Cancer and Genetics Help

By — McGraw-Hill Professional
Updated on Aug 23, 2011

Introduction to Cancer

Cancer is a genetic disease resulting from multiple mutational events and chromosomal rearrangements. These mutations alter the normal functioning of a cell so that it takes on the following characteristics: (1) it becomes immortal, i.e., it is capable of unlimited cell division, and (2) it becomes independent from normal cellular controls that limit growth and division some cancers become invasive by spreading to other tissues, in a process called metastasis. One cancer cell is capable of dividing into a clonal mass of cells called a tumor. Tumors are not necessarily life-threatening (e.g., warts or galls) and may occur in both plants and animals. Plants do not have cancers because their cell walls prevent metastasis of tumor cells.Oncogenesis is the process by which a normal cell becomes cancerous; oncology is the study of cancer.A neoplasmis a population of potentially cancerous cells growing out of control. If the neoplasm is confined to its place of origin and has no tendency to recur after removal, it is a benign neoplasm. If it metastasizes from its site of origin, it becomes a life-threatening malignant neoplasm.

Some oncogenic mutations may be inherited, and/or be induced by environmental exposure to mutagens that damage DNA. Oncogenic mutations may also occur spontaneously. A carcinogen is any agent (e.g., mutagenic chemicals, ionizing radiations, and certain viruses) that can promote a cancerous state. Aside from the irritant fibers of asbestos, all carcinogens are thought to be mutagenic (causing damage toDNA), but not all mutagens are carcinogenic.

EXAMPLE 11.10 Xeroderma pigmentosum is a genetic syndrome characterized by extreme sensitivity to ultraviolet light and the tendency to develop multiple skin cancers. It is inherited as an autosomal recessive trait that produces a defective enzyme. Individuals with this genotype are unable to repair ultraviolet-induced DNA damage. This disease provides strong evidence that cancer originates in cells that have sustained permanent damage to DNA.

EXAMPLE 11.11 A type of blood cell cancer known as chronic myelogenous leukemia is associated with a reciprocal translocation involving the tip of the long arm of chromosome 9 and a portion of the long arm of chromosome 22. The chromosome 22 that bears a piece of chromosome 9 is called a Philadelphia chromosome (Example 7.23). A cellular protooncogene called c-abl (normally located on chromosome 9) becomes activated to oncogenic status when translocated to chromosome 22. A homologus gene (v-abl) exists in the highly oncogenic Abelson murine (mouse) leukemia virus.

Cancer is generally conceded to involve at least two major steps. The first step, termed initiation, results from a single exposure to a carcinogen or the spontaneous generation of a mutation. The second step, called promotion, involves one or more exposures to the same initiator or even to unrelated substances called promoters that complete the conversion of a cell to the neoplastic state. The promotion stage is a gradual process, often requiring many weeks in rodents and years in humans. Phorbol esters are among the most well-known promoters. Further heritable changes of an unknown nature are thought to occur during the promotion phase. Some substances [e.g., benzo(a)pyrene and polycyclic hydrocarbons, at relatively high doses] can both initiate and promote tumor formation. Mutations in certain genes, such as BRCA-1, may predispose a person to cancer requiring fewer promoters to create a cancerous state.

Many carcinogens must undergo metabolic activation. In this process, enzymes in various tissues, especially those in the liver convert the inactive precarcinogens into active carcinogens (see Supplementary Problem 10.10). Not all species have the enzymes necessary to convert a given precarcinogen into a carcinogen; hence, such a species would not be susceptible to induction of cancer by that substance.

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