The FBI Is Very Excited About This Machine That Can Scan Your DNA in 90 Minutes
Rapid-DNA technology makes it easier than ever to grab and store your genetic profile. G-men, cops, and Homeland Security can’t wait to see it everywhere.
Nov. 20, 2014
By Shane Bauer
Illustration: Dan Bejar
Robert Schueren shook my hand firmly, handed me his business card, and flipped it over, revealing a short list of letters and numbers. “Here is my DNA profile.” He smiled. “I have nothing to hide.” I had come to meet Schueren, the CEO ofIntegenX, at his company’s headquarters in Pleasanton, California, to see its signature product: a machine the size of a large desktop printer that can unravel your genetic code in the time it takes to watch a movie.
Schueren grabbed a cotton swab and dropped it into a plastic cartridge. That’s what, say, a police officer would use to wipe the inside of your cheek to collect a DNA sample after an arrest, he explained. Other bits of material with traces of DNA on them, like cigarette butts or fabric, could work too. He inserted the cartridge into the machine and pressed a green button on its touch screen: “It’s that simple.” Ninety minutes later, the RapidHIT 200 would generate a DNA profile, check it against a database, and report on whether it found a match.
A scanner, quickly: The RapidHIT 200 can generate a DNA profile in about 90 minutes. IntegenX
The RapidHIT represents a major technological leap—testing a DNA sample in a forensics lab normally takes at least two days. This has government agencies very excited. The Department of Homeland Security, the Department of Defense, and the Justice Department funded the initial research for “rapid DNA” technology, and after just a year on the market, the $250,000 RapidHIT is already being used in a few states, as well as China, Russia, Australia, and countries in Africa and Europe.
“We’re not always aware of how it’s being used,” Schueren said. “All we can say is that it’s used to give an accurate identification of an individual.” Civil liberties advocates worry that rapid DNA will spur new efforts by the FBI and police to collect ordinary citizens’ genetic code.
The US government will soon test the machine in refugee camps in Turkey and possibly Thailand on families seeking asylum in the United States, according to Chris Miles, manager of the Department of Homeland Security’s biometrics program. “We have all these families that claim they are related, but we don’t have any way to verify that,” he says. Miles says that rapid DNA testing will be voluntary, though refusing a test could cause an asylum application to be rejected.
“We’re not always aware of how it’s being used. All we can say is that it’s used to give an accurate identification of an individual.”
Miles also says that federal immigration officials are interested in using rapid DNA to curb trafficking by ensuring that children entering the country are related to the adults with them. Jeff Heimburger, the vice president of marketing at IntegenX, says the government has also inquired about using rapid DNA to screen green-card applicants. (An Immigration and Customs Enforcement spokesman said he was not aware that the agency was pursuing the technology.)
Meanwhile, police have started using rapid DNA in Arizona, Florida, and South Carolina. In August, sheriffs in Columbia, South Carolina, used a RapidHIT to nab an attempted murder suspect. The machine’s speed provides a major “investigative lead,” said Vince Figarelli, superintendent of the Arizona Department of Public Safety crime lab, which is using a RapidHIT to compare DNA evidence from property crimes against the state’s database of 300,000 samples. Heimburger notes that the system can also prevent false arrests and wrongful convictions: “There is great value in finding out that somebody is not a suspect.”
But the technology is not a silver bullet for DNA evidence. The IntegenX executives brought up rape kits so often that it sounded like their product could make a serious dent in the backlog of half a million untested kits. Yet when I pressed Schueren on this, he conceded that the RapidHIT is not actually capable of processing rape kits since it can’t discern individual DNA in commingled bodily fluids.
Despite the new technology’s crime-solving potential, privacy advocates are wary of its spread. If rapid-DNA machines can be used in a refugee camp, “they can certainly be used in the back of a squad car,” says Jennifer Lynch, a senior staff attorney at the Electronic Frontier Foundation. “I could see that happening in the future as the prices of these machines go down.”
Democratic members of Congress have urged the FBI to look into the “broad deployment” of rapid DNA in police stations.
Lynch is particularly concerned that law enforcement agencies will use the devices to scoop up and store ever more DNA profiles. Every state already has a forensic DNA database, and while these systems were initially set up to track convicted violent offenders, their collection thresholds have steadily broadened. Today, at least 28 include data from anyone arrested for certain felonies, even if they are not convicted; some store the DNA of people who have committed misdemeanors as well. The FBI’s National DNA Index System has more than 11 million profiles of offenders plus 2 million people who have been arrested but not necessarily convicted of a crime.
For its part, Homeland Security will not hang onto refugees’ DNA records, insists Miles. (“They aren’t criminals,” he pointed out.) However, undocumented immigrants in custody may be required to provide DNA samples, which are put in the FBI’s database. DHS documents obtained by the Electronic Frontier Foundationsay there may even be a legal case for “mandating collection of DNA” from anyone granted legal status under a future immigration amnesty. (The documents also state that intelligence agencies and the military are interested in using rapid DNA to identify sex, race, and other factors the machines currently do not reveal.)
The FBI is the only federal agency allowed to keep a national DNA database. Currently, police must use a lab to upload genetic profiles to it. But that could change. The FBI’s website says it is eager to see rapid DNA in wide use and that it supports the “legislative changes necessary” to make that happen. IntegenX’s Heimburger says the FBI is almost finished working with members of Congress on a bill that would give “tens of thousands” of police stations rapid-DNA machines that could search the FBI’s system and add arrestees’ profiles to it. (The RapitHIT is already designed to do this.) IntegenX has spent $70,000 lobbying the FBI, DHS, and Congress over the last two years.
The FBI declined to comment, and Heimburger wouldn’t say which lawmakers might sponsor the bill. But some have already given rapid DNA their blessing. Rep. Eric Swalwell, a former prosecutor who represents the district where IntegenX is based, says he’d like to see the technology “put to use quickly to help law enforcement”—while protecting civil liberties. In March, he and seven other Democratic members of Congress, including progressive stalwart Rep. Barbara Lee of California, urged the FBI to assess rapid DNA’s “viability for broad deployment” in police departments across the country.

