Good Article Review About All Except One.

Type of paper: Article Review

Topic: Women, Health, Genetics, Family, DNA, Cancer, Medicine, Education

Pages: 2

Words: 550

Published: 2020/12/20

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Carl Zimmer “Seeing X Chromosomes in a New Light” nytimes.com JAN. 20, 2014 2
Alexandra Sifferlin  “Human Emotions Are Not as Complex as We Thought”. Time.com Feb. 5, 2014 6
Alexandra Sifferlin. “Humans and Dogs Process Emotions Similarly”. Time.com. Feb. 21, 2014 7
Nicholas Wade. “Researchers See New Importance in Y Chromosome”. nytimes.com. APRIL 23, 2014 8
P. Nash Jenkins   “Squid Protein: Our Best Defense Against Chemical Weapons?”. Time.com. June 17, 2014 10
KIM TINGLEY “The Brave New World of Three-Parent I.V.F.”. nytimes.com. JUNE 27, 2014 11
Kate Lunau “Mackenzee Wittke, a five-year-old Alberta girl with the body of an infant, might just hold the genetic key to how we age”. macleans.ca. July 20, 2014 15
ALAN BERNSTEIN. “Genomics will be at the centre of real health care innovation”. The Globe and Mail. Jan. 01 2015 24
George Johnson. “Random Chance’s Role in Cancer”. nytimes.com JAN. 19, 2015. 25
HELEN BRANSWELL. “Race may influence a woman's breast cancer outcome, study finds”. theglobeandmail.com. Jan. 13 2015 29
KATHRYN DOYLE. “Early childhood neglect hinders brain development”. theglobeandmail.com. Jan. 28 2015 31
Carolyn Y. Johnson. “New research sheds light on cancer, Alzheimer’s origins”. bostonglobe.com. FEBRUARY 18, 201 33
XUHUA XIA. “Even the best DNA databank might not put names to the missing”. theglobeandmail.com. Feb. 27 2015 36
Boston University Medical Center. “Genetic discovery may help determine effectiveness of Huntington's disease treatments”. ScienceDaily. March 2, 2015 38
INSERM (Institut national de la santé et de la recherche médicale). “Repairing the cerebral cortex: It can be done”. ScienceDaily. March 11, 2015 41
Walter and Eliza Hall Institute. “New genome-editing technology to help treat blood cancers”. ScienceDaily. March 12, 2015 42
International & American Associations for Dental Research. “Link between hair disorders and susceptibility to dental caries”. ScienceDaily. March 14, 2015 47
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Carl Zimmer “Seeing X Chromosomes in a New Light” nytimes.com JAN. 20, 2014
The term “X chromosome” has an air of mystery to it, and rightly so. It got its name in 1891 from a baffled biologist named Hermann Henking. To investigate the nature of chromosomes, Henking examined cells under a simple microscope. All the chromosomes in the cells came in pairs.

Henking labeled this outlier chromosome the “X element.” No one knows for sure what he meant by the letter. Maybe he saw it as an extra chromosome. Or perhaps he thought it was an ex-chromosome. Maybe he used X the way mathematicians do, to refer to something unknown.
Today, scientists know the X chromosome much better. It’s part of the system that determines whether we become male or female. If an egg inherits an X chromosome from both parents, it becomes female. If it gets an X from its mother and a Y from its father, it becomes male.
But the X chromosome remains mysterious. For one thing, females shut down an X chromosome in every cell, leaving only one active. That’s a drastic step to take, given that the X chromosome has more than 1,000 genes.
In some cells, the father’s goes dormant, and in others, the mother’s does. While scientists have known about this so-called X-chromosome inactivation for more than five decades, they still know little about the rules it follows, or even how it evolved.
In the journal Neuron, a team of scientists has unveiled an unprecedented view of X-chromosome inactivation in the body. They found a remarkable complexity to the pattern in which the chromosomes were switched on and off.
At the same time, each copy of the X chromosome contains versions of genes not found on its partner. So having two X chromosomes gives females more genetic diversity than males, with their single X chromosome. Because of that, females have a genetic complexity that scientists are only starting to understand.
“Females simply have access to realms of biology that males do not have,” said Huntington F. Willard, the director of Duke University’s Institute for Genome Sciences & Policy, who was not involved in the research.
But while the additional genes provided by their second X chromosome may in some cases provide females with a genetic advantage, X chromosomes also have a dark side. Their peculiar biology can lead to genetic disorders in males and, new research suggests, create a special risk of cancer in females. Understanding X-chromosome inactivation can also shed light on the use of stem cells in therapies.
A Japanese biologist, Susumu Ohno, first recognized X-chromosome inactivation in the late 1950s. In every female cell that he and his colleagues studied, they found that one of the two X chromosomes had shriveled into a dormant clump. Scientists would later find that almost no proteins were being produced from the clump, indicating that it had been shut down.
The British geneticist Mary F. Lyon realized that she could learn more about X-chromosome inactivation by breeding mice, because some color genes sit on the X. In 1961 she reported that female mice sported patches of hair with their mother’s color and others with their father’s.
Getting a deeper look at how females shut down their X chromosomes has remained a challenge in the decades since Dr. Lyon’s discovery. In recent years, Dr. Jeremy Nathans, a Howard Hughes Medical Institute investigator at Johns Hopkins University, and colleagues have developed a way to make X chromosomes from different parents light up. They inserted a set of genes into the X chromosomes of mice. The genes produced a green fluorescent protein, but only if their X chromosome was active and they were exposed to a particular chemical trigger.
Dr. Nathans and his colleagues engineered other mice to produce a red protein from active X chromosomes in response to a different chemical. The researchers bred the altered mice to produce female pups. The pups inherited a green X from one parent and a red one from the other.
The scientists then added both of their color-triggering chemicals to the mouse cells. The cells lit up in a dazzling mosaic of reds and greens. One cell might shut down the mother’s X, while its neighbor shut down the father’s.
In recent years, scientists have increasingly appreciated that our cells can vary genetically — a phenomenon called mosaicism. And X-chromosome inactivation, Dr. Nathans’s pictures show, creates a genetic diversity that’s particularly dramatic. Two cells side by side may be using different versions of many different genes. “But there is also much larger-scale diversity,” Dr. Nathans said.
In some brains, for example, a mother’s X chromosome was seen dominating the left side, while the father’s dominated the right. Entire organs can be skewed toward one parent. Dr. Nathans and his colleagues found that in some mice, one eye was dominated by the father and the other by the mother. The diversity even extended to the entire mouse. In some animals, almost all the X chromosomes from one parent were shut; in others, the opposite was true.
Dr. Nathans speculates that using chromosomes from both parents is especially useful in the nervous system. It could create more ways to process information. “Diversity in the brain is the name of the game,” he said.
But the X chromosome may also pose a risk to women. Dr. Lee and her colleagues have found that when they shut down Xist in female mice, the animals were more likely to develop cancer. She suspects that when a cell stops making Xist, its inactivated X chromosome wakes up. The extra proteins it makes can drive a cell to grow uncontrollably.
“That has bearing on stem cell therapy,” she added. When stem cells are reared in the lab, they sometimes stop making Xist as well. Dr. Lee is concerned that female stem cells may rouse sleeping X chromosomes, with devastating consequences.
Before stem cells can be safely used in medical treatments, we may finally need to solve the mystery that Henking originally labeled with an X.
Zimmer, Carl. “Seeing X Chromosomes in a New Light”. nytimes.com. 20 Jan. 2014. Web. 15 Mar. 2015. Available at http://www.nytimes.com/2014/01/21/science/seeing-x-chromosomes-in-a-new-light.html
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Alexandra Sifferlin  “Human Emotions Are Not as Complex as We Thought”. Time.com Feb. 5, 2014
 

