Category Archives: DNA

March 29, 2017 Credit: CC0 Public Domain

Researchers from King's College London have used a genetic scoring technique to predict reading performance throughout school years from DNA alone.

The study, published today in Scientific Studies of Reading, shows that a genetic score comprising around 20,000 of DNA variants explains five per cent of the differences between children's reading performance. Students with the highest and lowest genetic scores differed by a whole two years in their reading performance.

These findings highlight the potential of using genetic scores to predict strengths and weaknesses in children's learning abilities. According to the study authors, these scores could one day be used to identify and tackle reading difficulties early, rather than waiting until children develop these problems at school.

The researchers calculated genetic scores (also called polygenic scores*) for educational achievement in 5,825 individuals from the Twins Early Development Study (TEDS) based on genetic variants identified to be important for educational attainment. They then mapped these scores against reading ability between the ages of seven and 14.

Genetic scores were found to explain up to five per cent of the differences between children in their reading ability. This association remained significant even after accounting for cognitive ability and family socio-economic status.

The study authors note that although five per cent may seem a relatively small amount, this is substantial compared to other results related to reading. For example, gender differences have been found to explain less than one per cent of the differences between children in reading ability.

Saskia Selzam, first author of the study from the Institute of Psychiatry, Psychology & Neuroscience (IoPPN) at King's College London, said: 'The value of polygenic scores is that they make it possible to predict genetic risk and resilience at the level of the individual. This is different to twin studies, which tell us about the overall genetic influence within a large population of people.'

'We think this study provides an important starting point for exploring genetic differences in reading ability, using polygenic scoring. For instance, these scores could enable research on resilience to developing reading difficulties and how children respond individually to different interventions.'

Professor Robert Plomin, senior author from the IoPPN at King's College London, said: 'We hope these findings will contribute to better policy decisions that recognise and respect genetically driven differences between children in their reading ability.'

*Calculating an individual's polygenic score requires information from a genome-wide association study (GWAS) that finds specific genetic variants linked to particular traits, in this case educational attainment. Some of these genetic variants, known as single nucleotide polymorphisms (SNPs), are more strongly associated with the trait, and some are less strongly associated. In a polygenic score, the effects of these SNPs are weighed by the strength of association and then summed to a score, so that people with many SNPs related to academic achievement will have a higher polygenic score and higher academic achievement, whereas people with fewer associated SNPs will have a lower score and lower levels of academic achievement.

Explore further: Scientists herald 'tipping point' in ability to predict academic achievement from DNA

More information: Saskia Selzam et al, Genome-Wide Polygenic Scores Predict Reading Performance Throughout the School Years, Scientific Studies of Reading (2017). DOI: 10.1080/10888438.2017.1299152

Scientists from King's College London have used a new genetic scoring technique to predict academic achievement from DNA alone. This is the strongest prediction from DNA of a behavioural measure to date.

An international team of scientists, led by researchers at University of California San Diego School of Medicine and University of California San Francisco, has developed a novel genetic score that allows individuals to calculate ...

Psychological characteristics link genes with upward social mobility, according to data collected from almost 1000 individuals over four decades. The data suggest that various psychological factors play a role in linking ...

A study co-led by the University of East Anglia (UEA) has found that people with genes for high educational achievement tend to marry, and have children with, people with similar DNA.

Reading achievement at age 10 influences how much independent reading children do at age 11. However, independent reading doesn't directly improve children's achievement in reading, at least among children at the end of elementary ...

A first-of-its-kind, nationally representative study of siblings supports previously published research on unrelated individuals that links specific genotypes to educational attainment among adults in their mid-20s to early ...

Researchers from King's College London have used a genetic scoring technique to predict reading performance throughout school years from DNA alone.

The Liberty Mutual commercial mentions naming your car Brad and considering him part of your family.

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The reality that will emerge is that it will move to the lowest common denominator aspect, which is identifying and labeling types of people.

Brave new world people. alpha, beta, ceta, delta.... and then gamma.

Fully realized and idealized people sorting.

Human genetic separation into groups of desirables vs baskets of deplorables...

Humans and their rather pronounced unconscious aspects...becoming fully enabled in genetic selection... could easily fall into being a total disaster for forms of continuance in evolution.

