RCMP ties three ‘Highway of Tears’ cold cases to dead Oregon man

By Ken MacQueen - Tuesday, September 25, 2012 at 5:35 PM - 0 Comments

Her name was Colleen MacMillen, and in 1974—a more innocent time it seemed—the pretty 16-year-old thought little of hitch-hiking from her family’s lakeside home to visit a friend in the central B.C. town of Lac La Hache. Her body was found a month later south of 100 Mile House on a logging road off Highway 97. Her unsolved murder was swept into an RCMP investigation of 17 other tragically similar cases of girls and women who vanished from highways 16, 97 and 5 in central and northern B.C. between 1969 and 2006. On Tuesday, RCMP announced that advances in DNA technology had identified her murder as Bobby Jack Fowler, an Oregon man who died in prison in 2006 at age 66, while serving a 10-year sentence for kidnapping, attempted rape and assault.

Fowler had an “extensive violent history” in several U.S. states, and travelled and worked, in B.C. in the 1970s and possibly in the 1980s and 1990s, RCMP Insp. Gary Shinkaruk, head of the major crimes special projects unit, told a news conference in Surrey Tuesday. He said that the U.S.-born Fowler is “an incredibly strong suspect” in two other of the 18 murdered or missing women in the so-called Highway of Tears cases. He has been eliminated as a suspect in only eight of the 18 cases, Shinkaruk said, but investigators are also looking at other unsolved cases elsewhere in B.C., and in other provinces and states. Fowler is also “a person of interest” in at least two sets of murders of teen girls in Oregon in 1992 and 1995 and his movements in the state show a possible link with three other unsolved cases with similarities to the B.C. murder, Lincoln Country Ore., District Attorney Rob Bovett told the news conference.

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Proving his worth as Diefenbaker’s son

By Charlie Gillis - Sunday, September 9, 2012 at 5:00 AM - 0 Comments

BRJ/CP

A lot of people laughed. Internet trolls, talk-show callers, the self-appointed guardians of a dead prime minister’s reputation—they’ve all had their cracks over the past year at George Dryden and his claim that he’s the unacknowledged son of John Diefenbaker. Les MacPherson, a former newspaper editor from the Chief’s old riding of Prince Albert, Sask., admitted in an op-ed piece that Dryden looks like Canada’s 13th prime minister. “But so does my brother’s bloodhound, Beau,” he wrote. “It’s possible that the Dryden family’s milkman in 1968 looked like Diefenbaker, too, but that doesn’t mean they were related.”

The barbs could sting, the 43-year-old Dryden admits. “More than anything, it made me angry,” he says. But they failed to divert him from his mission, and this week the yuks are all his. On Aug. 28, Dryden emerged relieved and triumphant from the offices of a Toronto firm that had compared his genetic profile and that of an unidentified member of Diefenbaker’s extended family. The finding? Clear indications of common ancestry, typical of far-flung branches of the same family. “There is a familial linkage,” Harvey Tenenbaum, director of operations for Accu-Metrics, the nationally accredited company that performed the analysis, told Maclean’s. “I can’t say what it is, but it’s more than just strangers passing in the street.”

Tenenbaum cautions against leaping to conclusions. “They could be fifth cousins,” he said. “It’s impossible to pin down.” But to Dryden the results represent an enormous step forward. Stymied, stalled and plain unlucky in his attempts to obtain usable DNA samples of Diefenbaker himself, the Torontonian was running out of clues to justify his mission. Diefenbaker has no known direct descendents with whom to compare genes, and a previous test of cells gathered from personal articles that once belonged to the former PM, now stored at the Diefenbaker Canada Centre in Saskatoon, was inconclusive. He did test negative last winter against a sample of male DNA gleaned from the handle of a clothes brush. But the brush appeared to have been used by more than one person. No one could be sure whether the DNA tested was Diefenbaker’s.