Alexandra Sifferlin @acsifferlinNew study says we only have four: happy, sad, afraid/surprised, and angry/disgusted

Forget the conventional thinking that humans are complex creatures with a wide range of emotions. New research suggest we only have four.
The widely held scientific assumption is that we have six emotions: happy, surprised, afraid, disgusted, angry, and sad. But a new study from University of Glasgow scientists published in the journal Current Biology this week says humans may only have four biologically based emotions: happy, sad, afraid/surprised, and angry/disgusted.
Participants of the study were shown computer-generated facial expressions and asked to identify the emotion from among the six predominantly accepted ones. At the start, anger and disgust, as well as fear and surprise, looked very similar. For example, surprise and fear have similar eyebrow movements. As the expressions developed, though, participants were able to distinguish between them, but only over time, suggesting that differences in anger, disgust, surprise, and fear are the result of social evolution rather than biological.

Emo kids everywhere are processing this news with a much more limited scope of emotion than before.

Sifferlin, Alexandra. “Human Emotions Are Not as Complex as We Thought”. Time.com. 5 Feb. 2015. Web. 15 Mar. 2015. Available at http://time.com/4649/human-emotions-not-as-complex-as-we-think/
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Alexandra Sifferlin. “Humans and Dogs Process Emotions Similarly”. Time.com. Feb. 21, 2014

Similar areas of the brain are dedicated to recognizing voice and processing emotion

Oliver Rossi / Getty Images
Humans and dogs both have similar areas of their brains dedicated to processing voice and emotions, a new study finds.
Researchers scanned 11 dogs’ brains and 22 humans’ brains as they listened to dog and human sounds: barking, laughing, whining, and crying.
Similar regions of the brain lit up for dogs and humans when they listened to sounds made by their own species, according to the study published in the journal Current Biology. There were also similarities in brain reactions when the participants heard emotional sounds. Researchers remarked that the finding could explain why dogs tend to be attuned to humans’ emotions.
“At last we begin to understand how our best friend is looking at us and navigating in our social environment,” study author Attila Andics of MTA-ELTE Comparative Ethology Research Group in Hungary in a statement.
Sifferlin, Alexandra. “Humans and Dogs Process Emotions Similarly”. Time.com. 21 Feb. 2014. Web. 15 Mar. 2015. Available at http://healthland.time.com/2014/02/21/humans-dogs-brains/
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Nicholas Wade. “Researchers See New Importance in Y Chromosome”. nytimes.com. APRIL 23, 2014

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There is new reason to respect the diminutive male Y chromosome.
Besides its long-known role of reversing the default state of being female, the Y chromosome includes genes required for the general operation of the genome, according to two new surveys of its evolutionary history. These genes may represent a fundamental difference in how the cells in men’s and women’s bodies read off the information in their genomes.
When researchers were first able to analyze the genetic content of the Y chromosome, they found it had shed hundreds of genes over time, explaining why it was so much shorter than its partner, the X chromosome. All cells in a man’s body have an X and a Y chromosome; women’s have two X chromosomes.
The finding created considerable consternation. The Y had so few genes left that it seemed the loss of a few more could tip it into extinction.
But an analysis in 2012 showed that the rhesus monkey’s Y chromosome had essentially the same number of genes as the human Y. This suggested that the Y had stabilized and ceased to lose genes for the last 25 million years, the interval since the two species diverged from a common ancestor.
Two new surveys have now reconstructed the full history of the Y chromosome back to its evolutionary origin. One research group was led by Daniel W. Bellott and David C. Page of the Whitehead Institute in Cambridge, Mass., and the other by Diego Cortez and Henrik Kaessmann of the University of Lausanne in Switzerland. Their findings were reported on Wednesday in the journal Nature.
In the past 12 years, with the help of the genome sequencing centers at Washington University in St. Louis and the Baylor College of Medicine in Houston, Dr. Page’s group has decoded the DNA sequence of the Y chromosome of eight mammals, including the rhesus monkey and humans. The Y chromosome is so hard to decode that many early versions of the human genome sequence just omitted it. Dr. Kaessmann’s group, on the other hand, devised a quick method of fishing out Y chromosome genes by simply comparing the X and Y DNA of various species and assuming that any genetic sequences that did not match to the X must come from the Y.
Dr. Kaessmann calculates that the Y chromosome originated 181 million years ago, after the duck-billed platypus split off from other mammals but before the marsupials did so.
In some reptiles, sex is determined by the temperature at which the egg incubates. Genetic control over sex probably began when a gene on one of the X chromosomes called SOX3 became converted to SRY, the gene that determines maleness, and thus the Y chromosome came into being.
Recombination creates novel arrays of DNA that keep genes adapted to the environment; without recombination they decay and are shed from the genome.
The reconstructions by the Page and Kaessmann groups show that most such genes were shed almost immediately and that the few genes remaining on the Y have been stable for millions of years.
One of these genes is SRY, and others are involved in sperm production. A third category of genes is unusual in being switched on not just in the testis but in tissues all over the body. These active genes, of which there are 12 in humans, all have high-level roles in controlling the state of the genome and the activation of other genes.
The 12 regulatory genes have counterpart genes on the X with which they used to recombine millions of years ago. They escaped the usual decay caused by lack of recombination, presumably being kept functional by purifying selection, a geneticists’ term meaning that any mutations were lethal to the owner. They have, however, become somewhat different from their 12 counterpart genes on the X.
This means that female, or XX, cells have a slightly different set of these powerful genes from male or XY cells, since the X and Y genes are producing slightly different proteins. In females, usually one X chromosome is inactivated in each cell, but the 12 genes are so important that they escape inactivation, and XX cells, like XY cells, receive a double dose of the gene’s products.
“Throughout human bodies, the cells of males and females are biochemically different,” Dr. Page said. The genome may be controlled slightly differently because of this variation in the 12 regulatory genes, which he thinks could contribute to the differing incidence of many diseases in men and women.
Differences between male and female tissues are often attributed to the powerful influence of sex hormones. But now that the 12 regulatory genes are known to be active throughout the body, there is clearly an intrinsic difference in male and female cells even before the sex hormones are brought into play.
“We are only beginning to understand the full extent of the differences in molecular biology of males and females,” Andrew Clark, a geneticist at Cornell University, wrote in a commentary in Nature on the two reports.
Wade, Nicholas. “Researchers See New Importance in Y Chromosome”. nytimes.com. 23 Apr. 2014. Web. 15 Mar. 2015. Available at http://www.nytimes.com/2014/04/24/science/researchers-see-new-importance-for-y-chromosome.html
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P. Nash Jenkins   “Squid Protein: Our Best Defense Against Chemical Weapons?”. Time.com. June 17, 2014

