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Previously held beliefs about the role of genetic mutations incolon cancer development challenged by ferujkll sdff
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Previously held beliefs about the role of genetic mutations incolon cancer development challenged by FERUJKLL SDFF
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| Article Posted: 08/23/2012 |
| Article Views: 79 |
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Previously held beliefs about the role of genetic mutations incolon cancer development challenged |
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For the first time, researchers have found that the number of newmutations are significantly lower in cancers than in normal cells. "This is completely opposite of what we see in nuclear DNA,which has an increased overall mutation burden in cancer,"said cancer geneticist Jason Bielas, Ph.D., whose findings arepublished in the June 7 issue of PLoS Genetics . Mutations are changes in the genetic sequence of a cell's genomeand can occur as a result of environmental exposure to viruses,radiation and certain chemicals, or due to spontaneous errorsduring cell division or DNA replication. Mitochondria, which are primarily responsible for the cell's energyproduction, are semi-autonomous; similar to the nucleus, they havetheir own set of DNA, which encodes genes critical for thefunctioning of the cell. While the role of genomic instability hasbeen well characterized in nuclear DNA, this is the first attemptto determine whether instability in mitochondrial DNA may play asimilar role in cancer growth and metastasis.
"We were surprised to find that the frequency of new mutationsin mitochondrial DNA from tumor cells is decreased compared to thatof normal cells," said Bielas, an assistant member of thePublic Health Sciences and Human Biology divisions at theHutchinson Center. "By extension, this suggests, somewhatcounterintuitively, that higher mitcochondrial mutation rates mayactually serve as a barrier to cancer development, and drugs thatfocus directly on increasing mitochondrial DNA damage and mutationmight swap cancer's immortality for accelerated aging andtumor-cell death." For the study, the researchers used using an ultra-sensitive testto detect mutations in mitochondrial DNA from normal and cancerouscolon tissue resected from 20 patients prior to chemotherapy. Bielas and colleagues first set out to analyze mutation rates inmitochondrial DNA because they wanted to see if it could act as asurrogate for nuclear DNA as a cancer biomarker. "Cellscontain a thousandfold more mitochondrial genetic material thannuclear DNA, so theoretically you'd need a thousand times lesstissue to get the same genetic information to predict clinicaloutcomes such as how fast a tumor would progress or whether itwould be resistant to therapy," Bielas said.
While mitochondrial DNA proved to be an unreliable stand-in fornuclear DNA as a cancer biomarker, it offers promise as a new drugtarget. "If we could increase DNA damage and mutation within themitochondrial genome, theoretically we could decrease cancer,"Bielas said. "That's what we're testing now. This is a wholenew hypothesis." The way mitochondria maintain genetic stability in the face ofcancer, Bielas suggests, may be because unlike normal cells, cancercells do not need oxygen to survive.
In fact, cancer cells decreasethe process by which they get energy from the mitochondria and relyinstead on a process called glycolysis, which is a form of energyproduction in the absence of oxygen. "We believe less damageoccurs to mitochondrial DNA of cancer cells because they no longerneed oxygen," he said. "If we could program a cancer cellto once again need oxygen, we expect it would die -- with minimalside effects." Bielas and colleagues are now testing this theory in thelaboratory, seeing whether cancer cells that are reprogrammed toutilize oxygen and/or are targeted for mitochondrial DNA damagerespond better to certain therapeutic agents. "This finding is a game-changer because it challenges previousnotions about the role of mutations in cancer development,"said Bielas, who is also an affiliate assistant professor ofpathology at the University of Washington, where theultra-sensitive mutation-detection technology, called RandomMutation Capture, was developed.
The test is so sensitive that itcan detect the mutational equivalent of one misprinted letter in alibrary of a thousand 1,000-page books. "This work started with the idea that there would be a hugemutation burden in the mitochondrial DNA, but our findings werecompletely opposite of what we had expected. Hopefully ourdiscovery will open up new avenues for treatment, early detectionand monitoring treatment response of colon cancer and othermalignancies," he said. The National Institute of Environmental Health Sciences, theEllison Medical Foundation and Fred Hutchinson Cancer ResearchCenter funded this research. Collaborators included researchers atthe University of Washington, the University of North Carolina, andSt.
Vincent's University Hospital in Dublin, Ireland. I am a professional writer from Gifts & Crafts, which contains a great deal of information about babys first christmas , e27 led bulb, welcome to visit!
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