And the enabled Alpha aspects will have little to no form of any reasonable impetus to alter that coming path which they create and enable.

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Scientists predict reading ability from DNA alone - Phys.Org

Cortisol excess hits natural DNA process and mental health hard ... Science Daily High concentrations of the stress hormone cortisol in the body affect important DNA processes and increase the risk of long-term psychological consequences. and more »

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Cortisol excess hits natural DNA process and mental health hard ... - Science Daily

March 29, 2017 How can long DNA filaments, which have convoluted and highly knotted structure, manage to pass through the tiny pores of various biological systems? This is the fascinating question addressed by Antonio Suma and Cristian Micheletti, researchers at the International School for Advanced Studies (SISSA) in Trieste who used computer simulations to investigate the options available to the genetic material in such situations. The study has just been published in PNAS, the journal of the National Academy of Sciences of the Unites States. Credit: Antonio Suma, SISSA

Anyone who has been on a sail boat knows that tying a knot is the best way to secure a rope to a hook and prevent slippage. Similarly, knots in sewing threads prevent them slipping through two pieces of fabric. How, then, can long DNA filaments, which have convoluted and highly knotted structure, manage to pass through the tiny pores of various biological systems? This is the fascinating question addressed by Antonio Suma and Cristian Micheletti, researchers at the International School for Advanced Studies (SISSA) in Trieste, who used computer simulations to investigate the dynamics of the molecule in such situations. The study has just been published in PNAS, the journal of the National Academy of Sciences of the Unites States.

"Our computational study sheds light on the latest experimental breakthroughs on knotted DNA manipulation, and adds interesting and unexpected elements," explains Micheletti. "We first observed how knotted DNA filaments pass through minuscule pores with a diameter of about 10 nanometers (10 billionths of a meter). The behaviour observed in our simulations was in good agreement with the experimental measurements obtained by an international research team led by Cees Dekker, which were published only a few months ago in Nature Biotechnology. These advanced and sophisticated experiments marked a turning point for understanding DNA knotting. However, current experiments cannot detect how DNA knots actually pass through the narrow pore.

"In fact, the phenomenon occurs over a tiny spatial scale that is inaccessible to microscopes. This is why our group resorted to what the great German biophysicist Klaus Schulten called 'the computational microscope,' that is, computer simulations."

Suma and Micheletti explain: "The simulations revealed that the passage of the knot can occur in two distinct ways: One where the knot is tight, and the other where the knot is more delocalised. In both cases, the knot not only passes through the pore, but it does so in a very brief time."

Moreover, the knot usually passes in the final stages of the translocation, when most of the DNA strand has already passed. "But there is something more that is counterintuitive," state the authors. "The size of the knot, whether small or large, does not seem to affect the pore obstruction time by much. The latter depends instead on the translocation speed, which, in turn, depends on the initial position of the knot along the filament." These results, say the researchers, ought to help the design of future experiments probing the spontaneous knotting of DNA, a still largely unexplored venue, especially regarding the size of DNA knots.

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Advancing our current understanding of knots in biological molecules is important to clarify their implications in biological contexts as well as in applicative ones, such as DNA sequencing using nanopores. Suma and Micheletti hope that the promising directions suggested by their study can lead to a more detailed and accurate profiling of entanglement in DNA, RNA and proteins.

Explore further: New study shows that proteins are 'virtually' knotted

More information: Antonio Suma et al. Pore translocation of knotted DNA rings, Proceedings of the National Academy of Sciences (2017). DOI: 10.1073/pnas.1701321114

Journal reference: Proceedings of the National Academy of Sciences Nature Biotechnology

Provided by: Scuola Internazionale Superiore di Studi Avanzati

Many of the processes essential to life involve proteins - long molecules which 'fold' into three-dimensional shapes allowing them to perform their biological role.

DNA has the nasty habit of getting tangled and forming knots. Scientists study these knots to understand their function and learn how to disentangle them (e.g. useful for gene sequencing techniques). Cristian Micheletti, ...

