A blood smear from a person with acute myelogenous leukemia. The gigantic cells with irregularly shaped purple nuclei are leukemia cells. The small reddish-gray circular cells are normal red blood cells. [Margaret Cubberly/Phototake.]

Cancer causes about one-fifth of the deaths in the United States each year. Worldwide, between 100 and 350 of each 100,000 people die of cancer each year. Cancer is due to failures of the mechanisms that usually control the growth and proliferation of cells. During normal development and throughout adult life, intricate genetic control systems regulate the balance between cell birth and death in response to growth signals, growth-inhibiting signals, and death signals. Cell birth and death rates determine adult body size, and the rate of growth in reaching that size. In some adult tissues, cell proliferation occurs continuously as a constant tissue-renewal strategy. Intestinal epithelial cells, for instance, live for just a few days before they die and are replaced; certain white blood cells are replaced as rapidly, and skin cells commonly survive for only 2-4 weeks before being shed. The cells in many adult tissues, however, normally do not proliferate except during healing processes. Such stable cells (e.g., hepatocytes, heart muscle cells, neurons) can remain functional for long periods or even the entire lifetime of an organism.

The losses of cellular regulation that give rise to most or all cases of cancer are due to genetic damage (Figure 23-1). Mutations in two broad classes of genes have been implicated in the onset of cancer: proto-oncogenes and tumor-suppressor genes. Proto-oncogenes are activated to become oncogenes by mutations that cause the gene to be excessively active in growth promotion. Either increased gene expression or production of a hyperactive product will do it. Tumor-suppressor genes normally restrain growth, so damage to them allows inappropriate growth. Many of the genes in both classes encode proteins that help regulate cell birth (i.e., entry into and progression through the cell cycle) or cell death by apoptosis; others encode proteins that participate in repairing damaged DNA. Cancer commonly results from mutations that arise during a lifetime's exposure to carcino gens, which include certain chemicals and ultraviolet radiation. Cancer-causing mutations occur mostly in somatic cells, not in the germ-line cells, and somatic cell mutations are not passed on to the next generation. In contrast, certain inherited mutations, which are carried in the germ line, increase the probability that cancer will occur at some time. In a destructive partnership, somatic mutations can combine with inherited mutations to cause cancer.

Thus the cancer-forming process, called oncogenesis or tumorigenesis, is an interplay between genetics and the environment. Most cancers arise after genes are altered by carcinogens or by errors in the copying and repair of genes. Even if the genetic damage occurs only in one somatic cell, division of this cell will transmit the damage to the daughter cells, giving rise to a clone of altered cells. Rarely, however, does mutation in a single gene lead to the onset of cancer. More typically, a series of mutations in multiple genes creates a progressively more rapidly proliferating cell type that escapes normal growth restraints, creating an opportunity for additional mutations. Eventually the clone of cells grows into a tumor. In some cases cells from the primary tumor migrate to new sites (metastasis), forming secondary tumors that often have the greatest health impact.

10 Ways To Fight Off Cancer

10 Ways To Fight Off Cancer

Learning About 10 Ways Fight Off Cancer Can Have Amazing Benefits For Your Life The Best Tips On How To Keep This Killer At Bay Discovering that you or a loved one has cancer can be utterly terrifying. All the same, once you comprehend the causes of cancer and learn how to reverse those causes, you or your loved one may have more than a fighting chance of beating out cancer.

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