【medical-news】【资讯翻译】白血病相关的数百个随机突变是由年龄而非肿瘤引起的
发布于 2012-07-20 · 浏览 1851 · IP 山东山东
这个帖子发布于 12 年零 289 天前，其中的信息可能已发生改变或有所发展。
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Hundreds of Random Mutations in Leukemia Linked to Aging, Not Cancer
http://www.sciencedaily.com/releases/2012/07/120719132606.htm
ScienceDaily (July 19, 2012) — Hundreds of mutations exist in leukemia cells at the time of diagnosis, but nearly all occur randomly as a part of normal aging and are not related to cancer, new research shows.
Scientists at Washington University School of Medicine in St. Louis have found that even in healthy people, stem cells in the blood routinely accumulate new mutations over the course of a person's lifetime. And their research shows that in many cases only two or three additional genetic changes are required to transform a normal blood cell already dotted with mutations into acute myeloid leukemia (AML).
The research is published July 20 in the journal Cell.
"Now we have a very accurate picture of how acute leukemia develops," says senior author Richard K. Wilson, PhD, director of The Genome Institute at Washington University. "It's not hundreds of mutations that are important but only a few in each patient that push a normal cell to become a cancer cell. Finding these mutations will be important for identifying targeted therapies that can knock down a patient's cancer."
The study is the first to investigate how often mutations typically develop in healthy stem cells in the blood. These immature cells in the bone marrow give rise to all the blood cells in the body.
AML is a blood cancer that develops when too many immature blood cells crowd out the healthy cells. In recent years, Washington University researchers at the Siteman Cancer Center at Barnes-Jewish Hospital and Washington University School of Medicine have sequenced the genomes of 200 patients with AML to try to understand the mutations at the root of the disease.
Without fail, each patient's leukemia cells held hundreds of mutations, posing a conundrum for scientists, who have long believed that all the mutations in a cancer cell are likely to be important for the disease to progress.
"But we knew all of these mutations couldn't be important," says co-first author Daniel Link, MD, professor of medicine. "It didn't make any sense to us that so many mutations were present in all the cells in the tumor."
To investigate the origin of these mutations, the researchers isolated blood stem cells from healthy people of different ages. The youngest were newborns, and the oldest was in his 70s.
Every person has about 10,000 blood stem cells in their bone marrow, and the researchers found that each stem cell acquires about 10 mutations over the course of a year. By age 50, a person has accumulated nearly 500 mutations in every blood stem cell.
"Mutations are known to develop in cells as we age, but no one had any idea how many mutations occur in blood stem cells and how frequently they develop," Link says. "These random, background mutations occur during cell division and are unrelated to cancer. Our DNA can tolerate a huge number of these hits without any negative consequences. But if a cancer-initiating event occurs in one of these stem cells, it captures the genetic history of that cell, including the earlier mutations, and drives leukemia to develop."
As part of the study, the researchers sequenced the genomes of 24 patients with AML and compared the mutations in their leukemia cells to those that occurred in the blood stem cells of the healthy individuals. The scientists were surprised to see that the total number of mutations varied by age, not by whether a patient had leukemia. Thus, a healthy person in his 40s had just about the same number of mutations in his blood stem cells as a leukemia patient of the same age had in his cancer cells.
The study's results help to explain why leukemia occurs more frequently as people age.
"AML is relatively uncommon until about age 60," says co-first author John Welch, MD, PhD, assistant professor of medicine. "It is the persistent, random accumulation of mutations in blood stem cells that contributes to the risk of the disease."
By sequencing the genomes of the AML patients, the researchers also were able to identify 13 novel "driver" mutations that are likely to be important for leukemia to develop in other patients. They also identified a number of additional cooperating mutations that work together with the driver mutations to give blood stem cells a growth advantage over other cells. In many patients, it appeared that in addition to an initiating driver mutation, only a one or two additional cooperating mutations were important for cancer to occur.
While the findings are important to leukemia, they may also hold true for other cancers.
"Our study does not provide proof that this model applies to other cancers," says corresponding author Timothy Ley, MD, professor of medicine and of genetics. "But this research suggests that scientists should look. This model could explain the large numbers of mutations we and other researchers are finding in breast, lung and other cancers. The idea that the vast majority of mutations occur in a cell before it becomes cancer is completely novel and should be explored further."