Nanotechnologies require a detailed knowledge of the molecular state. For instance, it is useful to know when and how a generic polymer, a long chain of polymers (chain of beads), knots. The study of molecular entanglement ...

A simple and effective way of unravelling the often tangled mass of DNA is to 'thread' the strand into a nano-channel. A study carried out with the participation of the International School for Advanced Studies in Trieste ...

As sailors and mountaineers know very well, every knot carries out a specific function. There's a knot that slides, one that "floats", and one that comes undone with a single pull. In the field of nanotechnology as well, ...

Scientists at The University of Manchester have produced the most tightly knotted physical structure ever known - a scientific achievement which has the potential to create a new generation of advanced materials.

(Phys.org)Researchers from the University of Sheffield report a new continuous-breathing metal-organic framework (MOF), SHF-61, that has two different solvent-specific forms, a narrow-pore structure that is the result ...

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New study investigates the passage of knotted DNA through nanopores - Phys.Org

NBCBLK's Amber Payne and Rachel Dolezal John Makely / NBC News

These days, the former Spokane NAACP president unapologetically identifies as trans-Black but distinguishes between that term and transracial.

"Transracial it almost sounds like I'm neutral, and I'm not neutral on political and social issues," Dolezal told NBCBLK while on a press tour for her new memoir, "In Full Color: Finding My Place in a Black And White World."

She added: "If I was allowed a more complex term, I would say I'm pan-African, pro-Black, bisexual, mother, activist, artist, you know that's like too long. So trans-Black is quicker."

Related:

When

I heard from high school pals I hadn't talked to in years. Thousands of miles away, my expat friends in Japan and Berlin wanted to discuss. People of different ages, races, ethnicities, and sexual orientations filled my timeline. Even my mom weighed in.

While some of these eight questions are on the serious side, others more irreverent, all prove that the controversy around Dolezal's identity is also nothing short of fascinating.

I wrote the book to really to encourage and advance the conversation on race and yes to set the record straight about my whole life story. And also to encourage people to be exactly who they really are. And the essential essence of who I am is best defined in culture and in race terms as "Black."

Well I think that in America, even though race is a social construct, I mean, we say this in theory, but I think a lot of people don't believe that it really is. And so it's still a very racialized society. And so there's a line drawn in the sand. And there's a Black and white divide and I stand unapologetically on the Black side of that divide with my own internal sense of self and my values, and with my sons and my sister and with the greater cause of really undoing the myth of white supremacy.

It was actually given to me. Unfortunately, the press said I chose it randomly, which I didn't. And at the end of the book, I discuss that an Igbo man reached out to me and really just said that, "We see you. My tribe sees you for who you are, and you have this high frequency in your soul and you're incarnated into this white envelope. And you were brought here as a gift from the gods to challenge white supremacy spiritually."

That was in January 2016, and I fully embraced the name as my legal name in October, so a few months later.

Yea, I don't know about surprising. I guess have been a little bit surprised just at the polarization because it seems like it's either love or hate, as opposed to just like, OK, just cool be who you are whatever. It's not a big deal. Let's just work together and strive for common goals of freedom, justice, and equity. I mean that was kind of to some extent maybe more of what I anticipated.

Well, I wish that I could have had the chance to tell my whole story and introduce myself to the world instead of being introduced by others in a very negative connotation. So the oppositional people really came out with this narrative of a fraud, a liar and a con and all this kinda stuff before I had a chance to say, "Hello, my name is Rachel and this is who I am."

So I think it just kinda steamrolled and got so much momentum of negativity where my life just got shaped by that, and people's perceptions of me were shaped by that. And I knew very quickly that I wasn't going to be able to really describe my experience in full context in an interview and so I really needed to do that in book form.

I think that it is too common for white feminists to say, "We want some diversity, come join our movement about gender, but we want you to check the class and race at the door." And you can't undo that braid of race, class and gender, all three intersect with each other, so it's important for more education to be done about that. We talk about feminism, but I think even in the male world, that Donald Trump is white, rich, and male, like all those three are working together for his opportunities in his life.

Well, I think that it's important as a mother to support who our children are, and you kind of notice that as they grow and develop, whether it's gender or sexual orientation, culture, the music that they want to listen to, the food that they like, so I'll just be constantly encouraging him [her one-year-old] and guiding him toward what resonates with him. And he's one, so right now, what resonates with him are toys and gadgets and buttons.

