The data for the United Kingdom are similar. however, incidences are different in some other parts of the world, reflecting widespread exposures to different infectious agents and environmental toxins. (Data from American Cancer Society, Cancer Facts and Figures, 2014.)
Figure 20–3 Benign versus malignant tumors. A benign glandular tumor (pink cells; an adenoma) remains inside the basal lamina (yellow) that marks the boundary of the normal structure (a duct, in this example). In contrast, a malignant glandular tumor (red cells; an adenocarcinoma) can develop from a benign tumor cell, and it destroys the integrity of the tissue, as shown. There are many different forms that such tumors may take.
Figure 20–4 The growth of a typical human tumor, such as a tumor of the breast. The diameter of the tumor is plotted on a logarithmic scale. Years may elapse before the tumor becomes noticeable. The doubling time of a typical breast tumor, for example, is about 100 days. however, particularly virulent tumors may grow much more rapidly.
diameter of tumor (mm) how this particular translocation promotes the development of CML by creating a novel hybrid gene encoding a protein that promotes cell proliferation.
Many other lines of evidence, from a variety of cancers, point to the same con clusion: most cancers originate from a single aberrant cell.
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If a single abnormal cell is to give rise to a tumor, it must pass on its abnormality to its progeny: the aberration has to be heritable. Thus, the development of a clone of cancer cells depends on genetic changes. The tumor cells contain somatic mutations: they have one or more shared detectable abnormalities in their DNA sequence that distinguish them from the normal cells surrounding the tumor, as in the example of CML just described. (The mutations are called somatic because they occur in the soma, or body cells, not in the germ line). Cancers are also driven by epigenetic changes—persistent, heritable changes in gene expression that result from modifications of chromatin structure without alteration of the cell’s DNA sequence. But somatic mutations that alter DNA sequence appear to be a fundamental and universal feature, and cancer is in this sense a genetic disease.
Factors that cause genetic changes tend to provoke the development of cancer. Thus, carcinogenesis (the generation of cancer) can be linked to mutagenesis (the production of a change in the DNA sequence). This correlation is particularly clear for two classes of external agents: (1) chemical carcinogens (which typically cause simple local changes in the nucleotide sequence), and (2) radiation such as x-rays (which typically cause chromosome breaks and translocations) or ultraviolet (UV) light (which causes specific DNA base alterations).
As would be expected, people who have inherited a genetic defect in one of several DNA repair mechanisms, causing their cells to accumulate mutations at an elevated rate, run a heightened risk of cancer. Those with the disease xeroderma pigmentosum, for example, have defects in the system that repairs DNA damage induced by UV light, and they have a greatly increased incidence of skin cancers.
A Single Mutation Is Not Enough to Change a Normal Cell into a Cancer Cell