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Detection in two seconds

By Ken MacQueen - Thursday, November 17, 2011 at 10:40 AM - 5 Comments

Verisante

One in seven Canadians will develop skin cancer during their lifetime. The good news is the disease has a high survival rate—if detected early.

Enter the Aura, a world-beating device that detects if a lesion is cancerous in less than two seconds. The technology, developed by the B.C. Cancer Agency and the University of British Columbia, was recently approved by Health Canada. The Aura should be available to health professionals by summer, says Thomas Braun, founder of Vancouver-based Verisante Technology, which licensed the device. It uses a hand-held wand to optically analyze the skin, allowing early detection of deadly melanoma, and more common skin cancers. Variants of the technology are under development for detecting lung, colon, cervical and gastrointestinal cancers. Both in terms of treatment costs and unnecessary biopsies, says Braun, “it’s got great potential to save lives, and save money.”

Genetically modified mosquitoes could combat malaria

By macleans.ca - Thursday, April 21, 2011 at 2:20 PM - 19 Comments

Scientists say they will soon be able to change the DNA of wild mosquitoes to help curb malaria, an illness that caused nearly one million deaths worldwide in 2008 according to the World Health Organization. The BBC reports that researchers are getting closer to finding a gene that they could spread through most of the wild mosquito population in just a few years. Scientists at Imperial College London and the University of Washington have inserted a gene into mosquitoes that creates an enzyme to cut their DNA in two. The cell uses the gene as a template to fix itself , and the male mosquito’s sperm carries the gene on to its offspring. The gene was used in lab experiments to half of caged mosquitoes within 12 generations.

BBC News

Building a better mosquito

By Sarah Scott - Tuesday, April 19, 2011 at 9:00 AM - 7 Comments

David Scharf/Science Faction/Corbis

The East End district of Grand Cayman Island bills itself as an offbeat paradise for divers, a place where you can swim past spectacular coral reefs, practise yoga under water, and even get married in the process. But last summer, the wildest action was taking place on land, in a quiet village a couple of kilometres from the beach. Here, amid the town’s modest pastel bungalows, pest-control officials arrived with an unusual group of eager visitors: three million genetically modified mosquitoes.

They were brought in to fight a terrifying disease—dengue fever, which is racing through the tropics, infecting over 50 million people a year and killing more than 12,000 of them, often young children. You can’t prevent dengue, or stop it from killing you, which is why the island’s mosquito-control department treats the insect that spreads dengue, the yellow fever or Aedes aegypti mosquito, as a lethal invader. Insecticide was winning the war until 2006, when hurricane Ivan tore through the island and left debris that served as perfect nurseries for a new generation of local Aedes aegypti mosquitoes. That was when the island’s Scottish-born mosquito- control chief, Dr. Bill Petrie, decided to take radical action.

The problem clearly was the mosquito, the transmitter of disease, so maybe the solution was to get rid of it in a new way, without the blunt instrument of insecticide. An English company, Oxitec, was tweaking the DNA of mosquitoes in its Oxford lab, and its scientists had invented a new biological system called RIDL—Release of Insects carrying a Dominant Lethal. It was effectively a morning-after pill carried by the males. It would work like this: when a genetically modified male mated with a wild female, they would still produce progeny, but the offspring would die within a few days. This was a death sentence for the mosquito population—or at least it was in the lab.

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Cancer answer?

By Kate Lunau - Thursday, October 7, 2010 at 10:00 AM - 0 Comments

Photograph by Tsar Fedorsky/Getty ImagesLeif Ellisen says 'smart drugs' will one day change the way cancer is treated

This summer, Vancouver cancer researchers announced a medical first. Presented with an extremely rare case of tongue cancer—it was so unusual there were no standard treatments to use—they sequenced the DNA of the patient’s tumour, and discovered similarities with another cancer (renal cell carcinoma, a type of kidney cancer) for which there’s a known therapy. The patient received drugs tailored to these results, and the cancer stopped growing for several months. Steven Jones, a molecular biologist with the B.C. Cancer Agency Genome Sciences Centre and one of two lead researchers on the study, calls it a breakthrough. It isn’t standard in hospitals to genetically sequence a patient’s tumour, but “the goal would be, maybe in 10 years, this would be routine,” he says.

