Cancer predisposition

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  • Carcinogenesis covers molecular, biochemical and cellular processes that underpin this field. The complex nature of cancer means that a broad understanding of these processes is advantageous when designing novel preventative, therapeutic or diagnostic strategies. This book commences with chapters discussing cancer predisposition and pre-cancerous lesions. Factors that initiate or progress cancer development, including viral, hormonal, oncogenic and biochemical stimuli are then described, as are interactions with the cancer extracellular environment....

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  • Breast Cancer Breast self-examination, clinical breast examination by a care giver, and mammography have been advocated as useful screening tools. Only screening mammography alone and screening mammography with clinical examination have been evaluated in randomized controlled trials. MRI is being assessed and is more accurate than mammography in women at high risk due to genetic predisposition or in women with very dense breast tissue.

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  • Familial Cancer Syndromes A small fraction of cancers occur in patients with a genetic predisposition. In these families, the affected individuals have a predisposing loss-of-function mutation in one allele of a tumor-suppressor gene or caretaker gene. The tumors in these patients show a loss of the remaining normal allele as a result of somatic events (point mutations or deletions), in agreement with the Knudson hypothesis (Fig. 79-3).

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  • The Cancer Handbook is a major new reference work that provides a comprehensive overview of cancer, biology and medicine. All aspects of scientific and clinical information in cancer research and medicine are explored in this expansive resource for a wide audience including medical and life science students, as well as researchers, scientists and clinicians in the cancer field and related biomedical areas.

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  • The second requirement is a clear and well defined starting point. For popu- lation-based cancer registries, the starting date (from which the survival is calculated) is the incidence date (see Section 17.3.1). The third requirement is a clear and well defined outcome. Death is gener- ally the outcome of interest, but some registries collect enough data to allow them to conduct analyses using recurrence of tumour, or first recurrence of a particular complication, as the outcome of interest.

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  • A major pan-European study showed that survival rates in England and Scotland were lower than in other European countries in the 1980s. 6 This was probably due, at least in part, to the fact that British patients tended to have more advanced disease at the time of diagnosis. It is not yet known whether the discrepancy in outcomes has been reduced in the period since this study was carried out. Risk factors The causes of breast cancer are complex. It has been suggested that up to 10% of patients may have an inherited predisposition to the disease.

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  • Many disorders exhibit the feature of locus heterogeneity, which refers to the fact that mutations in different genes can cause phenotypically similar disorders. For example, osteogenesis imperfecta (Chap. 357), long QT syndrome (Chap. 226), muscular dystrophy (Chap. 382), homocystinuria (Chap. 358), retinitis pigmentosa (Chap. 29), and hereditary predisposition to colon cancer (Chap. 87) or breast cancer (Chap. 86) can each be caused by mutations in distinct genes.

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  • Inherited Predisposition to Lung Cancer While an inherited predisposition to develop lung cancer is not common, several features suggest a potential for familial association. People with inherited mutations in RB (patients with retinoblastomas living to adulthood) and p53 (LiFraumeni syndrome) genes may develop lung cancer. First-degree relatives of lung cancer probands have a two- to threefold excess risk of lung cancer or other cancers, many of which are not smoking-related.

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  • Pathogenesis The multicentric nature of the disease and high rate of recurrence has led to the hypothesis of a field defect in the urothelium that results in a predisposition to cancer. Molecular genetic analyses suggest that the superficial and invasive lesions develop along distinct molecular pathways in which primary tumorigenic aberrations precede secondary changes associated with progression to a more advanced stage.

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