The Cell Cycle and Cancer

author: Angelika Amon, Koch Institute, Massachusetts Institute of Technology, MIT
published: Feb. 21, 2011,   recorded: June 2006,   views: 329
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Description

We all start out as a single fertilized cell, and wind up, as fully formed humans, with 10 to the 13th cells. “The name of the game,” says Angelika Amon, is to replicate the genetic information in those cells accurately. “Only if that happens all the time and with high fidelity will you end up with a healthy individual.”

Amon shows a beautiful video of dance-like cell division in the African blood lily, which demonstrates the migration of chromosomes to opposite ends of the cell -- prelude to a single cell becoming two daughter cells. It’s “like a curtain opening,” Amon says in wonder. This process of cell division, she continues, is “highly conserved” among organisms. For instance, if a yeast cell contains a defect that prevents it from dividing correctly, plugging in the human equivalent of a protein to correct the defect will enable the yeast to begin dividing again.

Amon describes how cells contain special proteins called growth factors that work together to inhibit or initiate cell division. “The cell puts in place layers and layers of controls, like an onion,” says Amon. If someone inherits a mutation that affects one of these growth factors, then cells may proliferate uncontrollably. Another route to cancer is if a cell’s internal mechanisms for detecting DNA damage malfunctions, perhaps due to exposure to X-rays or UV rays. When these checkpoints break down, instead of putting the brakes on cell division, the cell will proceed unchecked through division with broken chromosomes, or extra chromosomes. Pieces of DNA lie around, information gets lost or amplified and “a mess ensues.”

Researchers have identified several key chromosomes in which defects lead to malfunctioning growth factors or checkpoints. And they’ve begun to design new drugs that target the specific proteins involved in these errant cell growth pathways.

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