 P. Nash Jenkins  

June 17, 2014
June 17, 2014
    

If engineered correctly, the enzyme can "chew up" toxic agents in the human body

A team of researchers at the University of Tennessee at Knoxville has identified an enzyme produced in the bodies of squid that may be effective in breaking down nerve gasses and other deadly chemical weapons.
The team’s study, recently published in the Journal of Physical Chemistry, focused on engineering the improvement of these proteins — known as “bioscavengers” — that “chew up” nerve agents like sarin, a chemical infamous for its use as a weapon in the ongoing Syrian civil war and in a terrorist attack on the Tokyo subway in 1995.
The team aspires to create a prophylactic drug from these enzymes that will mitigate their harmful effects on humans, but first they must modify the enzymes to ensure that the human body won’t destroy them first.
“Using an enzyme from a squid as a bioscavenger in humans is problematic because the human body will recognize it as a foreign substance and chop it up,” said research team member Jerry Parks, adding that “other groups have already shown possible ways to get around that problem.”
Jenkins, Nash. “Squid Protein: Our Best Defense Against Chemical Weapons?”. Time.com. 17 Jun. 2014. Web. 15 Mar. 2015. Available at http://time.com/2888387/squid-protein-our-best-defense-against-chemical-weapons/
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KIM TINGLEY “The Brave New World of Three-Parent I.V.F.”. nytimes.com. JUNE 27, 2014

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In August 1996, at St. Barnabas Medical Center in Livingston, N.J., a 39-year-old mechanical engineer from Pittsburgh named Maureen Ott became pregnant. Ott had been trying for almost seven years to conceive a child through in vitro fertilization. Unwilling to give up, she submitted to an experimental procedure in which doctors extracted her eggs, slid a needle through their shiny coat and injected not only her husband’s sperm but also a small amount of cytoplasm from another woman’s egg. When the embryo was implanted in Ott’s womb, she became the first woman on record to be successfully impregnated using this procedure, which some say is the root of an exciting medical advance and others say is the beginning of the end of the human species.
The fresh cytoplasm that entered Ott’s eggs (researchers thought it might help promote proper fertilization and development) contained mitochondria: bean-shaped organelles that power our cells like batteries. But mitochondria also contain their own DNA, which meant that her child could possess the genetic material of three people. In fact, the 37 genes in mitochondrial DNA pass directly from a woman’s egg into every cell of her offspring, including his or her germ cells, the sperm or eggs that eventually produce the next generation — so if Ott had a girl and the donor mitochondria injected into Ott’s egg made it into the eggs of her daughter, they could be passed along to her children. This is known as crossing the germ line, something that scientists generally agree is a risky proposition.

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Ott, who is Catholic, remembers weighing whether altering the makeup of her descendants in this way was O.K. “Being a person who’s been involved in science my whole life, the way I looked at it is: God gives us doctors to help us, and they help us with things like infertility,” she told me recently. As far as anyone knows, mitochondrial DNA (mtDNA) governs only basic cellular functions; Ott understood that her and her husband’s nuclear DNA would determine their child’s characteristics — height, eye color, intelligence and so on. “If I was doing something like, say, I only wanted a blond-haired girl, I would feel that was unethical,” she said. “But what I was trying to do was use whatever medical procedures were available to me to get pregnant, and I didn’t think that was unethical.” In May 1997, she gave birth to a healthy baby girl.
Two months later, her doctors published her case in the journal Lancet; soon, at least seven other U.S. clinics were doing the injection. Because the amount of donor mitochondria added to Ott’s egg was small, it was unclear how much third-party DNA would be present in the cells of her daughter. Ott says her doctors ran tests and did not find any, but it has been found in two other children born from the procedure. Although I.V.F. drugs and devices are regulated by the Food and Drug Administration, I.V.F. procedures (like all medical procedures) are generally not. But what media outlets came to call “three-parent babies” compelled the agency to take action. In 2001, the F.D.A. informed I.V.F. clinics that using a third person’s cytoplasm — and the mtDNA therein — would require an Investigational New Drug application.
A meeting before an F.D.A. committee followed, at which the clinics presented their research. While at least 30 women became pregnant through the injections, it was unclear what role the third-party cytoplasm played in their fertility. And there were safety concerns. Two embryos with Turner syndrome, typically a rare chromosomal abnormality, occurred after the procedure; one miscarried, the other was aborted. Further, not all of the children born from the procedure in the United States were being tracked. (They would be teenagers now, whose whereabouts and health are, for the most part, unknown.) “I think it is pretty ridiculous how little data there is to support any of this, and that worries me,” the acting chairman of the F.D.A. committee, Daniel Salomon, a professor at the Scripps Research Institute, told the embryologists in his closing remarks. The “drug,” such as it was, has never been approved.
But now, more than a decade later, two research groups in the United States and one in Britain each believes it has nearly enough data to begin clinical trials for a new technique based on the transfer of mitochondria — only in this case, researchers want to pair the nuclear DNA of one egg withall the mitochondria of another. Their aim is not to cure infertility. Rather, they hope to prevent a variety of devastating diseases caused by mutations in mtDNA. The new technique, which they call mitochondrial-replacement therapy, is far more advanced than the cytoplasm injection — and the researchers have studied the procedure’s impact on animals and human cells up to a pivotal point: They have created what appear to be viable three-parent embryos. They have yet to implant one in a woman, though. In Britain, national law prohibits altering the germ line, but Parliament is very likely to vote later this year on whether to allow mitochondrial replacement to move forward. Likewise, this February, the F.D.A. held a meeting to examine the possibility of allowing clinical trials. If either gives the go-ahead, it will be the first time a government body expressly approves a medical procedure that combines genetic material of three people in a heritable way. The historic nature of the moment has turned the technique into a symbol, a red line separating humanity from a dystopian or progressive future, depending on how you look at it. In the months leading up to the meeting, the F.D.A. received several hundred emails from members of the public objecting to the idea of three-parent embryos on grounds that included: “It’s bizarre”; “You are walking in Hitler’s footsteps if you allow this”; and “We will have a world of mad scientists.”
As the scientists who were pressing for mitochondrial replacement kept pointing out, these fears were somewhat unfounded. It cannot allow people to design babies to their specifications — in fact, it comes with most of the same risks and uncertainties that attend old-fashioned reproduction. It’s hard not to wonder if the argument is really about the technique or the sacrosanctity of DNA. Is our fear of crossing the germ line causing us to block a technology that could improve people’s lives, and if so, is the fear itself a thing we should also be afraid of?
What often gets lost in the loaded language of the debate over three-parent babies is the fact that ordinary human reproduction is, by definition, genetic modification. The risks involved are unpredictable and potentially tragic; the subject of the experiment is a future person who cannot consent. We constantly try to control this process, to “design” our children, starting with our choice of sexual partner. During pregnancy, we try to “enhance” them by taking folic acid, not smoking, avoiding stress; once they’re born, we continue the process with vaccines and nutritious food, education, clean air and drinking water. Some of these pre- and postnatal environmental factors, we now know, change their biology in heritable ways. Is mitochondrial replacement, because it takes place in a petri dish, any more unnatural or morally repugnant than this? Would the answer change if the technique turns out to cure age-related infertility in addition to preventing disease?
At first, Egli did not want me to watch him perform mitochondrial replacement on human eggs. He was afraid I would distract him. The eggs were precious: both challenging for researchers to obtain and a reminder of our fragile origins, and he was anxious not to slip and damage one. Several weeks after the F.D.A. meeting, he relented, on the condition that I camouflage myself among a cluster of CO2 tanks in the corner of the lab and not ask any questions. “If you look at what I’m doing,” he said, “there is really nothing to be afraid of, I think.”
The eggs arrived by cab, in an incubator shaped like a tackle box. An hour earlier, an embryologist in Midtown Manhattan suctioned them from a young donor; two lab technicians poured the musky pink fluid he had retrieved into dishes, which they slid under microscopes, searching for diamond-bright specks, counting, cleaning and packing them in vials. At the lab, uptown, Egli received the box in a darkened room. He opened it, took out a test tube, and used a pipette to transfer its contents into a dish. He peered at it through a microscope. His left hand twirled the knobs of the microscope, his right controlled a hollow extraction needle. His foot worked a pedal that lasered a hole in the coat of one of the eggs, the pretty zona pellucida. Bent over the viewfinder, only the muscles in his forearms twitched. For just a moment, he flicked on the monitor and the egg appeared, a luminous round moon, as if his instrument were a telescope aimed not at a single cell but at the night sky. He pointed at the faintest of shadows on its face — the spindle of chromosomes beneath the surface. The laser click-clicked, Egli maneuvered the needle into the hole it left behind and applied suction. The egg tugged back, released and then, there in the needle, was the genome, ready for transplant: an oblong seed, arbiter of all life.
Tingley, Kim.” The Brave New World of Three-Parent I.V.F.”. nytimes.com. 27 Jun. 2014. Web. 15 Mar. 2015. Available at http://www.nytimes.com/2014/06/29/magazine/the-brave-new-world-of-three-parent-ivf.html
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Kate Lunau “Mackenzee Wittke, a five-year-old Alberta girl with the body of an infant, might just hold the genetic key to how we age”. macleans.ca. July 20, 2014