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Lung cancer ‘risk’ for ex-smokers

August 24, 2007
Even years after quitting, former smokers still have a raised risk of lung cancer – and now scientists believe they know why.?

Smoking appears to permanently alter the activity of key genes, even though most cigarette damage is repaired over time.

Canadian researchers, writing in the journal BMC Genomics, looked at lung tissue of 24 people.

UK experts stressed that giving up still delivers massive health benefits.

It has been shown that the poisons in cigarette smoke can alter the activity of genes.

If you give up smoking, your risk of lung cancer falls significantly, but former smokers continue to have a slightly higher risk of lung cancer compared with someone who has never smoked.

We know that giving up smoking massively reduces your chances of developing lung cancer Spokesman, Action on Smoking and Health

The latest study from the British Columbia Cancer Research Centre in Vancouver suggests that some of these changes might be permanent.

They studied cell samples from the lungs of eight current smokers, 12 former smokers and four people who had never smoked.

Some gene changes appeared to be relatively short-lived, reversing after they had quit the habit for a year or more.

However, a small group of changes were more persistent, and some of these are thought to be involved in cancer susceptibility.

Self-repair

In particular three genes linked to the body’s ability to repair DNA had reduced activity levels.

Raj Chari, who led the research, said: “Those genes and functions which do not revert to normal levels upon smoking cessation may provide insight into why former smokers still maintain a risk of developing lung cancer.”

A spokesman for the pressure group Action on Smoking and Health (ASH) said that it was important for current smokers not to be put off trying to quit by the thought that genetic damage was irreversible.

She said: “We know that giving up smoking massively reduces your chances of developing lung cancer, and not only that, but your chances of heart disease and a number of other serious illnesses are also significantly reduced.

“Although former smokers do still have a slightly increased risk of lung cancer compared with someone who has never smoked, it is nowhere near as high as the risk of lung cancer to someone who is a current smoker.”

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Women with Certain Genes Have 90 Percent Risk of Developing Breast and/or Ovarian Cancer
By University of Colorado Cancer Center

Sep 11, 2006

Women with Certain Genes Have 90 Percent Risk of Developing Breast and/or Ovarian Cancer

(HealthNewsDigest.com).. AURORA, Colo. Sept. 6, 2006 – During September, Gynecologic Cancer Awareness Month, the University of Colorado Cancer Center at the University of Colorado at Denver and Health Sciences Center is joining with the Gynecologic Cancer Foundation (GCF) to educate women about familial breast-ovarian cancer syndrome.