Dr. Leif Ellisen, an associate professor of medicine at Harvard Medical School, is working to bring tumour genotyping from the lab into the clinic. He and a team have designed a system that can screen relatively large numbers of patients for a variety of mutations across different cancer genes. These genetic mutations are a tumour’s “Achilles’ heel,” noted a recent editorial in the journal EMBO Molecular Medicine. “Every tumour has a flaw,” says Ellisen, who’ll be discussing his work as part of the Scienta Health Series in Toronto on Oct. 7, and his goal is to find it.

It’s the mantra of a growing number of researchers, who tout personalized medicine—treatments tailored to each individual—as the future of cancer care. Traditionally, cancer treatment “has been one-size-fits all,” Ellisen says. “If it’s breast cancer, you treat it one way; if it’s lung cancer, you treat it another.” The downside is that costly drugs are administered to patients, sometimes with harmful side effects and no real promise they’ll work. “The treatment needs to be tailored to the individual characteristics of the patient and, we’re learning now, the characteristics of the tumour,” he says. Cancers are typically classified by the organs where they arise, but it’s possible that a breast cancer and a lung cancer, for example, might share a genetic abnormality. As a result, they might even respond to the same treatment.

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Der Führer's secret past

By Jane Switzer - Thursday, September 9, 2010 at 1:00 PM - 0 Comments

Imagno/Getty Images

Saliva samples taken from Adolf Hitler’s relatives show that the Nazi leader may have biological links to Africans and Jews. Belgian journalist Jean-Paul Mulder and historian Marc Vermeeren tracked down 39 of Hitler’s relatives earlier this year, among them Hitler’s cousin, an Austrian farmer identified only as Norbert H., and grand-nephew Alexander Stuart-Houston, a social worker from Long Island, N.Y. Results of their DNA tests found a chromosome called Haplogroup E1b1b1, which is rare in Western Europe but most commonly found in the Berbers of Morocco, Algeria and Tunisia, as well as among Ashkenazi and Sephardic Jews, Mulder said. The chromosome appears to be one of the major founding lineages of the Jewish population, and accounts for 8.6 per cent to 30 per cent of Sephardic Y-chromosomes. Their results, published in the Belgian magazine Knack, conclude that Hitler “was related to people whom he despised,” Mulder wrote.

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Methuselah's children

By Colby Cosh - Tuesday, July 6, 2010 at 9:19 AM - 0 Comments

A note on that Boston University study of centenarian genetics: it may represent a rare case of a piece of research being slightly undersold in the popular press. The CBC (to take an example at random) reports:

In Thursday’s online issue of the journal Science, researchers say their model of 150 genetic variants helped to predict exceptional longevity—living to late 90s or longer—among people in the study compared with people in the general population of North America and Europe.

…The researchers identified a group of 150 genetic variants that they say can predict exceptional longevity with 77 per cent accuracy. …The team found 19 genetic “signatures” in the subjects’ DNA that were associated with diseases such as dementia and hypertension.

…To make their findings, the researchers compared disease-associated variants in 801 unrelated subjects enrolled in the New England Centenarian Study with 926 controls with the same Caucasian genetic backgrounds.

It would not be particularly impressive if the researchers built a model of “signatures” based on its 1,727-person sample and then found that the model explained 77% of the longevity within that same sample. After building the model they actually collected a whole new group, a “replication set”, of ethnically paired, mostly-Caucasian centenarians and non-centenarians. The model works as well on the “replication set” of oldies and controls as it does on the original “discovery set”; the individual components strongly associated with longevity in the original data are, overall, associated about as strongly amongst the new people. So the finding looks very strong, at least for Caucasians who have genetic backgrounds of the sort one might find in New England.

