Letter to the editor: Family history and risk of ovarian cancer

Vecchia, Carlo La; Parazzini, Fabio; Negri, Eva; Pino, Del; Franceschi, Silvia

doi:10.1002/(sici)1097-0215(19960917)67:6<903::aid-ijc23>3.0.co;2-0

Cited by 5 publications

(2 citation statements)

References 7 publications

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“…These patterns are consistent with an autosomal dominant gene with variable penetration 38. The estimated relative risks from case‐control studies that included data on family history range from 2 to 10, but are between 3 and 5 in most studies 4, 39, 40, 41…”

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confidence: 54%

Ovarian cancer in Europe: Cross-sectional trends in incidence and mortality in 28 countries, 1953-2000

et al. 2004

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We have considered trends in incidence and mortality in 28 European countries using incidence data from successive volumes of Cancer Incidence in Five Continents and mortality from the WHO database. Countries with the highest rates in the early 1960s included the Nordic countries, Austria, Germany and the United Kingdom, but trends in these areas have tended to decline over recent calendar periods, particularly with regard to mortality. Southern European countries showed upward trends, at least until the early 1980s for France and Italy. Likewise, in most central and eastern European countries, ovarian cancer incidence and mortality rates were originally relatively low, but tended to rise over time. Falls in mortality, but not in incidence, over recent years were observed in the Czech Republic and Hungary. In several countries, mainly in northern Europe, trends were more favorable at younger age (25-49 years) than in the subsequent age groups. Thus, recent trends in ovarian cancer have led to a leveling of rates across various areas of the continent, although a 2.5-fold variation was still observed in the late 1990s between the highest mortality rate of 9.3/100,000 in Denmark and the lowest one of 3.6 in Portugal. These patterns should be viewed in the light of an observed reduction in parity, mainly in southern and eastern Europe, and the spread of oral contraceptive use, mainly in northern Europe, since these are the best recognized protective factors with regard to ovarian carcinogenesis. The declining mortality trends can also in part be ascribed to improvements in treatment. © 2004 Wiley-Liss, Inc. Key words: ovarian cancer; incidence; mortality; epidemiology; time trends; registries; European Union; female hormones; reproductive factors; diet In developed areas of the world, ovarian cancer is a common neoplasm, ranking 7th and 6th most frequent for incidence and mortality, respectively. 1 On a worldwide basis, the total number of cases has been estimated around 192,000, thus representing over 4% of all cancers in women and the 6th leading site for incidence. 1 There are, however, large variations in the incidence of ovarian cancer in different areas of the world. The highest incidence areas are in Europe (especially the Nordic countries and the United Kingdom) and North America, with a ratio of approximately 4 separating rates in the highest and the lowest incidence countries worldwide, and over 3 between the corresponding mortality figures. 1-3 Ovarian cancer is therefore an important public health issue in Western countries, although more than 50% of new cases diagnosed every year worldwide occur in developing countries. 1 Incidence and mortality rates in the highest-risk areas (the United States, Canada, Scandinavia and the United Kingdom) have remained approximately constant or have declined between 1980 and 1995, 3 while increasing trends were observed in previously low-risk areas, such as Japan, India and Singapore, and in southern and eastern Europe.Several factors have probably impacted on ovari...

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Ovarian cancer in Europe: Cross-sectional trends in incidence and mortality in 28 countries, 1953-2000

et al. 2004

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“…Gastric cancer remains a leading cause of cancer death worldwide and it has been estimated that up to 10% of gastric cancer cases have some kind of familial association 1, 2. Hereditary diffuse gastric cancer (HDGC) has been defined by the International Gastric Cancer Linkage Consortium (IGCLC) as: any family with two documented cases of diffuse gastric cancer in first‐ or second‐degree relatives with one case under the age of 50 years or three or more documented cases of diffuse gastric cancer in first or second degree relatives at any age 3, 4.…”

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Mechanisms and sequelae of E‐cadherin silencing in hereditary diffuse gastric cancer

Barber

Murrell

Itō

et al. 2008

The Journal of Pathology

120

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Around 25-40% of cases of hereditary diffuse gastric cancer (HDGC) are caused by heterozygous E-cadherin (CDH1) germline mutations. The mechanisms for loss of the second allele still remain unclear. The aims of this study were to elucidate mechanisms for somatic inactivation of the wild-type CDH1 allele and to seek evidence for cadherin switching. Archival tumour material was analysed from 16 patients with CDH1 germline mutations and seven patients fulfilling HDGC criteria without CDH1 germline mutations. The 16 CDH1 exons were sequenced. E-cadherin promoter methylation was analysed by bisulphite sequencing and pyrosequencing and allele specificity was determined using polymorphic loci. Loss of heterozygosity was analysed using microsatellite markers. Cadherin expression levels were determined by real-time RT-PCR and immunohistochemistry. Six of 16 individuals with germline mutations had at least one second hit mechanism. Two exonic mutations (exon 9 truncating, exon 3 missense) and four intronic mutations which may affect splicing were identified. Tumours from 4/16 individuals had promoter hypermethylation that was restricted to the A allele haplotype in three cases. E-cadherin loss (mRNA and protein) generally correlated with identification of a second hit. In cases without germline E-cadherin mutations there was no evidence for somatic mutation or significant promoter methylation. P-cadherin (>25% cells) was expressed in 7/13 (54%) and 4/5 (80%) with and without germline CDH1 mutations, respectively, independent of complete E-cadherin loss. Overall, inactivation of the second CDH1 allele occurs by mutation and methylation events. Methylation is commonly allele-specific and is uncommon without germline mutations. P-cadherin over-expression commonly occurs in individuals with diffuse type gastric cancer.

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