Cancer, a genetic disease, is known to affect more and more individuals as life spans increase. It is estimated that nearly one in three people will have neoplastic disease in his or her lifetime. However, the good news is that two out of three people remain unaffected. Even most heavy smokers, whose lungs are bombarded with carcinogens and tumor promoters over the years, are cancer free.
It has been proven that much of all men age 60 or older have microscopic prostate cancer when examined at autopsy. The majority of these microtumors never develop into cancer, though. Disseminated cancer cells are present throughout the body in most cancer patients, but only a small minority of these cells develop into secondary tumors as the rest is kept under control by the body.
Immune surveillance has played a major role in the defence against virus-associated tumors, where the virally encoded transforming proteins provide readily recognizable foreign targets. But nonviral tumors, composed of aberrant host cells, do not provide such targets, and the immune response is suppressed by defences against autoimmune reactions. Rather, it is now known that the main safeguards against cancer are not immunological at all.
Abnormal cell division is an indication of tumor cells as the mutated genes responsible for this proliferation are called cancer genes or oncogenes. Their normal function is not to cause cancer but to participate in the regulation of normal cell division. Meanwhile, also known as tumor suppressor, genes perceive the illegitimate activation of proliferation-driving genes and slow down.
There seem to be diverse mechanisms which protect against cancer. In addition to driving the proliferation of cancer cells, mutations or epigenetic changes may influence the ability of the cells to invade bordering tissues, giving rise to systemic metastasis, or resisting treatment. Notably, metastasis-favoring mutations may occur at a very early stage of tumor development, long before there are sufficient numbers of tumor cells to allow the manifestation of this property.
In the 1970s, American biologist Beatrice Mintz, discovered a defense against cancer while working with a highly malignant line of teratoma cells. Mintz found that adult mice subcutaneously inoculated with the cells all succumbed to teratomas. When the teratoma cells were introduced into very early embryos, however, no malignancies developed. The introduced cells simply became part of the organism, participating in the normal development of the mouse and contributing to many tissues of the embryo. This normalization of embryonic tumor cells in the early developmental environment is the most extreme example of the differentiation of malignant into normal cells. There are many other less spectacular examples in the later literature.
In sum, evolution has provided us and other animals with multiple mechanisms that stop normal cells from escaping into uncontrolled division. If they nevertheless escape, the cell mobilizes multiple mechanisms to stop the outlaw cell and preserve the normal organization of tissues. These mechanisms can stop life-threatening malignant growths early on. Only after the normal tissue neighborhood has been corrupted by the tumor cells so that it no longer inhibits, but rather stimulates, malignant growth can sail on uninhibited.
Adapted from: .
All of the words below are adverbs, except for:
