Solving a 100-year-old genetic puzzle, researchers at the University of California, San Diego (UCSD) School of Medicine have determined// that the same genetic mechanism that drives tumor growth can also act as a tumor suppressor. Their findings could lead to new drug targets for cancer therapies.
In a study published in the January 1 issue of Cancer Cell, Don Cleveland, Ph.D., UCSD Professor of Medicine, Neurosciences and Cellular and Molecular Medicine and member of the Ludwig Institute for Cancer Research, looked at a common characteristic of cancer cells called aneuploidy. Aneuploidy – the occurrence of one or more extra or missing chromosomes – was first proposed as the cause of cancerous tumors nearly a century ago by German biologist Theodor Boveri, but his hypothesis had remained unproven.
“We questioned whether the wrong number of chromosomes contributed to tumor growth, or was a consequences of the accrued damage in cancerous cells,” said Cleveland.
To find out, researchers in the Cleveland lab created and analyzed mouse models with cells having a highly variable number of chromosomes to discover if such aneuploidy made the mice more tumor-prone.
“We found that, with age, having cells which inherited the wrong composition of chromosomes resulted in a larger number of spontaneous tumors,” said Cleveland. But the more unexpected feature of their findings was discovered when the research team added other genetic errors to mice with a high rate of aneuploidy – tumor development was slowed.
The UCSD researchers also studied mice that were missing a tumor suppressor gene, which is a gene that acts to prevent cell growth. If a mutation occurs in this gene, it makes the individual – or in this case, the mouse – more susceptible to the development of cancer in the tissue in which the mutation occurs.
“When we created mice missing a tumor suppressor gene that also had a high rate of aneuploidy, tumor development wPage: 1 2 Related medicine news :1
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