The spread of cancer cells to distant sites implies a complex series of cellular abnormalities caused, in part, by genetic aberrations
Nothing has galvanized the biomedical research community as much as the study of cancer and how it spreads. And well it should. As it turns out, the events that allow a cell to become cancerous and then to metastasize alter just about every part of the cell—from its genes to its very skeletal structure. Mutated genes give rise to the aberrant growth patterns that characterize carcinogenesis. Later on, the genetically disorganized cancer cell breaks free of the molecular bonds that tether it to its host organ and eats through surrounding tissue to make its way to a blood vessel—its conduit to a new tissue. The previously sedentary cancer cell now becomes mobile, a feat that requires its underlying protein skeleton to become reconfigured for movement. The authors take us through these molecular steps and describe new anticancer therapies designed to interfere with these alterations.
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