Introduction

Colorectal carcinoma (CRC) represents a clinical and epidemiological relevant illness due to problems of acquiring an early diagnosis and the fact that it is a major cause of mortality worldwide and accounts for nearly 4% of all deaths in Western countries [1, 2]. Nearly 90% of CRC is the final result of a step-by-step progression from the normal mucosa to adenoma-tous polyps and finally to dysplasia and adenocarci-noma. The biological evolution takes many years and should allow enough time for early diagnosis and therapy, as it is widely accepted that endoscopic/sur-gical polypectomy prevents the otherwise natural progression to carcinoma.

The two major forms of hereditary CRC, which are quite different, include the hereditary non-polyposis colorectal cancer (HNPCC) and the familial adenomatous polyposis (FAP), which represents 5-10% of the total number of cases of CRC. Familial adenoma-tous polyposis is a troublesome autosomal dominant disease that evolves quietly until clinical manifestations appear, which means that the development of innumerable adenomatous polyps start to develop at puberty and gradually increase their growth to involve the whole colon at adulthood. The management of FAP represents a challenge for gastroen-terologists and surgeons in terms of history of the disease, evaluation of the clinical pattern, therapeutic options, follow up and chemoprevention of relapses.

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