Newborns carry more epigenetic markers than nonagenarians, providing clues to the mechanisms underlying aging.

Aging is associated with loss of an epigenetic marker that helps control gene expression, according to new research published today (June 11) in Proceedings of the National Academy of Sciences, with a centenarian carrying some 7 percent fewer methylated DNA bases than a newborn. Researchers posit that reductions in methylation may be one of the mechanisms underlying the aging process.

Its one of the first studies to look at aging from an epigenetic point of view, said Willis Li, at the University of California, San Diego, who did not participate in the research. Other research, including Lis own in Drosophila, has shown that the amount of heterochromatinhistone modifications that result in tight chromosome packingalso appears to decline with an organisms age. The new study further supports the idea that epigenetic modifications, in addition to genetic factors, play a critical role in aging, said Li.

Searching for clues to why some people live long healthy lives and some succumb to early to aging, scientists have discovered that genetic factors only contribute about 10 percent to longevity, while environmental factors contribute about 90 percent, said senior author Manel Esteller of the University of Barcelona. Knowing that epigenetic modifications, such as cytosine methylation, are responsive to environmental stimuli, Esteller and his collaborators wondered if they could be a reliable indicator of physiological aging.

The scientists first compared the DNA methylation epigenomethe genome-wide level and location of methylated cytosines located next to guanines (CpG)in circulating T cells from a newborn and a centenarian. The general level of methylation of the centenarians genome (73 percent), they found, was lower than the newborns (80 percent). Looking at a 26-year-olds genome, they found an intermediate level of methylation.

Examining more closely the patterns of methylation in the newborns and centenarians genomes gave hints that Esteller thinks may help explain how loss of methylation affects cellular function and leads to aging. While most areas of the centenarians genome were less methylatedsuch as genes with tissue-specific expression patterns, suggesting the possibility that the centenarians T cells were expressing genes they shouldnt, like neuron- or testes-restricted genesa few regions showed greater methylation. Many promoters of tumor-suppressor genes, for example, showed higher levels of methylation, suggesting a possible connection with age-associated increases in cancer risk, Esteller said.

When Esteller and his colleagues extended the study to 19 more newborns and 19 people in their 90s, they found similar differences in their genomes methylation patterns. Furthermore, explained Esteller, they were able to use the epigenetic patterns to predict the agenewborn or nonagenarianof their samples.

As tantalizing as these differences are, its still not clear how the epigenetic changes factor into the aging process, said Karl Kelsey, a molecular biologist who studies epigenetic biomarkers for cancer at Brown University, who was not involved in the study. We dont yet fully understand the phenotypic consequences of epigenetics, he said, and its unclear whats underlying the loss [of methylation].

It could be that DNA methyltransferases become less active as age progresses, for example, adding fewer methyl groups after each cell division. Alternatively, changes in metabolism and diet could change the intake of folate, the nutrient from which the methyl groups are derived. Understanding the mechanism of these epigenetic changes, as well as their consequences, will be an important next step for understanding how the new findings relate to aging, Kelsey said.

In the meantime, Esteller hopes to discover whether manipulating the epigenome of mice will extend their lifespans. If maintaining methylation really can stave off aging, it may offer therapies for preventing neurodegenerative disorders, he said, and possible aid children suffering from premature aging disorders, who show epigenetic changes similar to the nonagenarians.

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DNA Methylation Declines with Age

If you're arrested for even the most minor charge, police will check your fingerprints against the national IAFIS database, where more than 70 million prints are on file. So why shouldn't they be able to check your DNA, too?

That's the question raised by state Sen. Nicholas Sacco, an advocate for greater use of DNA since 1994, years before CSI and DNA became well-known terms. He and I were running mates for the first time in 1993 and after we'd won the primary, we compiled a list of things we intended to do in Trenton. Among them was to get New Jersey into the FBI's CODIS database. New, it was used chiefly to track sex offenders and only a dozen states were participating. We introduced legislation requiring New Jersey to join.

Since we were minority party freshmen, it was easy for leadership to ignore us. And they did. But good friends and good luck were on our side. I inveigled an invitation to visit the FBI lab in Washington, saw DNA evidence being processed, and became a DNA evangelist.

FBI agents in Newark agreed to help us to talk to other legislators, and by sheer coincidence Curtis Sliwa, founder of the Guardian Angels, also offered to travel around with us. We drew some pretty funny reactions from our colleagues when we showed up with two men in dark blue suits and a bunch of guys in red berets, but we sure did get their attention.

