Introduction to Cancer Genetics
published: Feb. 21, 2011, recorded: June 2006, views: 737
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During the human lifetime, there are 10 million billion cell divisions and each division represents, as Robert Weinberg puts it, “an opportunity for disaster, for chaos to occur.” The longer-lived the organism, the more likely it is that one cell eventually “will lose the ability to collaborate with its neighbors” in maintaining structure and function, and just start multiplying uncontrollably.
Weinberg and other researchers are delving at the molecular and genetic level to understand why and how this single cell begins to proliferate, leading over years and through different stages, to cancer. Weinberg offers a primer on the process of cancer formation, which he likens to Darwinian evolution but within the microcosm of human tissue.
Healthy organisms carry tumor suppressor genes, and proto-oncogenes. If these genes become corrupted somehow or prevented from functioning, the result may be cell proliferation. There are, unfortunately, lots of ways these genes become damaged: via a virus, or chromosomes changing places, or by chemical carcinogens, for instance. Weinberg describes how high rates of liver cancer in China were traced to a DNA-mutating mold found in damp rice, grain and fruit. Given the number of ways genetic alternations can come about, it’s a relief that as many as five changes are required to convert a normal human cell into a malignant one. “If single mutations sufficed, we would all be covered by tumors by age three. Our cells are wired to be highly resistant,” says Weinberg.
The latest cancer therapies attempt to capitalize on advancing knowledge of genetic and cellular networks. Weinberg points to two drugs that shut down growth stimulatory signals: Herceptin, which has proven very successful in a specific class of breast cancers, and Gleevec, for chronic myelogenous leukemia.
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