Well, what I found was kind of like, there's 10% African ancestry, 35% Iberian peninsula and all these things, and then when I asked the testing facility I'm not gonna reveal who I did the test with but they basically said, oh I asked them to make a certified record and they said, those weren't your real results, you're actually 100% European.

I mean, It was under Rachel Dolezal, as my name when I did that test. And I was asking them to certify the results cause I was gonna include it in the book. And really what it made me do is, I just kind of felt like, you know what, this is just b*******. I don't need a lab to tell me who I am, and if their results are that wishy washy anyway? I mean, we know that race is not biological and we teach this all the time in sociology courses so I just didn't get another one done.

1. As a fellow Black woman can you explain the difference between performative blackface and the experience of being Black?

2. What is your take on

3. Do you have any black friends? If so, are they still down?

4. Is it because you are a white woman that you feel entitled to everything including other people's cultures and experiences?

5. Can I touch your hair?

6. Tupac or Biggie? Prince or Michael Jackson?

7. Have you ever been called the N-word or been eyed as a shoplifter or denied service or strip-searched by a cop or otherwise gotten the "Black experience"?

8. WWWWWWWHHHHHHHHHHHYYYYYYYYYYYYYY?

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Rachel Dolezal on Rihanna, Her DNA Test, 'Fraud' Claims and Other Facebook Questions - NBCNews.com

LAURAN NEERGAARD

Last updated15:22, March 27 2017

Scientists in the US have published research showing that two-thirds of cancers are caused by DNA replication errors.

Cancer patients often wonder, "why me?'' Does their tumour run in the family? Did they try hard enough to avoid risks like smoking, too much sun or a bad diet?

Lifestyle and heredity get the most blame but new research suggests random chance plays a bigger role than people realise: Healthy cells naturally make mistakes when they multiply, unavoidable typos in DNA that can leave new cells carrying cancer-prone genetic mutations.

How big? About two-thirds of the mutations that occur in various forms of cancer are due to those random copying errors, researchers at Johns Hopkins University reported on Thursday in the journal Science.

Whoa: That doesn't mean most cases of cancer are due solely to "bad luck".It takes multiple mutations to turn cells into tumours -and a lot of cancer is preventable, the Hopkins team stressed, if people take proven protective steps.

READ MORE: *Why are we more likely to get cancer as we age? *Blood test picks up cancer before symptoms start to show *Why most cancer isn't due to 'bad luck'

Thereport is an estimate, based on a math model, that is sure to be hotly debated by scientists who say those unavoidable mistakes of nature play a much smaller role.

But whatever the ultimate number, the research offers a peek at how cancer may begin.

And it should help with the "why me'' question from people who have "done everything we know can be done to prevent cancer but they still get it",said Hopkins' Dr. Bert Vogelstein, a pioneer in cancer genetics who co-authored the study. "They need to understand that these cancers would have occurred no matter what they did.''

GENE MUTATIONS CAUSE CANCER BUT WHAT CAUSES THE MUTATIONS?

You might inherit some mutations, like flaws in BRCA genes that are infamous for causing aggressive breast and ovarian cancers in certain families.

More commonly, damage is caused by what scientists call environmental factors -the assault on DNA from the world around us and how we live our lives. There's a long list of risks: Cigarette smoke, UV light from the sun, other forms of radiation, certain hormones or viruses, an unhealthy diet, obesity and lack of exercise.

Then there are those random copy errors in cells -what Vogelstein calls our baseline rate of genetic mutations that will occur no matter how healthy we live.

One way to think of it: If we all have some mutations lurking in our cells anyway, that's yet another reason to avoid known risks that could push us over the edge.

123rf

New research has found most cancers are caused by random DNA 'mistakes'.

HOW CELLS MAKE TYPOS

New cells are formed when an existing cell divides and copies its DNA, one cell turning into two. Every time DNA is copied, about three random mutations occur, Vogelstein said.

