer risk depends on the number of cells at risk, the susceptibility of individual cells to malignant transformation, and on the degree of cellular proliferation, notably cells which can act as founders of breast cancer; (2) the number of target cells is determined by the hormonal environment mainly early in life, perhaps already in utero; (3) in adult life, hormones which are non-genotoxic, increase breast cancer risk by increasing selective cell proliferation and thus number of target cells and the risk of retention of spontaneous somatic mutations; (4) while a pregnancy stimulates the growth of already malignant cells or cells close to malignant transformation (and thereby entails a short-term risk increase) the dominating long-term protection occurs due to permanent structural changes, terminal differentiation and perhaps decreased cell proliferation and carcinogen-binding in combination.
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2.
  • Cnattingius, Sven, et al. (författare)
  • Prenatal and neonatal risk factors for childhood lymphatic leukemia
  • 1995
  • Ingår i: Journal of the National Cancer Institute. - 0027-8874 .- 1460-2105. ; 87:12, s. 908-914
  • Tidskriftsartikel (refereegranskat)abstract
    • BACKGROUND: Because the incidence of childhood acute lymphatic leukemia peaks between 2 and 4 years of age, the risk factors may exert their influence during the prenatal and/or the neonatal periods. Results of previous studies of perinatal risk factors have been contradictory, perhaps because most studies either have been hospital based or have been restricted to limited geographical areas. PURPOSE: A nationwide case-control study was carried out to identify maternal and perinatal risk factors for this disease. METHODS: The case-control study was nested in cohorts defined by all live births in Sweden recorded in the nationwide Medical Birth Register. Since 1973, this register has routinely collected information on all hospital births in regard to maternal demographic data, reproductive history, pregnancy, delivery, and the neonatal period. From the Swedish National Cancer Register, 613 case subjects were identified in successive birth cohorts from 1973 through 1989. Five control subjects per case subject were randomly selected from the pool of children matched by sex and month and year of birth. Conditional logistic regression was used to calculate the odds ratios (ORs) and 95% confidence intervals (CIs) for potential risk factors and to estimate their effects after adjustment for possible confounders. RESULTS: Risk of childhood lymphatic leukemia at all ages increased with Down's syndrome (OR = 20.0; 95% CI = 4.2-94.2), maternal renal disease (OR = 4.4; 95% CI = 1.6-12.1), use of supplementary oxygen (OR = 2.3; 95% CI = 1.5-3.6), postpartum asphyxia (OR = 1.8; 95% CI = 1.2-2.6), birth weight of more than 4500 g (OR = 1.7; 95% CI = 1.1-2.7), and hypertensive disease during pregnancy (OR = 1.4; 95% CI = 1.0-1.9). Down's syndrome affected risk mostly in children younger than 5 years, whereas other factors affected those children 5 years old or older. Being one of a multiple birth also increased risk among older children (OR = 2.5; 95% CI = 1.0-6.0). Use of supplementary oxygen may act as a causal intermediate (surrogate) for postpartum asphyxia and its causes, as would high birth weight for its causes. CONCLUSIONS: Several maternal and perinatal risk factors were found to be associated with childhood lymphatic leukemia, but they showed age-specific differences. Overall, only a few risk factors were identified, and these accounted for a small proportion of cases. We concluded that most risk factors for childhood lymphatic leukemia remain unidentified in very young children.
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3.
  • Lipworth, L., et al. (författare)
  • Maternal pregnancy hormone levels in an area with a high incidence (Boston, USA) and in an area with a low incidence (Shanghai, China) of breast cancer
  • 1999
  • Ingår i: British Journal of Cancer. - : Springer Science and Business Media LLC. - 0007-0920 .- 1532-1827. ; 79:1, s. 7-12
  • Tidskriftsartikel (refereegranskat)abstract
    • Characteristics probably associated with the fetal hormonal milieu have recently been shown to increase (birth size indicators, prematurity, neonatal jaundice) or decrease (pregnancy toxaemia) breast cancer risk in the female offspring. However, it is unknown whether differences in pregnancy hormone levels may contribute to the marked geographical variation in breast cancer incidence. We have compared, in a highly standardized manner, pregnancy hormone levels in a population with high incidence and one with low incidence of breast cancer. Three hundred and four pregnant Caucasian women in Boston and 334 pregnant Chinese women in Shanghai were enrolled from March 1994 to October 1995. Levels of oestradiol, oestriol, prolactin, progesterone, human growth hormone, albumin and sex hormone-binding globulin were measured in maternal blood at weeks 16 and 27 of gestation and compared between the two study sites using non-parametric Wilcoxon's rank-sum test. Demographical, anthropometrical and pregnancy characteristics were ascertained through interview, and relevant variables concerning delivery and the newborn were abstracted from medical records and paediatric charts. During the first visit, median serum levels of all studied hormones were statistically significant, and in most instances substantially, higher among Chinese women, who have a low incidence of breast cancer, compared with American women, who have a high incidence of breast cancer. An analogous pattern was evident during the second visit, although the relative differences tended to be smaller. Further research is needed to identify lifestyle or other exogenous determinants of pregnancy hormone levels, as well as possible mechanisms by which they may influence carcinogenic processes in the breast and possibly other organs.
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4.
  • Thurfjell, Erik, et al. (författare)
  • Breast size and mammographic pattern in relation to breast cancer risk
  • 1996
  • Ingår i: European Journal of Cancer Prevention. - 0959-8278 .- 1473-5709. ; 5:1, s. 37-41
  • Tidskriftsartikel (refereegranskat)abstract
    • The relation of Wolfe's parenchymal patterns and radiographically-assessed breast size with breast cancer risk was evaluated in a population-based nested case-control study in Uppsala, Sweden. All women who attended a mammographic screening programme in Uppsala county starting in 1988 have been followed for the occurrence of breast cancer through 1993. The analysis was based on 295 cases and 589 age-matched controls, whose mammograms were blindly evaluated for parenchymal pattern and breast size. Women with P2 or DY pattern had a significantly elevated risk of breast cancer compared with women with N1 or P1 (OR = 2.09; 95% CI = 1.52-2.86). There was an inverse association of breast size with breast cancer risk, which disappeared after adjusting for parenchymal pattern, because breasts of smaller size tended to have high-risk parenchymal patterns. It is concluded that in Swedish women, and perhaps in Caucasian women in general, small breast size is associated with increasing breast risk through its association with high-risk parenchymal pattern. This is in contrast to the fact that Asian women, who in general have breasts of smaller size, have low prevalence of high-risk parenchymal pattern as well as low rates of breast cancer.
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