In:
eLife, eLife Sciences Publications, Ltd, Vol. 4 ( 2015-10-24)
Abstract:
Sarcoma is a type of cancer that forms in the connective tissues of the body, such as bone, cartilage, muscle and fat. Usually, treatment involves surgical removal of the tumor and/or radiation to kill the tumor cells. However, if sarcomas spread to other parts of the body, the treatment options are limited. Genetic studies have revealed several genetic changes that contribute to the formation of sarcomas. Many sarcomas have a mutation in a gene that encodes a protein called Ras. In 2011, researchers found that injecting Ras mutant muscle cells into the muscles of mice could lead to the formation of sarcomas. Next, the researchers compared gene expression in the mouse sarcoma cells with gene expression in normal mouse muscle cells and found that certain genes appeared to be more highly expressed in the sarcoma cells. These genes were also hyperactive in human sarcoma cells and may promote the growth of sarcomas carrying mutant forms of Ras. Now, Hettmer et al. – including some of the same researchers involved in the earlier work – show that targeting one of these hyperactive genes can slow sarcoma growth. The experiments made use of a technique called ribonucleic acid interference (or RNAi for short) to specifically switch off the expression of the hyperactive genes and then observed how this affected sarcoma growth. Hettmer et al. found that blocking the expression of one particular gene, which encodes an enzyme called asparagine synthetase, slowed down the growth of the sarcoma the most. Asparagine synthetase makes the amino acid asparagine, which is needed to make proteins in cells. Further experiments showed that reducing the amount of asparagine in human and mouse sarcoma cells slowed down the growth of these cells. A drug that lowers the amount of asparagine in cells is already used to treat some blood cancers. Hettmer et al.’s findings suggest that drugs that alter the availability of asparagine in the body might also be useful to treat sarcomas with mutant forms of Ras.
Type of Medium:
Online Resource
ISSN:
2050-084X
DOI:
10.7554/eLife.09436.001
DOI:
10.7554/eLife.09436.002
DOI:
10.7554/eLife.09436.003
DOI:
10.7554/eLife.09436.004
DOI:
10.7554/eLife.09436.005
DOI:
10.7554/eLife.09436.006
DOI:
10.7554/eLife.09436.007
DOI:
10.7554/eLife.09436.008
DOI:
10.7554/eLife.09436.009
DOI:
10.7554/eLife.09436.010
DOI:
10.7554/eLife.09436.011
DOI:
10.7554/eLife.09436.012
DOI:
10.7554/eLife.09436.013
DOI:
10.7554/eLife.09436.014
DOI:
10.7554/eLife.09436.015
DOI:
10.7554/eLife.09436.016
DOI:
10.7554/eLife.09436.017
DOI:
10.7554/eLife.09436.018
DOI:
10.7554/eLife.09436.019
DOI:
10.7554/eLife.09436.020
DOI:
10.7554/eLife.09436.021
DOI:
10.7554/eLife.09436.022
Language:
English
Publisher:
eLife Sciences Publications, Ltd
Publication Date:
2015
detail.hit.zdb_id:
2687154-3
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