We all harbor these kinds of mutations and most don't hurt us because they're in genes that have nothing to do with cancer or the body's defense mechanisms spot and fix the damage, said DrOtis Brawley of the American Cancer Society, who wasn't involved in the new research.

But sometimes the errors hit the wrong spot and damage genes that can spur cancerous growth or genes that help the cell spot and fix problems. Then the damaged cells can survive to copy themselves, allowing important mutations to gradually build up over time. That's one reason the risk of cancer increases with age.

THE STUDY FINDINGS

Thursday's study follows 2015 research by Vogelstein and statistician Cristian Tomasetti that introduced the idea that a lot of cancer may be due to "bad luck",because those random DNA copying mistakes are more common in some kinds of cancer than others. Cancer prevention advocates worried the idea might sway people to give up on healthier lifestyles.

This time around, the duo analysed mutations involved in 32 types of cancer to estimate that 66 per cent of the gene flaws are due to random copy errors. Environmental and lifestyle factors account for another 29 per cent, while inherited genes made up just 5 per cent of the mutations.

DIFFERENT ORGANS, DIFFERENT RISKS

The same person can harbor a mix of mutations sparked by random DNA mistakes, heredity or environmental factors. And which is the most common factor differs by cancer, the Hopkins team said.

For example, they estimate that random cell errors account for 77 per cent of critical mutations in pancreatic cancer -while still finding some caused by lifestyle risks like smoking. And the random DNA mistakes caused nearly all the mutations leading to childhood cancers, which is not surprising because youngsters have had little time to be exposed to environmental risks.

In contrast, most lung cancer mutations were the result of lifestyle factors, mainly from smoking. And while lung tissue doesn't multiply frequently, the small number of mutations caused by chance DNA errors might explain rare cases of never-smokers who still get sick.

"This paper is a good paper,'' said the cancer society's Brawley. "It gives prevention its due respect.''

OTHER SCIENTISTS SEE MORE TO THE STORY

Estimates from Britain suggest 42 per cent of cancers are potentially preventable with a healthy lifestyle, and the Hopkins team says their mutation research backs that idea.

But Dr Yusuf Hannun, Stony Brook University's cancer centre director, contends that's just the number known to be preventable today -researchers may discover additional environmental risks we can guard against in the future.

He said the Hopkins paper exaggerates the effect of the unavoidable DNA mistakes. His own 2015 research concluded they account for 10 to 30 per cent of cancer cases.

This project by the Associated Press was produced in collaboration with the Howard Hughes Medical Institute's Department of Science Education.

-AP

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Unavoidable DNA errors help fuel cancer - Stuff.co.nz

Sally Martin backs DNA Parentage test.

DNA parentage testing of progeny from multiple sire mating groups significantly improves the accuracy of breeding values associated with their bloodlines, a new trial has found.

A genomic validation trial conducted in conjunction with Australian Wool Innovation, Sally Martin Consulting, Moses & Son, and Bluechip Livestock, used Sheep CRC DNA tests to identify parentage of the progeny of 300 ewes that had been joined in a syndicate mating program and found huge variation in the number of progeny sired by each ram.

Rather than an even spread of offspring per sire, the number of progeny per sire ranged from 4 percent up to 30pc, with the dominant ram varying from year to year.

Similar results were recorded in an AI backup program, with a range of progeny per syndicate sire from 1pc to 58pc, Ms Martin said.

This variation in the number of progeny per sire helps to explain the reason why Sheep Genetics adjusts results from syndicate sire groups compared to single sire matings when calculating Australian Sheep Breeding Values (ASBVs).

ASBVs provide breeders with an estimate of the genetic potential a ram or ewe will pass on to its progeny for a range of economically important traits. ASBVs account for the environmental effects, allowing the comparison of sheep based on the genes they will pass on to their progeny.

Ms Martin said variation in parentage even extended to twins, where the results of DNA Parentage testing showed that on average 50 percent of twins were half-siblings (i.e. the same dam but different sire).

DNA Parentage testing provides a great opportunity to account for the variability in the number of progeny per ram by providing accurate pedigree data, and this in turn improves the accuracy of the ASBVs, she said.

