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Cancer Prevention Overview (PDQ®): Prevention - Health Professional Information [NCI] - Description of the Evidence

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.

About the PDQ Cancer Prevention Summaries

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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

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 [1] and Hanahan and Weinberg.[2] 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.

The model of Hanahan and Weinberg focuses on the hallmark events at the cellular level that lead to a malignant tumor. In this model, the hallmarks of cancer include sustained angiogenesis, limitless replicative potential, evading apoptosis, self-sufficiency in growth signals, and insensitivity to antigrowth signals, leading to the defining characteristics of malignant tumors by giving them the ability to invade and metastasize. This model highlights the fact that malignant tumors arise and flourish within the environment of a whole organism. The tissue organizational field theory,[3] posits that carcinogenesis is better conceptualized at the level of tissues rather than cells. This theory is based on the dual premise that carcinogenesis is driven by defects in tissue organization and that all cells are inherently in a proliferative state.

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