Women with this syndrome have a 90 percent risk of developing breast and/or ovarian cancer during their lifetime. By contrast, women without this syndrome have about a 10 percent chance of developing breast cancer and an almost 2 percent chance of developing ovarian cancer. Approximately 10 percent of all cancers have a strong hereditary component.

About one out of every 500 individuals in the general population are members of a family that inherit and pass on a mutation or change in the breast cancer 1 (BRCA1) or the breast cancer 2 (BRCA2) gene, the cause of familiar breast-ovarian cancer syndrome. Women with changes in the BRCA1 gene have an 80 percent chance of developing breast cancer and a 20 percent to 40 percent chance of being diagnosed with ovarian cancer. Changes in the BRCA2 gene result in the same sharply higher risk of developing breast cancer as the BRCA1 gene, but fewer women, 10 percent to 20 percent, will be diagnosed with ovarian cancer.

“While these statistics sound alarming,” said Susan Davidson, MD, a gynecologic oncology specialist at UCDHSC Cancer Center, “there are steps every woman can take to manage this increased risk. First, it is extremely important for women to know their family history of these cancers. Second, if it is determined that a woman is at increased risk after undergoing genetic testing, she should discuss the various strategies for managing this risk with her health care provider.”

Women who are found to have these changes in the BRCA1 or BRCA2 genes should consider more intense clinical monitoring, including mammograms, pelvic exams and a blood test called a CA 125 test. Medication, lifestyle changes and preventive surgery also should be considered.

“It is our hope that during September, Gynecologic Cancer Awareness Month, and October, Breast Cancer Awareness Month, women will have an opportunity to learn more about the inherited link between breast and ovarian cancer, and take appropriate measures,” said Karl C. Podratz, MD, PhD, chairman of the Gynecologic Cancer Foundation.

The Cancer Center is the only National Cancer Institute-designated comprehensive cancer center in the Rocky Mountain Region. Headquartered primarily at the University of Colorado at Denver and Health Sciences Center, its four-part mission is excellence in cancer research, treatment, prevention and education. For more information, visit the Web site at www.uccc.info.

The Gynecologic Cancer Foundation (GCF) was established by SGO in 1991 to develop educational programs for women, and create awareness about the prevention, early detection and treatment of gynecologic cancers. The foundation also supports research and training related to gynecologic cancers.

As a 501(c)(3) non-profit charitable organization, GCF raises funds to support these programs from both public and private sources. To learn more, visit our Web sites at www.thegcf.org or the Women’s Cancer Network at www.wcn.org.

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Article Date: 25 Jan 2006

A study to be published in the European Respiratory Journal (ERJ) demonstrates that most Japanese smokers’ cigarette consumption is conditioned by their genetic heritage. This discovery opens new horizons for stop-smoking treatments.

Nicotine, an alkaloid found in concentrations of 10 to 20 mg per gram of dried tobacco leaf, is known to be the main agent causing cigarette addiction.

However, under the influence of a particular enzyme known to specialists as CYP2A6, nicotine, with its strong effect on the nervous system, can degrade into an inactive substance named cotinine.

The latest data suggest that it is the fall in nicotine levels in the blood and cerebrospinal fluid, caused by the degradation process, that gives rise to the more or less irresistible desire to light another cigarette.

These were the considerations that inspired a Japanese team from Keio University and the Tokyo Electronic Power Company Hospital, led by Hidetoshi Nakamura and Naoto Minematsu, to examine the influence of genetic variations of the enzyme on smoking habits.

For the gene that causes synthesis of the CYP2A6 enzyme can present in various forms, known as alleles, which can be expected to affect nicotine degradation rates and hence the severity of tobacco addiction.

The authors of the study published in February’s ERJ decided to focus on the three alleles most commonly found in Asian populations, namely the *4, *7 and *9 forms of the CYP2A6 gene, which slow nicotine degradation to a greater or lesser degree.