Kate Lunau

July 20, 2014
Todd Korol for Maclean’s
Every year, on her birthday, Mackenzee Wittke gets the same cake. It’s a homemade Rice Krispies treat, gooey with marshmallows and butter, moulded into the shape of a number: one for her first birthday, two for her second, and so on. Every year, as she hits another milestone, her parents, Kim and Matt Wittke—who live in the Edmonton suburb of Sherwood Park—snap a photo of her next to the cake. These pictures are a timeline of five-year-old Mackenzee’s life so far, and they reveal something startling: From one year to the next, as the number-shaped cakes tick upward, this girl has barely aged. Today, about to turn six, Mackenzee weighs 16 lb. and measures just under 30 inches. Doctors and specialists say that, physically and cognitively, she’s the age of a six-month-old baby.
No medical expert has ever been able to explain Mackenzee’s condition; all genetic and chromosomal tests come back normal. One scientist, who has dedicated his career to understanding aging, has a theory about what affects her. Solving the mystery of why Mackenzee Wittke seems frozen in time will, Richard Walker believes, answer one of life’s biggest questions: how we grow old.
The Wittkes are among a tiny group of families participating in his new study, which will sequence the genomes of seven girls (six in the U.S., and Mackenzee) who all seem impervious to aging. For the Wittkes, it’s an opportunity to better understand their daughter’s condition. Mackenzee wears baby onesies, and rides in an infant car seat. She can’t walk or speak, but she will giggle and coo; when she’s upset or hurt, she cries. Her condition has brought with it a suite of medical problems, which flare up unpredictably, and have seen her in and out of hospital. Her life expectancy is unknown. As for Walker’s study, “I think this may be our biggest shot at finding some answers,” says Kim Wittke, 37.
Walker’s work could finally shed light on what ails Mackenzee. “What if there’s another Mackenzee born tomorrow?” Kim says. “Those parents could have some answers, where we never did.” For Walker, now 74, this would be a welcome outcome. But he also sees in Mackenzee a chance to find a way to slow aging, or maybe even to stop it altogether.
Aging is a part of life, one we accept as a given. But, while there are lots of theories—maybe it’s preprogrammed into our genes; maybe environmental factors gradually damage our cells and, like a rusted old car, we begin to break down—scientists still can’t say exactly why our muscles slowly weaken, and our organs fail. For Walker, a retired professor of biochemistry and molecular biology at the University of South Florida in Tampa, and editor-in-chief of the journal Clinical Interventions in Aging, this question has been a lifelong fixation. During the Vietnam War, he served with the military medical corps, on the island of Guam, where he saw his share of wartime injuries. But many types of injury, he notes, are still more treatable than age-related diseases, like cancer. “Aging has always been repugnant to me,” he says. “I didn’t like the way my grandparents suffered. My grandma died of pancreatic cancer. Something in me found that to be abysmal.”
Walker, whose career spans almost 50 years, crafted his own hypothesis to explain the decay of age. “We start off life as two cells,” he says. “These have to become a mature man or woman.” He believes each of us may contain a genetic program that pushes us toward sexual maturity, while coordinating the body’s systems to grow and work together, like instruments playing in an orchestra. But once we reach our physical peak, our body’s tendency to remodel itself doesn’t switch off. Something, perhaps a gene (or genes), keeps driving it forward, and problems begin to accumulate. Its systems fall out of sync, and the music, so to speak, grows dissonant. As age grinds away at us, its accompanying diseases—cancers, Alzheimer’s, heart disease—start to show up.
Walker saw no way of testing his theory, until one evening in 2005. “I was sitting at my desk, and my wife was in another room,” he recalls. “She yelled, ‘Rich, you’d better come look at what’s on TV.’ That’s when I discovered Brooke.” Brooke Greenberg, who lived near Baltimore with her family, was a preteen at the time; she resembled an infant. Nobody could say why. (Her pediatrician referred to her condition as “syndrome X,” which is sometimes applied to others in Walker’s group, too.) “I thought, ‘Maybe she has a mutation of this theoretical gene,’ ” Walker says. He reached out to the Greenbergs, who let him examine Brooke. Her genetic markers were normal; her condition couldn’t be pinned on disruptions in her hormones, chromosomes, or anything else known to cause developmental delays. Brooke’s development was not only stalled, but “disorganized,” as Walker puts it, which his theory predicted: Her various physical parts weren’t developing in sync. Her program had gone out of whack, and the instruments in the orchestra weren’t playing together.
At 16, Brooke’s height and weight were those of an 11-month-old; she showed no signs of puberty. Her teeth and bones resembled those of a preteen, yet the length of her telomeres (the tiny caps on our chromosomes whose length corresponds to biological age) were right for her 16 years. A bona fide medical mystery, Brooke’s story attracted national media attention—she was on TLC, Katie Couric, in People—and other families reached out to Walker about their kids. In most cases, he could find a cause for the child’s condition. But, in a few of them, he couldn’t.
About four years ago, Kim Wittke, who used to work in the insurance industry but now stays home with Mackenzee, also watched a TV show about Brooke Greenberg. “At the time, I think she was 15 or 16, but she looked like a toddler,” Kim says. “Something resonated with me. Mackenzee was 18 months, but she looked like a newborn. I remember them saying, ‘Nothing grows but her hair and fingernails.’ And I said, ‘Yeah. That’s the same with Mackenzee.’ ” She reached out to Walker, but it wasn’t until last summer that the Wittkes felt ready to work with him. “We’ve kind of run out of options here,” Kim says. “There are days where it just turns in you, and you’re ready to find out what’s going on.”
It was around that time that Brooke’s father abruptly broke off contact with Walker. (Howard Greenberg declined to comment for this story.) As Walker set out to find other subjects like Brooke, the Greenbergs formed a new alliance, with Eric Schadt, director of the Icahn Institute for Genomics and Multiscale Biology at Mount Sinai Hospital in New York. When Greenberg first told Schadt that his daughter, then 19, resembled a toddler, “I was a little skeptical,” Schadt tells Maclean’s. “It seemed hard to believe.”
Schadt sequenced Brooke’s genome, parsing six billion letters of DNA to search for tiny quirks that might have contributed to her condition. (His team sequenced the genomes of her parents and three developmentally normal sisters, too.) That left him with a handful of genes that “look interesting,” Schadt says. His team has created a line of stem cells from Brooke’s skin, and are using them to grow liver cells, fat cells, neurons, and other building blocks of her body, to study the impact of each mutation, and how it may relate to aging and disease. If any of these genes are connected to aging, Schadt suggests, manipulating them could boost longevity and help erase age-related disease. “We’re on a path where we will absolutely gain control over aging,” he says.
Walker sees it, too. Imagine switching off the right gene in a healthy 20-year-old, he suggests, whose body is developmentally mature, its systems working perfectly in sync, and hasn’t yet begun to crumble with age. “Here’s the science fiction,” Walker says. “We could create a biological immortal.”
Schadt and Walker praise each other’s work, although, in a sense, they’re rivals; each takes a different approach. Walker, for his study, has collected blood samples from seven girls and their family members: 36 people, all told. Each will have his or her genome sequenced. At the University of California at Los Angeles, a collaborator will also perform epigenetic studies to help determine these girls’ “biological age,” Walker says. One of his subjects is 25, he notes, but looks like she’s about seven years old. “So, biologically, is she 25, or seven?” After identifying the most interesting mutations, Walker plans to test any that seem related to growth or aging, in a mouse. “You take a young mouse, shut that gene off,” and see if the mouse is still able reproduce past the point when fertility would normally be lost to old age, Walker explains. If so, it’s possible this scientist will have finally found his long-hypothesized aging switch.