请根据自己专业背景选择认领，如使用翻译软件翻译，被发现者扣分1-2分
请根据自己的专业背景选择相应的资讯认领，经常认领而不能及时提供优质稿件者将被列入黑名单，取消认领资格，请大家注意！
新近参与本次活动的会员请查看：【公告】动态版重启资讯翻译计划：我为人人，人人为我，共同提高
寻找最近的翻译贴请查看：http://search.dxy.cn/?words=%E8%B5%84%E8%AE%AF%E7%BF%BB%E8%AF%91&bid=116&t=1&c=1&age=7&bid=116&limit=30&o=1
翻译时请参照版规 【版务】科技动态版版规及加分细则（ 2014-02-21 更新）
希望参与动态版其他活动的会员请查看版面右边栏的置顶部分。
Hundreds of Random Mutations in Leukemia Linked to Aging, Not Cancer
http://www.sciencedaily.com/releases/2012/07/120719132606.htm
ScienceDaily (July 19, 2012) — Hundreds of mutations exist in leukemia cells at the time of diagnosis, but nearly all occur randomly as a part of normal aging and are not related to cancer, new research shows.
Scientists at Washington University School of Medicine in St. Louis have found that even in healthy people, stem cells in the blood routinely accumulate new mutations over the course of a person's lifetime. And their research shows that in many cases only two or three additional genetic changes are required to transform a normal blood cell already dotted with mutations into acute myeloid leukemia (AML).
The research is published July 20 in the journal Cell.
"Now we have a very accurate picture of how acute leukemia develops," says senior author Richard K. Wilson, PhD, director of The Genome Institute at Washington University. "It's not hundreds of mutations that are important but only a few in each patient that push a normal cell to become a cancer cell. Finding these mutations will be important for identifying targeted therapies that can knock down a patient's cancer."
The study is the first to investigate how often mutations typically develop in healthy stem cells in the blood. These immature cells in the bone marrow give rise to all the blood cells in the body.
AML is a blood cancer that develops when too many immature blood cells crowd out the healthy cells. In recent years, Washington University researchers at the Siteman Cancer Center at Barnes-Jewish Hospital and Washington University School of Medicine have sequenced the genomes of 200 patients with AML to try to understand the mutations at the root of the disease.
Without fail, each patient's leukemia cells held hundreds of mutations, posing a conundrum for scientists, who have long believed that all the mutations in a cancer cell are likely to be important for the disease to progress.
"But we knew all of these mutations couldn't be important," says co-first author Daniel Link, MD, professor of medicine. "It didn't make any sense to us that so many mutations were present in all the cells in the tumor."
To investigate the origin of these mutations, the researchers isolated blood stem cells from healthy people of different ages. The youngest were newborns, and the oldest was in his 70s.
Every person has about 10,000 blood stem cells in their bone marrow, and the researchers found that each stem cell acquires about 10 mutations over the course of a year. By age 50, a person has accumulated nearly 500 mutations in every blood stem cell.
"Mutations are known to develop in cells as we age, but no one had any idea how many mutations occur in blood stem cells and how frequently they develop," Link says. "These random, background mutations occur during cell division and are unrelated to cancer. Our DNA can tolerate a huge number of these hits without any negative consequences. But if a cancer-initiating event occurs in one of these stem cells, it captures the genetic history of that cell, including the earlier mutations, and drives leukemia to develop."
As part of the study, the researchers sequenced the genomes of 24 patients with AML and compared the mutations in their leukemia cells to those that occurred in the blood stem cells of the healthy individuals. The scientists were surprised to see that the total number of mutations varied by age, not by whether a patient had leukemia. Thus, a healthy person in his 40s had just about the same number of mutations in his blood stem cells as a leukemia patient of the same age had in his cancer cells.
The study's results help to explain why leukemia occurs more frequently as people age.
"AML is relatively uncommon until about age 60," says co-first author John Welch, MD, PhD, assistant professor of medicine. "It is the persistent, random accumulation of mutations in blood stem cells that contributes to the risk of the disease."
By sequencing the genomes of the AML patients, the researchers also were able to identify 13 novel "driver" mutations that are likely to be important for leukemia to develop in other patients. They also identified a number of additional cooperating mutations that work together with the driver mutations to give blood stem cells a growth advantage over other cells. In many patients, it appeared that in addition to an initiating driver mutation, only a one or two additional cooperating mutations were important for cancer to occur.
While the findings are important to leukemia, they may also hold true for other cancers.
"Our study does not provide proof that this model applies to other cancers," says corresponding author Timothy Ley, MD, professor of medicine and of genetics. "But this research suggests that scientists should look. This model could explain the large numbers of mutations we and other researchers are finding in breast, lung and other cancers. The idea that the vast majority of mutations occur in a cell before it becomes cancer is completely novel and should be explored further."
最后编辑于 2022-10-09 · 浏览 1851
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