The study covered a population of 200 Japanese smokers aged 50 or over, who had smoked the equivalent of at least a pack of cigarettes daily for 10 years and had no particular respiratory disease (other than chronic obstructive pulmonary disease, from which 70 per cent of them suffered).

Three-quarters of Japanese smokers affected

Just over a quarter (26%) of the subjects were found to carry the normal form of the gene (allele *1) on the relevant two chromosomes (homozygotes). In these subjects nicotine degradation is not slowed, and they were found to be the heaviest smokers (almost two packs a day on average).

Conversely, subjects with homozygotic allele *4, who represented 3.5% of the study population, were found to smoke the least on a daily basis (just under one pack a day).

The various combinations of alleles, meanwhile (*1/*9, *1/*7,*1/*4, _ _ *4/*9, *4/*4), give rise to a daily consumption mid-way between the two extremes.

The significance of these data becomes more obvious when one looks at the frequency with which the relevant alleles were found.

“We found a polymorphism for allele *4, *7 or*9 in almost three-quarters of the Japanese subjects”, the authors explain. “One could legitimately suppose that the higher nicotine concentrations in these subjects, whose CYP2A6 activity is reduced, make them less likely to light another cigarette.”

Most importantly, this study sheds light on the role – previously unknown – of alleles *7 and *9, which are widespread among Asian populations, running at 11% and 20% respectively.

Moreover, the research team believes the results could also give rise to improvements in stop-smoking methods, which consist mainly of nicotine replacement therapies. The data published in the ERJ could thus lead to the development of stop-smoking programmes tailored to the needs (i.e. the genetic profile) of the individual.

“Identification of these polymorphisms should represent the first tangible stage of stop-smoking programmes, in order that nicotine replacement therapies can be adjusted”, the authors add.

Finally, it should be noted that, while these data are of direct concern to Asian populations, they have broader significance for the human race.

Allele *9, in particular, is relatively common in certain white populations, including those of Sweden and Turkey, where the results published in February’s ERJ could easily be applied.

Title of the original article:
Limitation of cigarette consumption by CYP2A6*4, *7 and *9 polymorphisms

EUROPEAN RESPIRATORY JOURNAL

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Feb. 08, 2006

In his State of the U nion address, President Bush proposed programs for helping students who struggle with math. That’s certainly a worthy objective, but not strictly for the stated purpose of graduating more American scientists and engineers.

Government policy is increasingly justified by appeal to scientific and statistical analysis. Unfortunately, many policy-makers eschew the hard work required to understand scientific research and use statistics the way a drunk uses a street light — for support rather than illumination. Equally unfortunate, too few of us object.

A couple of Saturdays ago, I hosted “The Patriot Insider” radio program on WWTC, AM 1280. My guests were St. Paul City Council Member Dave Thune and Hennepin County Commissioner Penny Steele. I asked Thune what scientific evidence convinced him that secondhand smoke posed a danger that necessitated a government-imposed smoking ban. Could he pluck from the “mountains of evidence” he leaned on for support just one study and generally explain how it illuminated the dangers of secondhand smoke?

“I’m not a scientist,” Thune responded. “And I didn’t do very well in that class about numbers, you know… .”

“Statistics?” prompted Steele.

“Yeah, that’s it,” Thune said. “I flunked it badly.”

That notwithstanding, Thune concludes that government intervention is necessary to protect people from a danger that he cannot define. Lacking the skill and will to read past the executive summary of a research report, Thune has no choice but to make policy decisions based on the credibility of business cards rather than the content of research.

“We have to believe the experts,” he said. “And when health experts say that secondhand smoke kills, I believe them.”

I think Thune “analyzes” economic data in a like manner; he leans for support on experts who say smoking bans cause no economic harm. He ignores that this research relies on aggregate tax data that necessarily hide the negative impact of smoking bans on neighborhood taverns and the businesses that serve them.

I don’t intend to rehash the science and economics of smoking bans. A productive discussion among parties requires knowledge, which brings us back to the State of the U nion address and the president’s call for educational emphasis on science and math.

Of equal if not greater urgency than producing scientists and engineers who churn out data is graduating students who have sufficient skills to understand scientific research and protest policy based on unfounded conclusions, whether they are perpetuated by utopian policy-makers or practitioners of sky-is-falling journalism.

