“암 예측” 더 이상 꿈이 아니다 ‘Death clock’ in cells could tell you when you’ll get cancer

‘Death clock’ in cells could tell you when you’ll get cancer

영국 생거(Sanger)연구소 소장 유전자학자 Michael Stratton

암환자 1만명 상대 체내 ＤＮＡ 순서 연구

source newscientist.com

edited by kcontents 

케이콘텐츠 편집

현재까지도 인간은 수명을 예측할수 없다.  그러나 “언제쯤 자신이 암에 걸릴 것”인지를 알게될 날이 멀지 않은듯 하다. 영국 생거(Sanger)연구소 소장인 유전자학자 Michael Stratton는 “네이처 유전학” 잡지에서 “우리 팀원들은 암환자 1만명을 상대로 그들 체내의 ＤＮＡ 순서를 연구함으로써 대표성을 지닌 유전자의 변이를 탐색하려 시도했다”고 서술했다. 스트라튼(Stratton)은 인체내 매개 세포마다 ＤＮＡ가 존재하고 ＤＮＡ는 변이를 발생한다고 지적했다. 대량의 햇빛에 노출되거나 혹은 장기적인 흡연으로 비롯된 일부 변이는 돌발성을 지녔으나 다른 일부 변이는 완만하고 안정된 상태로 진행되는데 이는 시간의 흐름과 더불어 손상된 ＤＮＡ를 하나둘씩 추이하다가 궁극적으로 암을 유발하게 된다. 스트라튼과 그의 팀원들은 두가지 전형적인 변이를 발견했는데 일반상황에서 사람은 나이가 들수록 이런 유전자의 변이가 더 많이 발생한다. 만약 개인에게 상술한 두개 변이의 속도가 일반인에 비해 빠르다면 그가 암에 걸릴 확율이 높다는 것을 뜻한다. 그들의 이와같은 발견은 의사들이 암을 “예측”하거나 환자를 위해 의료팀이 치료방안을 제시하는 등 과정에 도움을 줄 것이라 스프라튼이 피력했다. 언젠가 과학자들이 변이의 “속도”를 늦추는 방식으로 사람들에게 영구불멸의 청춘을 선사할 그날이 올지도 모른다. [글/ 신화사 기자 징징(荊晶), 번역/ 신화망 한국어판] [신화사 베이징 11월 16일]

Tick-tock, tick-tock. How fast we age and whether we get cancer may be predetermined by two “clocks” discovered in almost every cell in the human body.

Each tick of these clocks is a DNA mutation, and these build up at a constant rate throughout your life. The discovery will give us a deeper understanding of the causes of cancer, and an insight into healthy ageing. But here’s the twist: if you could slow the rate at which these clocks tick, it might be possible to alter the rate of cancer – and even the rate at which we age.

Every cell in the body contains DNA, which acquires mutations – changes in individual genes – over time. Some of these mutations occur in bursts, say, from smoking or too much sun exposure. Others build up slowly over decades.

Some mutations seem to build up at a constant rate year by year, causing DNA damage, which can lead to cancer. Now, Michael Stratton at the Wellcome Trust Sanger Institute in Cambridge, UK, and his colleagues have identified two such mutational clocks in almost every cell in the body. They have also figured out how fast these clocks tick in different tissues.

They started by studying the DNA sequences of more than 10,000 individual cancers, encompassing 36 different types of cancer. An algorithm allowed them to search the cancer genomes for complex patterns of mutations – what they call signatures.

The team discovered more than 30 different signatures. Next, they looked at which of these occur in a clock-like manner, with the mutations appearing at a steady rate that correlates with the age of the person who provided the sample. Two signatures – numbers one and five – fitted the bill. This also means they would have begun in healthy tissue before it became cancerous. “The cancer tissues are the cracked and dirty lens that allow us to look back in time to look at what’s been happening in normal cells,” says Stratton.

Faulty replicator

Stratton’s team believes signature one is a “mitotic clock”, a mutation that occurs as a result of cell division. “The rate of mutations correlate with the rate of cell turnover in tissues,” he says. “So in future we’ll be able to use the number of mutations from this signature to know how many times a cell has divided – giving us a deep insight into the biology of human tissues.”

Far less is known about signature five. Preliminary hypotheses suggest it may be linked to DNA repair. Over time, as DNA gets damaged it has to be patched up, which involves replicating small sections. “The machinery that replicates DNA occasionally makes mistakes and signature five might be the outcome of that,” says Stratton.

For both signatures, the number of mutations correlated with the age of the person the sample came from. This allowed the team to figure out how fast the clocks were ticking in each tissue. For instance, signature one ticked quickest in stomach and colon cells – which resulted in about 23 mutations, per cell, per year, and slowest in breast and ovarian cells, which had three to four mutations per year.

Counting down

Because the clocks continue to tick once a healthy cell becomes cancerous, they could be used to tell how fast a cancer may metastasise and spread around the body, or become resistant to a drug, meaning doctors could plan the best course of action for a patient. They might even be used to predict cancer before it starts.

“It’s not an inevitability for an individual to get cancer, but it’s an inevitability for us as a species,” says Stratton. “We accumulate mutations over a lifetime and in some people the correct combination leads to a cancer emerging. Further research will discover if our mutation rates differ between individuals. If that is the case, the expectation would be that those rates could be read out to predict the time they might take to become cancerous.”

Stratton adds that in theory if you could alter the rate at which the mutations are occurring you might be able to change the rate at which cancer occurs. “I’m not saying this as a definite possibility – these mutations are so deeply embedded in our biology – but nevertheless this discovery inevitably leads you onto that kind of thinking. Every time we find something that causes cancer we think about how we can reduce it.”

Is it possible then that human ageing could also be predetermined by one or both of these clock processes? The answer depends on the extent to which ageing is determined by the accumulation of mutations in individual cells, says Stratton. “If so, then certainly these two processes could contribute to ageing and their presence at a constant rate could predetermine the rate of ageing.”

Darryl Shibata, at the USC Norris Comprehensive Cancer Centre and Hospital in Los Angeles, California, says that the team’s work is important because there is high interest in discovering which mutations best represent age-related processes. “Ageing is fundamental to health and many diseases,” he says. “This is a fantastic paper.”

https://www.newscientist.com/article/dn28466-death-clock-in-cells-could-tell-you-when-youll-get-cancer/

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