The authors of the study are excited about the possibility of their complex gene-hunting approach being adapted to questions about inheritable illnesses—and most of our biggest killers are, to a surprising degree, inherited. The same study could also just be done over for other ethnicities. At the same time, there’s a depressing deterministic quality to the outcome here. The genes that contribute most to extreme longevity don’t seem to be the ones that were previously known to be specifically connected to some disease.

It appears that the people who live to 100 and beyond don’t do so because they have strong genetic defences against stroke or Alzheimer’s or cancer, but because their overall aging clock is slower, and the diseases and disabilities to which they would otherwise be prone are all mutually delayed—in the wording of the study, “compressed”—into the tenth decade of life. More and more, one’s natural lifespan, as Bertrand Russell (1872-1970) joked, appears to depend on a careful choice of ancestors.

It’s alive! A primer on synthetic life

By Colby Cosh - Wednesday, May 26, 2010 at 8:21 AM - 55 Comments

I’ve got a neglected heap of notes for weblogging topics, but Craig Venter’s latest biotechnology stunt metaphorically swept them clear from my desk. It is not easy to comprehend by means of plain English what Venter and his research institute have achieved. The title of their paper for Science offers the best possible short summary: “Creation of a bacterial cell controlled by a chemically synthesized genome.” Reactions range from the alarmist—dear God, he’s created synthetic life!—to the dismissive—bah, it’s not synthetic life at all! (The Raelians, for their part, take the view “He’s created synthetic life, and we think it’s awesome!”)

Here’s the strictly technological significance of what Venter has done: he used computers to create a synthetic genome that never previously existed in nature, turned that information into physically existing DNA, replaced the DNA of an existing organism with the new DNA, and successfully showed that his artificial software “worked”—that it could self-reproduce and serve as the design for functioning progeny. It is the production of an all-new life form from human programming. I do not think Scots SF author Ken MacLeod goes too far when he writes “This is a moment in evolution, the origin of a new kingdom: the Synthetica, as artist Daisy Ginsberg has suggested we call it, supplementing nature’s bacteria, eukarya, and archaea.”

Creationists and Catholics are putting on a brave face, and they have a basic point that cannot be gainsaid. Venter had to follow “God’s” existing “literary rules” of genome construction, so to speak; his artificial genome had to contain essential bits of programming plagiarized from nature, some of which are not fully understood. And nobody can yet imitate “God” in building a cell from scratch: an existing bacterium had to have its own chromosomes scraped out to provide a platform for Venter to build upon. It’s a bit like observing that, yes, this sentence I’m writing right now is completely original in the usual sense, but I haven’t made up any of the words in it completely from scratch, and to be understood as a message, it must follow a certain accepted structure.

That being said, once you’ve gone Gutenberg, there is no going back. The key passage in the Venter paper is perhaps this one [emphasis mine]:

We refer to such a cell controlled by a genome assembled from chemically synthesized pieces of DNA as a “synthetic cell”, even though the cytoplasm of the recipient cell is not synthetic. Phenotypic effects of the recipient cytoplasm are diluted with protein turnover and as cells carrying only the transplanted genome replicate. Following transplantation and replication on a plate to form a colony (>30 divisions or >10⁹-fold dilution), progeny will not contain any protein molecules that were present in the original recipient cell. This was previously demonstrated when we first described genome transplantation. The properties of the cells controlled by the assembled genome are expected to be the same as if the whole cell had been produced synthetically (the DNA software builds its own hardware).

If I had a way of putting that last parenthetical in double-bold face, I’d do it. No, we can’t yet build a cell from scratch, but if we can edit the software of an existing cell to any degree we please—although the process described in the paper is still of a crudity that bleeds forth from its every line—it really doesn’t matter. The descendants will reproduce according to our program, and will be indistinguishable from the descendants of a cell created by God, Klingons, or Santa’s elves. The software builds its own hardware. Sixty-seven years after DNA’s role as a genetic information carrier was confirmed, and 57 years after its structure was ascertained, we can now say that there exists, in the parlance of mathematics, a true constructive proof of this.

