Leukoplakia of the oral cavity, vulva, and penis, which may progress to squamous cell carcinoma (Chapters 15, 18, and 19)
Villous adenoma of the colon, associated with a high risk for progression to colorectal carcinoma (Chapter 15)
In this context it also may be asked, “What is the risk for malignant change in a benign neoplasm?”—or, stated differently, “Are benign tumors precancers?” In general the answer is no, but inevitably there are exceptions, and perhaps it is better to say that each type of benign tumor is associated with a particular level of risk, ranging from high to virtually nonexistent. As cited earlier, adenomas of the colon as they enlarge can undergo malignant transformation in up to 50% of cases; by contrast, malignant change is extremely rare in leiomyomas of the uterus.
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Cancer behaves like an inherited trait in some families, usually due to germ line mutations that affect the function of a gene that suppresses cancer (a so-called “tumor suppressor gene,” discussed later). What then can be said about the influence of heredity on sporadic malignant neoplasms, which constitute roughly 95% of the cancers in the United States?
While the evidence suggests that sporadic cancers can largely be attributed to environmental factors or acquired predisposing conditions, lack of family history does not preclude an inherited component. It may in fact be difficult to tease out hereditary and genetic contributions because these factors often interact. Such interactions may be particularly complex when tumor development is affected by small contributions from multiple genes. Furthermore, genetic factors may alter the risk for developing environmentally induced cancers. Instances where this holds true often involve inherited variation in enzymes such as components of the cytochrome P-450 system that metabolize procarcinogens to active carcinogens. Conversely, environmental factors can influence the risk for developing cancer, even in individuals who inherit well-defined “cancer genes.” For instance, breast cancer risk in females who inherit mutated copies of the BRCA1 or BRCA2 tumor suppressor genes (discussed later) is almost three-fold higher for women born after 1940 than for women born before that year, perhaps because of changes in reproductive behavior or increases in obesity in more recent times.
Theincidenceofcancervarieswithage,geographicfactors,andgeneticbackground.Thegeographicvariationincancerincidenceresultsmostlyfromdifferentenvironmentalexposures.Cancercanoccuratanyage,butismostcommoninolderadults.
Environmentalfactorsimplicatedincarcinogenesisincludeinfectiousagents,smoking,alcohol,diet,obesity,reproductivehistory,andexposuretocarcinogens.
Cancerriskrisesincertaintissuesinthesettingofincreasedcellularproliferationcausedbychronicinflammationorhormonalstimulation.
Epithelialcellliningsmaydevelopmorphologicchangesthatsignifyanincreasedriskfordevelopingcancer;suchlesionsarereferredtoasprecursor lesions.
Theriskfordevelopingcancerismodifiedbyinteractionsbetweenenvironmentalexposuresandgeneticvariants.