If a true biological clock does exist, in these girls it’s broken. Because their development is “disorganized,” they have been left vulnerable to disease. Each girl (all of Walker’s subjects are girls, but he doesn’t know why; it could be meaningful, or just a coincidence) suffers from multiple health problems. Mackenzee has pulmonary hypertension and serious stomach issues that led to the removal of half her colon. She takes several medications daily, including heart medication, a diuretic and an antibiotic. She consumes baby formula through a feeding tube and needs her oxygen intake topped up through nasal prongs. Her “perpetual youth,” for what it’s worth, has come at a high cost.
It’s a Thursday in June, around 4 p.m., and Matt Wittke is coming home from work. He pulls into the garage, in a neatly kept cul-de-sac surrounded by parks, walking trails, highways and strip malls, and heads inside. His oldest daughter, Emilee, who’s about to finish Grade 3, sits at the table working on an origami project, as Kim bustles around the kitchen. Mackenzee, reclined in a baby bouncer seat, smiles brightly when she sees her dad. Matt, who works for Bradken, a major supplier of pipe to the Alberta oil sands, picks up his daughter and holds her in his lap, as Kim gets dinner ready. “Matt, would you carve the chicken?” Kim asks, and he puts The Little Mermaid on TV for Mackenzee, and goes to help Kim.
The first sign Mackenzee was different came during Kim’s pregnancy, when doctors detected heart and brain abnormalities on her standard 20-week ultrasound scan. This prompted a series of tests, from more ultrasounds to blood work to an MRI, but no real answers. Fearing possible complications, Kim declined amniocentesis, which can diagnose chromosomal problems in a fetus, including Down’s syndrome. (The test, which involves inserting a needle into the uterus, slightly ups the risk of miscarriage.) She’s happy she made that decision. “The amnio would have shown that all her chromosomes are normal,” Kim says. “I think I would have prepared myself a bit differently, hearing that.”
As it was, doctors told her Mackenzee was extremely small for her gestational age. She was in the 10th percentile; then the fifth; then the third; finally, she dropped off the charts. Four weeks shy of the due date, doctors determined they’d need to deliver the baby. Kim’s voice still gets shaky when she recalls Mackenzee’s first days. As she recovered from delivery, “my parents and Kim’s and I sat down with the doctor,” Matt says. “They said, ‘Take lots of pictures. She’ll be gone in a week.’ ”
Doctors tested for “one syndrome after another,” Kim says, from Down’s to trisomy 18 (half of all infants with this genetic disorder don’t survive beyond their first week). Mackenzee spent her first six months in hospital before coming home. Doctors said there was a slim chance she’d see her fifth birthday, yet she has survived. To this day, her only medical diagnosis is pulmonary hypertension, Kim says.
Of the genetic and chromosomal testing she’s since undergone, “what we have is all normal,” says Lyle McGonigle, Mackenzee’s trusted pediatrician since she was two months old. With no better explanation for her condition, the front of her chart says “ECS” in big, handwritten letters: “Extremely cute syndrome,” a joke Kim likes to make. (“It’s inherited from the mother,” Kim says.) McGonigle, who’s been practising for 30 years, focuses on special-needs kids. “I’d say she has the Mackenzee Wittke syndrome,” he says, “because she’s unique.”
The Wittkes long ago adapted to a new way of life—one that, today, feels normal. Because of a sensitivity to light, Mackenzee can’t be outside in the bright sun, and family outings take a fair bit of planning. They find other ways of including their little daughter: In their “family dance parties,” Kim, Matt and Emilee play music and dance around Mackenzee, as she giggles away. “Emilee’s taken her hits sometimes, when we’ve planned something fun and it has to be cancelled because Mackenzee was sick,” Kim says, but they’ll bring in respite care now and then to look after Mackenzee, and take Emilee out somewhere, maybe to a movie. Emilee dotes on her sister. Despite an age gap of just three years, Emilee can cradle Mackenzee—“Kenzee,” she calls her—in her lap. “We’ve been told many times, when she’s sick even with a bad virus: This may be what takes her,” Kim says. “We’ve learned to take it one day at a time. Sometimes that’s too much, and it’s five minutes at a time. I put her to bed every night, give her a kiss, tell her how much I love her, and pray I get another day with her.”
If anyone can relate, it’s Mary Margret Williams, mother of Gabrielle (who goes by Gabby), a nine-year-old in Billings, Mont., and another participant in Walker’s study. Gabby’s symptoms aren’t identical to Mackenzee’s—she can feed from a bottle and is partially blind—but she also wears baby onesies and travels in a stroller. Gabby weighs 12 lb., five ounces. “All her life now, they’ve told me: ‘This little girl’s not going to last very long,’ ” says Williams, who has six children (Gabby is second-oldest). “Whenever she gets sick, it’s like, this is it. But she pulls herself back up, and sticks with us.”
In October 2013, Brooke Greenberg died at age 20. No cause of death was publicly disclosed, but, like Mackenzee and Gabby, she’d suffered various health problems. That’s the irony: These ageless children remain, in reality, quite fragile. When McGonigle speaks about Mackenzee, he’s blunt. “The prognosis is grave,” he says. “She could die anytime, and someday she will, from the complications of one of the problems she has. But that day is not today; and it wasn’t yesterday; and it may not be tomorrow. It may be six months from now. It may be 10 years from now; I don’t know. As long as her life is good, we should support her.” Mackenzee is happy and well cared for, he says, despite all the tests and procedures she’s undergone. “It’s a tribute to her parents. They’ve dedicated themselves to making this child’s life as good as it can be.”
Neither Kim nor Mary Margret shares Walker’s desire to find an off switch for aging—for us all to remain perfect 22-year-olds forever. “Our goal is not to have a fountain of youth,” says Mary Margret, a staunch Catholic. “I think we’re all meant to be babies, and grow old and die, and that’s the way God made our world.” Although she and Kim have never met or spoken, both express a desire for Walker’s research to help slow the age-related diseases that are on the rise, such as Alzheimer’s, cancer and heart disease. “If my daughter can help with that, I think it would be astounding,” Kim says. “But the main thing, for us, is to find out something for Mackenzee.”
When asked whether we’ll truly understand aging within his lifetime, Walker acknowledges that the answer is probably no. Despite his vigorous exercise regimen, and the vitamins he takes, “I don’t expect to live beyond the normal lifespan,” he says, “maybe another 10 years.” Both he and Schadt know immortality is a polarizing topic. “Most people I’ve talked to want to live forever,” Schadt says. “But there are such dramatic social implications, it’s overwhelming.” Walker has heard the objections—that the planet is overpopulated; that we weren’t meant to live forever—but he doesn’t entertain them. “These are not issues I’m willing to enter into. I’m strictly a scientist,” Walker says. “Even if I find out I’m wrong, I will be happy.”
Time is ticking down, and he’s moving as fast as he can. By August, Walker expects to have results from sequencing the genomes of the seven girls; then, he’ll start drilling into the various mutations to see which ones are good candidates for further examination. That same month, Mackenzee will hit another landmark: her sixth birthday. There will be another photo taken, of her next to a six-shaped Rice Krispies cake. Although she won’t be able to eat a slice, her parents will touch it to her lips. She likes the sweet taste.
In September, for the first time, Mackenzee is going to school. Kim has enrolled her in a Grade 1 program in Sherwood Park, for medically fragile kids (there will be only five or six in her class). They’re having a tiny wheelchair built, to “give her a different perspective on the world,” Kim says. Instead of facing backward toward her parents, as she does in the stroller, Mackenzee will look forward. For Kim and Matt both, Mackenzee’s transition into Grade 1 is “nerve-wracking,” Kim says. They worry about exposure to germs; about this little girl being out of their sight, even for a few hours a day. “She’s been my sidekick for almost six years,” Kim says. But the days keep moving forward, and her parents don’t want her to miss out. As Kim says, “Mackenzee’s got to live her life.”
Lunau, Kate. “The little girl who may hold the secret to aging”. Maclean`s. 20 Jul. 2014. Web. 15 Mar. 2015. Available at http://www.macleans.ca/society/health/the-little-girl-who-may-hold-the-secret-to-aging/
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ALAN BERNSTEIN. “Genomics will be at the centre of real health care innovation”. The Globe and Mail. Jan. 01 2015