But then again, no biologist or other sane person really needed such a proof. The best lay summary of Venter’s achievement that I have found is provided by robotics professor Rodney Brooks, a man who has thought a great deal about the operational definition of life.

..the fact that [Venter's] genome works as a genome is not a surprise to molecular biologists. They have long believed that life is chemistry, and that one string of connected atoms is just as good as another having the same arrangement. They have long ago discounted the idea that there is any sort of specialness imparted to a molecule by its history of production. Molecules have no souls.

But the new cells are also not synthetic life in that the ancestor cell was an existing live cell. It was not built from pieces in the same way that the synthetic genome was built. That is another, perhaps harder technological challenge, but also one that there may be no imperative to try to achieve in the short term; hijacking existing cells may be all that we need to develop all sorts of new synthetic forms.

The press has both overplayed that what has been done is a surprise, and underplayed the interesting challenges that lie ahead, in that their biggest fears do not automatically follow from the current achievement.

Brooks is saying that there are no new theoretical implications from the Venter team’s accomplishment, as there actually were from the Venterian work that preceded the demonstration of synthetic life—namely, paring the smallest genome known to exist in nature down to an even smaller instruction set, and getting humans closer (closer than God or natural selection ever managed) to the theoretical minimum of information needed for a DNA sequence to be meaningful. Playing God? Hell, that’s for amateurs!

That DNA can practically be edited will come as a shock only to those whose anti-materialist or vitalist views depend on clinging to some particular state of human technological ignorance. There are no longer very many biologists in that category. If life can be designed and mass-produced synthetically like machines, there won’t be much ground left on which to argue that living things aren’t machines.

Biologists presented with the Venter news are instinctively contemplating the revival of familiar old forms previously discarded by natural selection, and the synthetic genome adds spice to the ethical debates over whether we would be justified in making a Neanderthal or a woolly mammoth. This is not really a big theoretical deal either. The more important, wider prospect on offer is the ability to recover biodiversity by artificial means, and the eventual end of the rule than “extinction” is the definitive end for a species. The thought of one day being able to see a dodo strut and squawk and lay eggs is romantic (in a way that warms even the stony heart of Darwinian tough-guy Richard Dawkins) and missions of that sort are now one big step closer to fruition.

But the really exciting and scary idea here is the customizability of life, and as Brooks says, we don’t know what limits, other than the obvious physical ones, scientists might ultimately run up against. Let’s note, though, that so-called “genetic modification” in agriculture has already accomplished a lot, even with one hand tied behind its back by trade rules and consumer fears. (What we refer to as “genetic modification” is really just genetic modification 2.0. The hybridization and artificial selection that humans were busily engaged in for several millennia beforehand was 1.0; the stuff we’re talking about in this article is, if you like, version 3.0.) Journalist Quinn Norton offers some wild thoughts about bacteria that “pee out biofuels or Prozac, eat Gulf of Mexico oil, or glow in the presence of melamine, cancer, or anger”. These dreams may transcend what is ultimately feasible. Or they may hint only at a thousandth of a thousandth of the possibilities.

Eating for your genes

By Cathy Gulli - Thursday, May 6, 2010 at 8:00 AM - 0 Comments

ZUMA/KEYSTONE

Few physicians have the cachet or the captive audience of Dr. Mehmet Oz. He’s written half a dozen books, and has been on the The Oprah Winfrey Show no less than 55 times. She nicknamed him “America’s doctor,” and every weekday he hosts his own radio and television talk shows. So, last month, when a segment of Dr. Oz was devoted to “exploring the perfect diet for your genes,” the nascent field of “nutrigenomics” was catapulted into pop science stardom.

“It’s totally sexy,” says Christopher Gardner, a Stanford University researcher who co-authored the study featured on Dr. Oz, which had not yet been published in a peer-reviewed journal as of late April. The study suggests that a simple genetic test (a mouth swab) may pinpoint for individuals exactly what kind of diet they should be on—low-fat, low-carb or balanced—to drop the maximum number of pounds. “Lots of people know they should go on a diet. Lots of people are pissed because they went on the same diet that their friend went on and their friend lost more weight than they did,” muses Gardner, who is also a professor at Stanford’s medical school. Hopefully, this study, he says, “will explain part of that.”