The DNA Parentage test provided by the Cooperative Research Centre for Sheep Industry Innovation (Sheep CRC), can be used either for full pedigree that is linking a lamb to its ewe and sire or breeders may choose to only link the lambs with their sires. To use the test, breeders need to collect either blood or tissue samples from all of the animals that need to be matched up.

The DNA Parentage test is a great tool.

For producers to extract full value out of this technology it is best to measure a whole syndicate group rather than sub-sampling within a syndicate group to ensure effective progeny groups are not compromised when submitting data to Sheep Genetics, Ms Martin said.

More information on DNA Parentage testing is available at http://www.sheepcrc.org.au

Source: Sheep CRC.

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DNA parentage testing improved breeding value accuracy in research trial - Sheep Central

A special New York State panel of experts is scheduled Monday to discuss and possibly propose ways of using an emerging DNA testing procedure to help state and local law enforcement solve cold cases.

The use of familial searching, as the technique is called, is one of the main items on the agenda of a special DNA subcommittee meeting Monday morning in Manhattan.

Outside experts familiar with the issue believe the subcommittee may reveal proposed regulations to govern the procedure in New York.

Prudent, appropriate, limited safeguards can be put in place, Queens District Attorney Richard Brown said recently.

Familial searching involves a two-step process to analyze crime-scene DNA not matched to existing profiles in databases. First, the DNA is compared with known genetic profiles by using probability rankings of potential family relationships. If any partial similarities emerge, an analysis of the Y chromosome is done to identify who may be actual relatives of an unknown suspect.

Once relatives are identified, police can use traditional investigative techniques to develop reasonable suspicion and retrieve a DNA sample of the person of interest.

The process is used in 10 states and a number of countries, including Britain. Interest in New York arose as an offshoot of the case of Karina Vetrano, the Howard Beach jogger who was found strangled last August in Spring Creek Park. Police had DNA of a suspect but couldnt match it to any known genetic profile in state databases, and the investigation seemed stalled.

After a story last November in Newsday highlighted familial searching and its potential use in the Vetrano case, interest grew. Brown and NYPD Commissioner James ONeill issued strong statements in support of the procedure.

Vetranos parents, Philip and Catherine Vetrano, support the use of familial searching and testified in February at a special meeting of a state forensic science commission. Police made an arrest in the Vetrano case in early February as a result of tracking old police reports.

Still, the Vetrano family supports the technique. Now more than ever, Philip Vetrano said last week in an email.

Some civil libertarians are concerned about the impact on privacy and have likened it to a form of genetic stop-and-frisk. But advocates said such concerns are off the mark and note that familial searching is a valid scientific tool that can actually clear innocent people.

NYPD Deputy Chief Emanuel Katranakis has said that 10 percent of last years unsolved homicides in the city an estimated 12 cases have DNA evidence with no match and could benefit from familial searching. Suffolk County Assistant District Attorney Robert Biancavilla testified in February that the county had 200 unsolved homicides since 1960, cases in which families such as the Vetranos dont have closure.

However, Erin Murphy, a professor at New York University School of Law, testified at the February hearing that familial searching has an inherent racial bias because the genetic profiles in the state database are disproportionately those of people of color, who are convicted in greater numbers.

Former Denver District Attorney Mitch Morrissey countered such criticism when he testified that people of color also make up 91 percent of homicide victims and 71 percent of rape cases. NYPD data for 2015 showed that known homicide and rape suspects were identified as people of color in 91.7 percent and 85 percent of cases, respectively.

Rockne Harmon, a former prosecutor and proponent of familial searching, said last week that there is evidence that criminal tendencies tend to run in families, creating a strong chance that familial matching may uncover suspects.

One thing you can be certain of is the next step the state takes will not be the last, said UC Berkeley School of Law professor Franklin Zimring about New York. There will be inevitable pressure to making the system a standard part of a citizens profile.

The rest is here:
New York mulls use of DNA familial matching to solve cold cases - Newsday

Two thirds of the mutations that cause cancer may be due to random, unpredictable DNA copying "mistakes," according to scientists from the Johns Hopkins Kimmel Cancer Center in Baltimore, MD. These errors are reported to occur regardless of lifestyle and environmental factors.