ALAN BERNSTEIN

Contributed to The Globe and Mail
Published Thursday, Jan. 01 2015, 8:00 AM EST
Last updated Thursday, Jan. 01 2015, 8:00 AM EST
26 comments
 
 
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Alan Bernstein is the president and CEO of CIFAR (the Canadian Institute for Advanced Research), and was the founding president of the Canadian Institutes of Health Research.
In June of last year, federal Minister of Health Rona Ambrose launched a new Advisory Panel on Healthcare Innovation. This important panel, chaired by Dr. David Naylor, is charged with advising government on areas of innovation that could bring the greatest value to Canada’s health care system.
Two months later, British Prime Minister David Cameron launched the 100,000 Genomes Project. Its goal is to sequence the complete genomes of 100,000 people with cancer or other diseases and ultimately relate these genetic changes to better diagnostics and treatments. This project is feasible because the cost and time required to sequence complete human genomes has fallen from $3-billion and four years, to about $1,000 and less than a week.
The information emerging from genomics heralds a new era of personalized or precision medicine. New ways of diagnosing, treating and preventing disease will be based on our rapidly emerging understanding of human health and disease.
Treating disease based on understanding seems intuitively obvious: how can you fix a car if you don’t know what’s wrong with it? But when I started out in cancer research in the 1970s, there were only vague hints of what lay behind the abnormal behavior of cancer cells. Consequently, there was no obvious path forward.
Today, we know that all cancers result from changes in our genes. And we now have the molecular and computational tools to scan the three billion bases of DNA that make up our genome, and identify the changes that are contributing to the cancer in any given patient.
Contrast this with schizophrenia, bipolar disease, and age-related dementia. Twenty per cent of Canadians will experience a mental illness sometime over their lifetimes. Despite their importance, this large and diverse group of brain disorders is poorly understood. As a result, diagnostic and therapeutic approaches are neither precise nor effective, nor do we have a clear path forward. But our experience cracking the cancer problem will soon transform how we diagnose, treat or prevent this complex set of human illnesses.
At a recent meeting of CIFAR’s program in genetic networks, CIFAR Fellows from the University of British Columbia, the University of Toronto and the Hospital for Sick Children presented groundbreaking research on new ways to analyze and understand genomic alterations involved in cancer, autism, spinal muscular atrophy and other diseases. This research is opening up new understanding of the consequences of these genetic alterations, and new ways of diagnosing disease, identifying at-risk individuals, and developing better drugs.
As the Naylor panel contemplates changes in health care delivery, there is a larger lesson to learn from this research: a modern, cost-effective health care system is not the old system plus genomics. It will be a new health care system, an entirely new paradigm for organizing and implementing care based on our emerging understanding of human biology and the complex interactions between our genetic inheritance and our life experiences. It is not nibbling around the edges of the health care system, tinkering with the odd change here or there. Rather, it will demand a new way of organizing health care, requiring new skills and new infrastructure.
I have two recommendations for the Naylor Committee: first, don’t focus on process and governance. That’s a uniquely Canadian pastime and an excuse for avoiding real change. Instead, focus on building a health system for the 21st centure, not the 20th. In partnership with the provinces, the federal government should launch a decade-long multimillion dollar initiative whose goals are threefold: first, to employ the new science of “omics” to understand the underlying biology of human health and disease and to integrate that understanding into rapid and precise clinical diagnostics; second, to harness that understanding to develop, in partnership with industry, precision therapies that are targeted to the molecular alterations responsible for disease; and third, to develop targeted prevention strategies based on our emerging ability to identify individuals at risk based on the interplay between our genetic inheritance and lifestyle.
The Naylor panel can chart a course for Canada’s health system based on the revolution in our understanding of the biology of human disease. Canada has the opportunity to lead the world in building a health system that takes full advantage of today’s science, and that stands ready to contribute to and benefit from tomorrow’s science. That would be true healthcare innovation.
Bernstein, Alan. “Genomics will be at the centre of real health care innovation”. The Globe and Mail. 1 Jan. 2015. Web. 15 Mar. 2015. Available at http://www.theglobeandmail.com/globe-debate/genomics-will-be-at-the-centre-of-real-health-care-innovation/article22247987/
9
George Johnson. “Random Chance’s Role in Cancer”. nytimes.com JAN. 19, 2015.

JAN. 19, 2015

George Johnson
Unlike Ebola, flu or polio, cancer is a disease that arises from within — a consequence of the mutations that inevitably occur when one of our 50 trillion cells divides and copies its DNA.
Some of these genetic misprints are caused by outside agents, chemical or biological, especially in parts of the body — the skin, the lungs and the digestive tract — most exposed to the ravages of the world. But millions every second occur purely by chance — random, spontaneous glitches that may be the most pervasive carcinogen of all.
