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癌症的誘因 > 研究發現癌症常由不到10個基因突變造成

研究發現癌症常由不到10個基因突變造成

21-10-2017

 

一項新研究19日説,平均而言,導致一種癌症發生的基因變異數量介于1到10個之間。

  這項發表在新一期美國《細胞》雜志上的研究説,對不同癌症類型,所需的致癌基因突變數量大不相同。比如,肝癌大約需要4個突變,而結腸直腸癌需要10個突變。

  “我們解答了自20世紀50年代以來癌症研究領域一個長期爭論的問題:一個正常細胞需要多少個(基因)突變變成癌細胞?”研究負責人、英國桑格研究所的彼得·坎貝爾在一份聲明中説,“我們的答案是:少數幾個就夠了。”

  研究人員採用分子進化相關方法,對29種癌症的7664個腫瘤樣本進行分析後得出上述結論。

  該研究還發現,這些關鍵性致癌突變幾乎有一半發生在尚未被確定與癌症相關的基因中,説明更多致癌基因仍有待被發現。

 

http://www.cancerresearchuk.org/about-us/cancer-news/

 

‘A handful’ of gene faults can turn a healthy cell cancerous

 

Fewer than 10 errors in the DNA inside cells are enough to drive development of a cancer, according to new estimates. 

Researchers at the Wellcome Trust Sanger Institute found that different types of cancer are triggered by a different number of genetic changes (mutations).

“The most surprising finding from this research was that most genetic faults didn’t harm the cell but rather accumulated over time.” – Dr Nicholas McGranahan, Cancer Research UK

Professor Sir Mike Stratton, director of the institute, said the research shows that a small number of mutated genes are responsible for converting a single normal cell into a cancer cell. The specific genes that are affected vary according to cancer type.

Cancers evolve in a similar way to species, with some genetic faults helping the cell survive, and some holding it back or causing it to die.

Dr Nicholas McGranahan, an expert in cancer evolution from the Cancer Research UK Lung Cancer Centre of Excellence at the UCL Cancer Institute, said that using ideas from species evolution can help scientists work out the genetic faults that cause a cancer to grow.

The researchers looked at the patterns of genetic changes of 7,664 tumours spanning 29 types of cancer. They found that on average tumours have around 4 genetic faults that drive them. 

The results are published in the journal Cell(link is external).

Testicular and thyroid cancers were among those that needed the fewest faults to develop (less than 1 on average), while melanoma, bowel and endometrial cancers needed the most (more than 10 on average).

“The most surprising finding from this research was that most genetic faults didn’t harm the cell but rather accumulated over time,” said McGranahan.

While it’s known that hundreds of genes can become faulty and fuel growing cancers, around half of the faults found in the study were in genes that haven’t yet been linked to cancer. 

Stratton said these genes will be the target of future studies. 

“This increasingly precise understanding of the underlying changes that result in cancer provides the foundation for the discovery and use of targeted therapies that treat the disease," he said. 

Dr Peter Campbell, who led the study, said they had addressed a long-standing question. In relation to how many mutations are needed for a normal cell to turn into a cancer cell, “the answer is a small handful”, he said. 

McGranahan added that the ways cancers evolve are complex, and this focuses on one part of the puzzle. 

“Other components such as how DNA is packaged into chromosomes are also key in how a tumour progresses and will need to be looked at to give us a clearer picture of how cancer evolves,” he said.

 

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