It is not entirely understood why some people develop cancer while others do not. There are lifestyle and environmental risk factors that make a person more likely to develop cancer, such as smoking, drinking alcohol, obesity, and exposure to harmful chemicals.

While these risk factors can be avoided to lower the risk of cancer, the majority of cancer cases occur in people with no known risk factors and no family history of the disease.

For people that try to actively decrease their chances of disease by living a healthy lifestyle and avoiding known risk factors and yet still develop cancer, they may question what they are doing wrong. Bert Vogelstein, co-director of the Ludwig Center at the Johns Hopkins Kimmel Cancer Center says: "It's not your fault. Nothing you did or didn't do was responsible for your illness."

Even with the best health intentions, cancer may still develop due to mistakes that crop up when cells divide to form new cells.

The team at the Johns Hopkins Kimmel Cancer Center conducted a study to find out what fraction of mutations in cancer DNA copying errors are responsible for. Their findings were published in the journal Science.

"It is well-known that we must avoid environmental factors such as smoking to decrease our risk of getting cancer. But it is not as well-known that each time a normal cell divides and copies its DNA to produce two new cells, it makes multiple mistakes," says Cristian Tomasetti, Ph.D., assistant professor of biostatistics at the Johns Hopkins Kimmel Cancer Center and the Johns Hopkins Bloomberg School of Public Health.

"These copying mistakes are a potent source of cancer mutations that historically have been scientifically undervalued, and this new work provides the first estimate of the fraction of mutations caused by these mistakes," he adds.

"We need to continue to encourage people to avoid environmental agents and lifestyles that increase their risk of developing cancer mutations," says Vogelstein. "However, many people will still develop cancers due to these random DNA copying errors, and better methods to detect all cancers earlier, while they are still curable, are urgently needed."

Tomasetti and Vogelstein's research agrees with previous studies that show that around 40 percent of cancers could be prevented "by avoiding unhealthy lifestyles and environments."

The researchers say that while efforts to reduce environmental risk factors will have a significant impact on cancer incidence, the new research highlights that there is little attention given to early cancer detection strategies that would tackle the considerable number of cancers that are caused by DNA copying errors. "These cancers will occur no matter how perfect the environment," explains Vogelstein.

Mutations that are behind abnormal cell growth in 32 types of cancer were observed. According to the researchers, it typically takes two or more critical gene mutations to cause cancer. These mutations can be due to inherited genes, the environment, or random DNA copying errors.

The team developed a new mathematical model using DNA sequencing data from The Cancer Genome Atlas and epidemiologic data from the Cancer Research UK database to find out what fraction of cancer mutations are due to DNA copying mistakes.

Using the mathematical model, Tomasetti and Vogelstein could add together the critical mutations in each of the 32 cancer types and determine what percentage of mutations were due to DNA copying errors, the environment, and hereditary factors. For example, for pancreatic cancer, when the critical mutations were added together, 77 percent were a result of random DNA copying errors, 18 percent were due to environmental factors, and 5 percent down to heredity.

In cancers of the bone, brain, and prostate, more than 95 percent of mutations were the result of random DNA copying mistakes.

In contrast, lung cancer painted a different picture: 65 percent of mutations were a result of environmental factors, predominantly smoking. The other 35 percent of mutations were attributed to copying errors. It is not thought that inherited factors have a part in the development of lung cancers.

Overall, the team estimated that across the 32 types of cancer, 66 percent of cancer mutations are due to random DNA copying mistakes, 29 percent result from lifestyle and environmental factors, and the remaining 5 percent are down to hereditary factors.

Tomasetti, Vogelstein, and colleagues likened the reasons that mutations occur to why "typos" happen during the typing of a 20-volume book. Typos often happen when people are tired, representing environmental factors, or if a key on the keyboard is missing or stuck, representing inherited factors. Some typographical errors just randomly happen, which represents DNA copying errors.

"You can reduce your chance of typographical errors by making sure you're not drowsy while typing and that your keyboard isn't missing some keys. But typos will still occur because no one can type perfectly. Similarly, mutations will occur, no matter what your environment is, but you can take steps to minimize those mutations by limiting your exposure to hazardous substances and unhealthy lifestyles."