It’s a truth that grates against our deepest nature. That was clear earlier this month when a paper in Science on the prominent role of “bad luck” and cancer caused an outbreak of despair, outrage and, ultimately, disbelief.
The most intemperate of this backlash — mini-screeds on Twitter and hit-and-run comments on the web — suggested that the authors, Cristian Tomasetti and Bert Vogelstein of Johns Hopkins University, must be apologists for chemical companies or the processed food industry. In fact, their study was underwritten by nonprofit cancer foundations and grants from the National Institutes of Health. In some people’s minds, those were just part of the plot.
What psychologists call apophenia — the human tendency to see connections and patterns that are not really there — gives rise to conspiracy theories. It is also at work, though usually in a milder form, in our perceptions about cancer and our revulsion to randomness.
It takes several mutations, in specific combinations, for a cell to erupt into a malignant tumor. The idea that random copying errors are prominent among them is thoroughly mainstream. What was new about the paper wasits attempt to measure this biological bad luck and see how it compares with the two other corners of the cancer triangle: environment and heredity — mutations we inherit from our parents that can give cancer a head start.
The mix of these influences varies. A lifetime of heavy smoking has been shown to multiply the risk of lung cancer — the most common malignancy in the world — by some twentyfold, or about 2,000 percent. But that is an anomaly. One of the great frustrations of cancer prevention has been the failure to find other chemical carcinogens so definitive or damaging, especially in the dilute amounts in which they reach most of the public.
For a handful of cancers, biological agents are important, like human papilloma virus in cervical cancer and helicobacter pylori in stomach cancer. On another level, inflammation and hormonal imbalances, like those associated with obesity and diabetes, can drive cells to multiply more frequently, increasing the chance of mutations causal and accidental.
Finally, heredity — like the BRCA mutations involved in some breast cancers — can have a profound effect in individual cases. But inheritance appears to be involved in just 5 to 10 percent of all cancers.
What that leaves is a large role for random, spontaneous mutations — the ones that just happen because of the microscopic grind of life.
That is not a reason for resignation. It is frequently estimated that some 40 percent of cancers are preventable. But that means some 60 percent are not.
Then they compared that number with the likelihood that a tissue would develop a malignant tumor. The result was a strong correlation, a steep sloping line suggesting that two-thirds of the difference in cancer susceptibility could be explained by spontaneous errors.

Tissues that deviated from the relationship, contracting cancer at a higher rate, were presumably swayed more strongly by something else. 

For cancers like those of the bone and brain, chance seemed to rule. But at the other end of the spectrum were those that were more “deterministic” — like lung cancer and basal cell carcinoma, a usually harmless skin malignancy where sunlight plays a deciding part. Also at that extreme were rare cancers mostly determined by inherited defects, like some familial forms of colon cancer.
The more common colon cancers were near the middle of the range. Random mutation was important, but environment — like the carcinogens in digestive waste — seemed to hold a modest edge.
There are still ambiguities to resolve. The cellular dynamics of two of the most common cancers, breast and prostate, were not certain enough to be included in the analysis. But however they might tilt the lineup, random mutations will remain a dominant driver.
It is always possible that what we call randomness will turn out to be complexity in disguise. Some mutations attributed to chance may eventually be revealed to have subtle causes.
Over the years, however, the scale seems to be tipping the other way, with the discovery that some long-suspected agents like dietary fat and artificial sweeteners may not be so potent after all.
For all our agonizing, it can be liberating to accept and even embrace the powerful role chance plays in the biology of life and death. Random variation, after all, is the engine of evolution.
Because of spontaneous mutations in germ cells — sperm and eggs — each generation of our species is subtly different. Some of the variations confer an advantage and others a vulnerability. They are sifted by natural selection, and so we adapt and evolve. 
In the ecosystem of the body, cancer cells go through a much faster version of this same process. The fittest of the bunch develop the weaponry to invade and destroy their surroundings, like a fractal reflection of what humans do in their own world. 
The evolution of our brains, so compelled to find patterns, has given us an edge — discovering cancers that can be avoided or, failing that, identified and excised before their deadly storm. But try as we might, we can never be in complete control of a condition so deeply rooted in the trade-offs of being alive. 
Johnson, George. “Random Chance’s Role in Cancer”. nytimes.com. 19 Jan. 2015. Web. 15 Mar. 2015. Available at http://www.nytimes.com/2015/01/20/science/though-we-long-for-control-chance-plays-a-powerful-role-in-the-biology-of-cancer-and-the-evolution-of-life.html?ref=topics&_r=0
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HELEN BRANSWELL. “Race may influence a woman's breast cancer outcome, study finds”. theglobeandmail.com. Jan. 13 2015

