Titlebook: Genetic Predisposition to Cancer; Rosalind A. Eeles (Senior Lecturer and Honorary Co Book 1996 Springer Science+Business Media Dordrecht 1

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,Die Entstehung des Warenhauses (1860–1880),e attempted to quantify the risks of breast cancer associated with a positive family history. Attempts have also been made to examine whether the pattern of related individuals with breast cancer are consistent with the effects of a single gene of large effect, shared environmental effects, many gen

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https://doi.org/10.1007/978-3-642-91200-9e of a high risk gene. Over the past 5 years a number of the genes responsible for inherited predisposition to breast and/or ovarian cancer have been identified or localized. In particular, .1 [1], .2 [2], the ataxia-telangiectasia gene [3,4], the .53 gene [5,6] and the androgen receptor gene [7] ar

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https://doi.org/10.1007/978-3-642-92212-1The multiple endocrine neoplasia (MEN) syndromes comprise dominantly inherited predisposition to tumours of specific endocrine glands. Two distinct syndromes are recognized:

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Genetic predisposition to cancer: an introductionEvidence that inherited susceptibility plays a role in the risk of malignancy comes from three separate sources. These observations are that:

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Multiple endocrine neoplasiaThe multiple endocrine neoplasia (MEN) syndromes comprise dominantly inherited predisposition to tumours of specific endocrine glands. Two distinct syndromes are recognized:

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From families to chromosomes: genetic linkage, and other methods for finding cancer-predisposition gd since then genes for all the major ‘inherited cancer syndromes’ (that is, those rare syndromes where evidence for Mendelian inheritance was apparent from clinical studies) have now been either identified or at least mapped precisely within the human genome (see Chapter 1). Genetic linkage analysis

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The Li-Fraumeni syndrome and the role of ,53 mutations in predisposition to cancer were due to inherited predisposition to the observed cancers [1]. In a more detailed report, a second pair of cousins with childhood soft tissue sarcoma were identified, and the finding of adrenocortical carcinoma and brain tumours in first-degree relatives of children with soft tissue sarcoma sugg

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Xeroderma pigmentosum, Cockayne syndrome and trichothiodystrophy: sun sensitivity, DNA repair defectiduals with XP alone, XP with CS, or TTD alone. In order to understand the relationship between DNA damage/repair and cancer revealed in XP, it is necessary to study all three conditions at the clinical, cellular and molecular levels.

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