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Aliens among us?

By Kate Lunau - Thursday, April 8, 2010 at 12:30 PM - 3 Comments

Photograph by NASA/Kepler mission/Wendy Stenzel

This month marks the 50th anniversary of a day some say changed the course of science. In April 1960, Frank Drake, an astronomer at the National Radio Astronomy Observatory in West Virginia, turned a radio telescope (basically a huge antenna) toward two nearby stars. Drake thought he might—just might—hear signals broadcast from another planet. “For the first time in history, we had the chance of detecting a civilization no more advanced than our own,” he says today. “For all we knew, every star in the sky had a civilization that was transmitting.”

Of course, Drake didn’t hear any alien broadcasts. But his experiment (dubbed Project Ozma for the princess of the land of Oz) marked the beginnings of what’s called SETI: the search for extraterrestrial intelligence. He’s spent half a century trying to answer one of our most enduring questions: are we alone? Today, an answer seems tantalizingly close. Scientists have now found hundreds of previously unknown planets, and even water in our own solar system; the new Allen Telescope Array, with 350 interlinked radio dishes, promises to vastly improve the search. (It’s run by the University of California, Berkeley and the SETI Institute, where Drake now works.) If the universe really is teeming with life, though, why haven’t we found it yet?

Physicist Paul Davies, who directs Arizona State University’s Beyond Center for Fundamental Concepts in Science, addresses this in his new book, The Eerie Silence: Renewing Our Search for Alien Intelligence. “We need to think more creatively, and give up hope that some benevolent alien community will send us a ‘Hi guys’ message,” says Davies. After all, it takes time for radio signals to travel through space; if we found a civilization 1,000 light years away, it’d take at least 2,000 years for us to send them a message, and get a response back. (“However powerful their instruments, they can’t go faster than light,” Davies says.) Luckily, we don’t need to pick up a message to know for sure we’re not alone. “We merely have to see a footprint,” he says. And scientists are chasing that footprint not only in distant galaxies, but in our own solar system—and here on earth.

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The DNA discount

By Nancy Macdonald - Thursday, July 23, 2009 at 10:20 AM - 3 Comments

Geoffrey Shmigelsky says the best money he ever spent on his health was a $1,000 test he took a year ago. The 41-year-old—who sold Calgary’s largest internet service provider, PSINet, for a “stupid amount of money” a decade ago—spat into a test tube and FedExed the vial to biotech start-up 23andMe in California. Eight weeks later, he sat down to find out his risk for developing everything from heart disease to Alzheimer’s, schizophrenia to prostate cancer—even how likely he was to go bald.

Most of the information was interesting, but benign. However, Shmigelsky did discover that he’s 10 times more likely than average to develop glaucoma and 50 per cent more likely to develop age-related macular degeneration of the eyes. So now he takes lutein, a dietary nutrient that significantly decreases his risk of developing the ocular disease. He’s also learned that he carries a gene putting him at “extremely high risk” for developing gallstones, so he has frequent, thorough ultrasounds to screen for them. “I can do something today to reduce my risks going forward,” he says. “It’s empowering.” Continue…

So who did it? DNA test fingers twins.

By Philippe Gohier - Thursday, March 5, 2009 at 8:00 AM - 0 Comments

One of the most spectacular robberies in German history could end in an acquittal because one of the accused shares his DNA with a twin.

Last January’s multi-million-dollar heist at Berlin’s famous Kaufhaus des Westens department store had all the trappings of a big-budget action flick. Local police believe thieves climbed onto the store’s roof before carefully lowering themselves into its main hall. Once there, they broke into display cases and lifted their contents—all without setting off any motion detectors or alarms. By the time they were done, nearly $10 million worth of jewels and luxury watches were gone.

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