State Police leaders were a tougher sell. Many felt DNA was pseudo-science and said their old, inadequate laboratory couldn't handle it anyway. That opposition melted, however, when our bill passed as part of the Megan's Law package and NJSP got funding for a new lab. As use of DNA expanded, more lawbreakers were convicted with the help of DNA evidence and some unjustly jailed persons were freed when DNA analysis proved they didn't do it.

In the late '90s, credible studies by experts in the criminal justice field reported few people start out committing major crimes. However, petty offenders are likely to escalate their criminal activities, so the experts said that identifying them early and offering alternatives could prevent that escalation. Sacco then introduced legislation calling for the collection of DNA from all convicted persons for inclusion in an all-crimes database.

That bill sparked another tough legislative battle. The ACLU and defense lawyers fought it every step of the way. Eventually it passed in a watered-down version that required only persons convicted of violent crimes to give DNA samples.

Collecting DNA is not invasive, just a swab of the inner cheek. It is as quick and easy as taking a photograph, an eye scan or a fingerprint. So Sacco feels there's no legitimate reason for anyone to refuse to give a sample. With a reliability factor of almost a billion to one, DNA can identify missing persons, convict guilty persons, and exonerate innocent persons. Sacco sees all good in that. He wonders "What's not to love?"

But some people don't love it at all. They include conspiracy theorists who believe Big Brother will use their DNA for nefarious purposes and privacy-rights folks protesting that recording their DNA is unconstitutional. Sacco politely listens to their arguments and then reminds them he's not giving up on his quest.

He is convinced that maintaining a DNA database of all convicted persons is inexpensive, easy to use, and will go a long way to keep the public safe. Maybe this is the year he'll get the chance to prove he's right.

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Quigley: Expanding the DNA database

11 June 2012 Last updated at 10:51 ET

A rapist has been jailed for eight-and-a-half years after being convicted of attacking a 15-year-old girl in an Essex woodland almost 15 years ago.

Jon Molt, 34, was traced after his father provided a DNA sample as part of the police inquiry into the rape in Ten Metre Wood, Harlow, in December 1997.

Chelmsford Crown Court heard the sample provided a "familial match". Molt, from Rushes Mead, Harlow, had denied rape.

His victim said she was "extremely grateful" to police for catching him.

Prosecutor Carolyn Gardiner said the girl had attended a Christmas concert at her school and became concerned that her boyfriend, who played in the band, was not there and decided to walk to his house.

As she passed through a secluded area of the wood she became aware of somebody running behind her, the court heard.

Ms Gardiner said as the attacker tried to remove the girl's school uniform, she said: "Please don't hurt me, I'm only 15."

The prosecutor said: "She screamed and he struck her and said 'If you scream again I'm going to kill you and I'm going to kill you bad'."

I would like to thank them not only on my behalf, but for any future victims of this man who will now never have to go through the ordeal that I have had to endure

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Rapist caught by DNA match jailed

ScienceDaily (June 10, 2012) Decoding the DNA of patients with advanced breast cancer has allowed scientists to identify distinct cancer "signatures" that could help predict which women are most likely to benefit from estrogen-lowering therapy, while sparing others from unnecessary treatment.

Researchers at Washington University School of Medicine in St. Louis uncovered mutations linked to whether or not women respond to aromatase inhibitors, drugs often prescribed to shrink large tumors before surgery. These mutations also correlate with clinical features of breast tumors, including how likely they are to grow quickly and spread.

The research, which also involved physicians and scientists at the Alvin J. Siteman Cancer Center at Barnes-Jewish Hospital and Washington University School of Medicine and The Genome Institute, is published June 10 in the advance online edition of Nature.

"This is one of the first cancer genomics studies to move beyond cataloging mutations involved in cancer to finding those linked to treatment response and other clinical features," says senior author Elaine Mardis, PhD, co-director of The Genome Institute. "If our results are validated in larger studies, we think genomic information will be one more data point for physicians to consider when they select among several treatment options for their patients."

The study involved DNA from 77 post-menopausal women with stage 2 or 3 estrogen-receptor-positive breast cancer, the most common form of the disease. Estrogen stimulates the growth of these tumors, and all the women received aromatase inhibitors to lower estrogen in the body. The drugs can reduce the size of breast tumors, enabling many women to receive breast-conserving surgery rather than a mastectomy. But aromatase inhibitors only work in some women, and doctors don't know why.