HELEN BRANSWELL

The Canadian Press
Published Tuesday, Jan. 13 2015, 1:00 PM EST
Last updated Tuesday, Jan. 13 2015, 7:15 PM EST
Race may influence whether women diagnosed with breast cancer will survive, suggests a new study which found black women are more likely to die even when their tumours are found when they are small and theoretically easier to treat.
The study, which is based on U.S. data, said that even when breast cancer is diagnosed at Stage 1, black women have a higher risk of dying than women of Japanese ethnicity or white women.
Senior author Steven Narod said it had long been thought differences in outcomes between white and black women with breast cancer related to access to quality health care in the United States, where before the Affordable Care Act came into effect more black women may have been without health insurance.
But he said that by mining a large U.S. database that registers breast cancer cases by stage at diagnosis, income status, race and ethnicity, he and his colleagues concluded that is not the case.
“The assumption that we’re going to eliminate differences in cancer outcomes by eliminating differences in health care is not that well founded,” said Dr. Narod, a leading breast cancer researcher who is based at Toronto’s Women’s College Hospital.

“There may be intrinsic biological differences that account for some of the differences in outcomes that cannot be eliminated.”

Dr. Narod said he thinks similar results would be seen if a matching study was done in Canada, but without doing the work he cannot be sure.
Dr. Narod and his co-authors analyzed data on nearly 375,000 women with invasive breast cancer that was diagnosed between 2004 and 2011. The study is published in the Journal of the American Medical Association.
They looked at the stage of the cancer at diagnosis, in particular focusing on women whose cancers were found at the earliest stage, when the cancers were less than two centimetres.
With some types of breast cancer, the earlier the tumour is found the more likely it is that the woman will survive. So looking only at cancers diagnosed early should have eliminated the survival differences one might have expected if one racial group’s problems accessing care meant their cancers were typically found later.
The researchers saw that black women were less likely to be diagnosed with Stage 1 cancer than women of Japanese heritage. But even if they were first diagnosed with a Stage 1 tumour, black women were more likely to die from the cancer than white women or women of Japanese ethnicity.
For one thing, the cancer was more likely to have spread at the time of diagnosis, even though the tumours were small. And black women were more likely to have the hardest form of the disease to treat, known as triple negative breast cancer.
“It’s more likely to have already spread when it’s detected. And if it hasn’t spread when it’s detected, it’s more likely to spread in the future. Both things are true, compared to a white woman,” Dr. Narod said.
An editorial that accompanied the study suggested the survival gap will be closed only when large numbers of women from minority groups are included in studies aimed at finding the genomic basis of different types of breast cancers.
Editorial co-author Olufunmilayo Olopade called the paper “fundamentally important,” saying she has been pressing the breast cancer research field to look at racial differences for some time.
“Yes, you can talk about access [to care],” said Dr. Olopade, director of the Center for Clinical Cancer Genetics at the University of Chicago Medical School.
“But if you treat all cancers the same in all populations, you are not recognizing the biological differences that happen in human beings.”
She said the advent of registries like the one Dr. Narod and his colleagues mined finally gives researchers granular data to study. “The data are speaking to us in very different ways than we had been accustomed to because they now break everybody down by their race and their ethnicity.”
But Otis Brawley, chief medical officer of the American Cancer Society, suggested the differences in survival outcomes may not be down to race but rather socio-economic factors.
He said girls who are born into poor families have poorer diets, are more likely to gain weight in childhood and are more likely to start menstruating early. Early start of menstruation is linked to an increased risk of breast cancer.
Dr. Brawley said studies done in Scotland — in an all-white cohort — showed that women who were economically deprived in childhood had higher rates of breast cancer later in life and were more likely to develop breast cancer at a younger age than women who were more economically advantaged.
He said the American Cancer Society would expect to see similar survival outcomes among poor white women as among poor black women — and even middle- and upper-income black women who grew up poor.
“I believe it’s race for social reasons, and not race for biologic reasons,” Dr. Brawley said. “There are a lot of lifestyle factors that actually do affect biology and change biology.”
Dr. Olopade disputed Dr. Brawley’s position, saying there are many poor Asian immigrants in the United States but their breast cancer outcomes are not on a par with those of black women.
Dr. Narod said that among all racial or ethnic groups, the seven-year survival rates were good when breast cancers were detected when the tumour was under two centimetres in size.
For women of Japanese heritage, the survival rate was nearly 99 per cent. For white women, it was 95 per cent, and for black women it was 91 per cent, he said.
“Those are all pretty good, but there’s a hell of a big difference between a 1-per-cent chance of dying and a 9-per-cent chance of dying,” Dr. Narod said. “That’s an extraordinary difference from that point of view.”
Branswell, Helen. “Race may influence a woman's breast cancer outcome, study finds”. theglobeandmail.com. 13 Jan. 2015. Web. 15 Mar. 2015. Available at http://www.theglobeandmail.com/life/health-and-fitness/health/race-influences-breast-cancer-outcome-study-finds/article22426124/
11
KATHRYN DOYLE. “Early childhood neglect hinders brain development”. theglobeandmail.com. Jan. 28 2015

KATHRYN DOYLE

Reuters
Published Wednesday, Jan. 28 2015, 2:54 PM EST
Last updated Wednesday, Jan. 28 2015, 3:00 PM EST
0 comments
 
Kids who were raised in a Romanian institution for abandoned children have smaller heads, smaller brains and different white-matter structure than similar children who were moved into high-quality foster care at an early age.
Even those who were moved into foster care by age two have noticeably different brains from children raised in biological families.
The Bucharest Early Intervention Project began in 2000 with 136 abandoned babies who had spent more than half of their lives in institutions, which was the standard at the time. At the age of two, researchers randomly selected half of the babies and arranged for them to be moved into high-quality foster homes.
Ever since then, the researchers have been comparing the children to similar youngsters in biological families who were never institutionalized. The institutions had high ratios of babies to

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