This little chunk of blue landed in a recent Pioneer Press column advocating more government involvement in health care — “about half of the people who file for bankruptcy do so because of illness or medical costs.”

Now, that sounds pretty scary — unless one asks the obvious question, “Just how many people are we talking about?” The columnist, however, didn’t ask that question. Hers was not the honest intent of illuminating the extent of medical bankruptcy. She was simply leaning on her statistic to support her intoxication with government-run health care.

Had the columnist taken the time to look at the data she was referencing, she would have found that medical bankruptcies affect about 2 million Americans a year, including both individuals who actually declare bankruptcy and their dependents. In a population of 298 million, 2 million equals about seven-tenths of 1 percent of the population.

“Seven-tenths of 1 percent” doesn’t sound nearly as frightening as “half of all bankruptcies.” However, might not a policy-maker who doesn’t question the statement “half of all bankruptcies are for medical reasons” lean toward a policy more extensive than is warranted by the problem? Would not a wise policy-maker focus on easing the situation of the seven-tenths of 1 percent rather than inflicting government health care on the other 296 million of us?

More so than a lack of scientists and engineers, the bigger problem we face today is policy-makers drunk with power leaning on scientific testimony they do not understand to support unwarranted regulations and programs.

“Common sense” means making policy consistent with data, not ignoring it. Deferring to experts as an excuse for willful ignorance is unacceptable public leadership.

Westover is an Afton writer who blogs at www.craigwestover. blogspot.com. E-mail him at westover4@yahoo.com. Warning: This column contains math and science content that may not be suitable for some policy-makers and journalists. Reader discretion is advised.

Interesting developments. Are you smoking/drinking because your grandfather experienced a lot of stress? For ETS/smoking research it means that we have another, very complex, cofactor in the equations…

Biology stands on the brink of a shift in the understanding of inheritance. The discovery of epigenetics – hidden influences upon the genes – could affect every aspect of our lives.

At the heart of this new field is a simple but contentious idea – that genes have a ‘memory’. That the lives of your grandparents – the air they breathed, the food they ate, even the things they saw – can directly affect you, decades later, despite your never experiencing these things yourself. And that what you do in your lifetime could in turn affect your grandchildren.

The conventional view is that DNA carries all our heritable information and that nothing an individual does in their lifetime will be biologically passed to their children. To many scientists, epigenetics amounts to a heresy, calling into question the accepted view of the DNA sequence – a cornerstone on which modern biology sits.
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Smoking, breast cancer and genotype

Epidemiologic studies have examined the association between cigarette smoking and breast cancer risk according to genotype with increasing frequency, commensurate with the growing awareness of the roles genes play in detoxifying or activating chemicals found in cigarette smoke and in preventing or repairing the damage caused by those compounds. To date, approximately 50 epidemiologic studies have examined the association between smoking and breast cancer risk according to variation in genes related to carcinogen metabolism, modulation of oxidative damage, and DNA repair. Some of the findings presented here suggest possible effect modification by genotype.

In particular, 14 epidemiologic studies have tended to show positive associations with long-term smoking among NAT2 slow acetylators, especially among postmenopausal women.

Summary analyses produced overall meta-relative risk (RR) estimates for smoking of 1.2 [95% confidence interval (95% CI), 1.0-1.5] for rapid acetylators and 1.5 (95% CI, 1.2-1.8) for slow acetylators. After stratification by menopausal status, the meta-RR for postmenopausal slow acetylators was 2.4 (95% CI, 1.7-3.3), whereas similar analyses for the other categories showed no association. In addition, summary analyses produced meta-RRs for smoking of 1.1 (95% CI, 0.8-1.4) when GSTM1 was present and 1.5 (95% CI, 1.1-2.1) when the gene was deleted.

Overall, however, interpretation of the available literature is complicated by methodologic limitations, including small sample sizes, varying definitions of smoking, and difficulties involving single nucleotide polymorphism selection, which likely have contributed to the inconsistent findings. These methodologic issues should be addressed in future studies to help clarify the association between smoking and breast cancer. (Cancer Epidemiol Biomarkers Prev 2006;15(4):602-11).
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