Bert Vogelstein

The researchers compared the total numbers of stem cell divisions with worldwide cancer incidence data. They found a strong correlation between cancer incidence and normal cell division in 17 types of cancer, despite the state of the countries' environment or economic development.

The more cells divide, the higher is the likelihood that DNA copying errors will occur in cells of an organ. These errors will only get more important as "societies face aging populations," among which cells are given the opportunity to produce an increasing amount of copying errors, concludes Tomasetti.

Learn how a cancer diagnosis impacts young adults in the long-term.

Link:
Most cancer mutations result from DNA copying errors - Medical News Today

Researchers have identified a cellular mechanism that allows them to reverse ageing in mouse DNA and protect it from future damage.

They've shown that by giving a particular compound to older mice, they can activate the DNA repair process and not only protect against future damage, but repair the existing effects of ageing. And they're ready to start testing in humans within six months.

"The cells of the old mice were indistinguishable from the young mice, after just one week of treatment," said lead researcher David Sinclairfrom the University of New South Wales (UNSW) in Australia and the Harvard Medical School in Boston.

"This is the closest we are to a safe and effective anti-ageing drug that's perhaps only three to five years away from being on the market if the trials go well."

Sinclair and his team made headlines back in 2013 when they found that the cells of younger mice contained more of a compound called nicotinaminde adenine dinucleotide, or NAD+, than their older counterparts.

Not only that, but when they gave the older mice more NAD+, they started to look younger, too.

It was a big deal at the time, but one of the tricky things about medicine is that in order to show that something could work as a potential treatment, you need to first understand how it's acting in the body.

And although the researchers knew NAD+ was having an impressive effect, they couldn't say for sure how it was doing it.

Now, Sinclair and his team have released a new study, where they outline in detail the mechanism through which NAD+ protects DNA from the damage of ageing and radiation in mice.

So how does it work? When we're born, all of our cells have the ability to repair DNA damage, which we experience constantly through random mutations when our cells divide, or whenever we go out in the sun.

But as we get older, our ability to patch up this damage declines, and our cells being to age.

What the researchers have now shown in this latest study is that a lot of this damage comes down to a DNA-repair compound called PARP1.

When there's a lot of NAD+ in a cell, PARP1 does its job and keeps our DNA healthy. But when NAD+ drops naturally with age, PARP1 starts to decline, and damage builds up.

To see whether they could take advantage of this cellular mechanism, Sinclair and his team developed a drug that contains the precursor to NAD+, known as NMN, or nicotinamide mononucleotide.

In mice, boosting older mice with NMN was enough to kick DNA repair into action and even reverse existing DNA damage.

They now plan to trial a similar drug in humans before the end of the year - and not just for anti-ageing purposes, but also to protect against DNA damage of any kind.

In fact, the team is collaborating with NASA to see if NMN could help protect its astronauts against harsh space radiation on their four-year journey to Mars, during which it's predicted that 5 percent of the astronauts' cells would die, and their chances of cancer would approach 100 percent.

The drug could also be useful for groups that are particularly vulnerable to the effects of radiation, such as frequent fliers and those who undergo frequent CT scans or X-rays.

"The idea is to protect the body from radiation exposure here on earth, either naturally occurring or doctor-inflicted," Sinclair told Time.

"If I were going to have an X-ray or a CT scan, I would take NMN beforehand."

Survivors of childhood cancer could also benefit - right now, 96 percentgo on to suffer a chronic illness by age 45, including cardiovascular disease, Alzheimer's, or cancers unrelated to their original cancer.

"All of this adds up to the fact they have accelerated ageing, which is devastating," said one of the researchers, Lindsay Wu. "It would be great to do something about that, and we believe we can with this molecule."

Before we get too excited, we need to keep in mind that many, many studies in mice are not replicated in humans.

So until the results of these early clinical trials in people begin to trickle in, there's no promise that NMN will help protect human DNA.

But understanding this mechanism of DNA ageing is a big step towards better understanding how to keep our cells healthier for longer, and that's pretty exciting.

The research has been published inScience.

See the rest here:
It's Happening: Scientists Can Now Reverse DNA Ageing in Mice - ScienceAlert

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