To answer that question, the researchers compared the DNA in the tumor samples to matched DNA from the same patients' healthy cells, which allowed them to identify mutations that only occurred in the cancer cells. This "unbiased" approach finds all the mutations underlying a patient's cancer not just those that would be expected to occur.

The tumor samples came from women enrolled in one of two aromatase inhibitor clinical trials sponsored by the American College of Surgeons Oncology Group. As part of those trials, researchers had collected detailed information about the women's tumors and whether they responded to a four-month course of aromatase inhibitor therapy before surgery. Twenty-nine of the tumor samples came from women whose tumors were resistant to aromatase inhibitors, and 48 came from patients whose tumors responded.

Over all, the scientists noted that tumors in women who responded to the estrogen-lowering drugs had relatively few mutations, while those whose cancers were resistant to the treatment had higher mutation rates and were genomically more complex.

"This makes sense in hindsight but it's not something that we would have predicted," Mardis says.

The researchers identified 18 significantly mutated genes in the tumor samples, meaning the genes were altered more often than would have been expected. Some of these genes were already known to be important in breast cancer but others were completely unexpected, including a handful that are well-recognized for their role in leukemia.

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Decoding DNA finds breast tumor signatures that predict treatment response

By Tom Schoenberg - 2012-06-11T21:00:49Z

U.S. prosecutors sought to bolster the credibility of their DNA and drug use evidence against former New York Yankees pitcher Roger Clemens, accused of lying to Congress by denying that he used steroids and human growth hormone, as testimony in his perjury trial ended in Washington.

The government, which completed its case against Clemens today, put on three witnesses to rebut defense allegations that the evidence linking Clemens to a needle and cotton balls containing anabolic steroids was contaminated or faked.

U.S. District Judge Reggie Walton scheduled closing arguments for tomorrow and the jury may begin deliberating Clemenss fate in the afternoon.

Clemens, a seven-time Cy Young Award winner as the best pitcher in his league, is charged with one count of obstructing a congressional investigation into the use of performance- enhancing drugs by professional athletes.

Hes also charged with three counts of making false statements and of perjury stemming from his testimony to a House panel. If convicted, he faces as long as 21 months in prison.

The prosecutions evidence includes a needle and cotton with Clemenss DNA that tested positive for steroids. The material was given to prosecutors by Brian McNamee, Clemenss former trainer. McNamee, who spent six days testifying, told jurors that he gave the ballplayer injections of steroids and HGH during the 1998, 2000 and 2001 baseball seasons while both men worked for the Toronto Blue Jays and the Yankees.

McNamee told jurors he saved needles, gauze and vials from one of the injections in 2001 and kept some of the items in a Miller Lite beer can that he took from the recycling bin in Clemenss apartment.

Walton, for a second time, denied a defense motion to dismiss the case. He did say hes considering whether to throw out one of the 13 false or misleading statements in the charges having to do with Clemenss denial that he attended a pool party at the home of fellow Toronto Blue Jays teammate Jose Canseco in 1998.

The case is U.S. v. Clemens, 1:10-cr-00223, U.S. District Court, District of Columbia (Washington).

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Clemens Prosecutors Revisit DNA Evidence as Testimony Ends

Article updated: 6/11/2012 4:23 PM

Tyrone M. Young

DNA evidence has led to charges against an Aurora man for an August 2010 sex attack at the Oakhurst Forest Preserve community garden plots on the Auroras east side.

Tyrone M. Young, 30, who already faces charges for an attack in the womens bathroom of a home improvement store last summer, recently was indicted on 14 charges stemming from the garden plot attack, according to court records.

Young, of the 800 block of Sard Avenue, is charged with four counts of aggravated criminal sexual assault, three counts of criminal sexual assault, two counts of aggravated criminal sexual abuse, four counts of aggravated battery and one count of unlawful restraint, the court records said.

We had DNA evidence that was slowly working its way through the state crime lab that came back as positive for Mr. Young, said Kane County Forest Preserve Police Chief Michael Gilloffo.

He also credited Forest Preserve Police Officer Patti Bowker for working with Aurora police on the case.

Authorities said a then-29-year-old woman told police she was gardening at about 1:30 p.m. Aug 28, 2010, when a man walked into the garden and suddenly attacked her and sexually assaulted her.

According to court documents, the woman was choked to the point of losing consciousness.

Several people pulled into the parking lot, called police and the attacker fled in a dark green, four-door Pontiac Grand Prix.

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DNA leads to charges in 2010 Aurora garden plot attack