Prevention is defined as the reduction of cancer mortality via reduction in the incidence of cancer. This can be accomplished by avoiding a carcinogen or altering its metabolism; pursuing lifestyle or dietary practices that modify cancer-causing factors or genetic predispositions; medical intervention (e.g., chemoprevention); or early detection strategies that can result in removal of precancerous lesions, such as colonoscopy for colorectal polyps.
Although they comprise fewer than 1% of all gastrointestinal (GI) tumors, gastrointestinal stromal tumors (GIST) are the most common mesenchymal tumors of the GI tract. It has been estimated that there are 3,300 to 6,000 new GIST cases per year in the United States. A study based on Surveillance, Epidemiology and End Results (SEER) registry data found that the age-adjusted yearly incidence of GIST in the United States was 6.8 per million from 1992 to 2000. However, the...
The PDQ cancer prevention summaries are primarily organized by specific anatomic cancer site to facilitate consideration of the unique characteristics of specific malignancies. In this section, an overview of cancer prevention strategies is provided, including a summary of evidence for selected preventive strategies used in the prevention of a broad spectrum of malignancies. The strength of evidence and magnitude of effects of these strategies, however, may vary by cancer site. Other PDQ cancer prevention summaries address the prevention of specific types of cancer and provide more detailed descriptions of the evidence.
There are many common beliefs or speculations about causes of cancer. However, putative causes of cancer for which there exist very little scientific evidence, positive or negative, are not considered in these summaries. Therefore, absence of an environmental, dietary, or lifestyle factor from these summaries implies insufficient evidence for detailed consideration and not necessarily absence of effect. Many such factors are deserving of research regarding their potential roles in cancer, but if that research does not exist, has not been published, or the Editorial Board judges the research to be of poor quality, then they are not addressed in these summaries.
Carcinogenesis refers to an underlying etiologic pathway that leads to cancer. Several models of carcinogenesis have been proposed. Knudson proposed a "two-hit" model requiring a mutation in both copies of a gene resulting in cancer. Expansion of this concept has resulted in other widely cited models of carcinogenesis including those of Vogelstein and Kinzler  and Hanahan and Weinberg. The model of Vogelstein and Kinzler emphasizes that cancer is ultimately a disease of damaged DNA, comprised of a series of genetic mutations that can transform normal cells to cancerous cells. The genetic mutations include inactivation of tumor suppressor genes and activation of oncogenes. Compared with cancers arising in the general population, individuals with a major inherited predisposition to cancer are born with inherited (i.e., germline) mutations in genes involved in cancer causation, giving them a head start on the pathway to cancer. Similar mutations would be expected to result in cancer progression among all individuals; however, in those without a major inherited cancer predisposition, the mutation would occur as a somatic mutation later during their lifetime.