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Clinical Trials, Ethics, Genetics, NIH, Pediatrics

The promise and peril of genome sequencing newborns

NICUEven though doctors and researchers have made great strides in caring for patients in the past few decades, there are still many illnesses that are difficult to diagnose, let alone treat. Among the most heartbreaking cases are those newborns who come down with mysterious illnesses that defy medical expertise. But in recent years, doctors have turned to genetic sequencing in some of these cases to identify the culprit causes of the illnesses.

Last year, the National Institutes of Health funded four pilot projects looking into the efficacy and ethics of genetic screening for otherwise inexplicable illnesses in newborns. The first of the trials will begin next week at Children’s Mercy Hospital in Kansas City, Missouri, as reported in a recent story from Nature. The trial at Children’s Mercy Hospital will focus on rapid genome sequencing with a 24-hour turn-around. Genetic sequencing normally takes weeks, but some of these infants don’t survive that long. Doctors have used similar rapid genome sequencing to diagnose an infant with cardiac defects at Lucile Packard Children’s Hospital Stanford.

Earlier this year, I had the opportunity to report on a rare genetic mutation that leads young infants to develop inflammatory bowel disease. I spoke with some parents of children with the mutation, which was identified by sequencing the children’s exome – just the protein-producing part of the genome – as part of a new project (separate from the NIH trials) at the University of Toronto in Canada. As I explain in the piece, getting a bone marrow transplant early enough can help alleviate symptoms and save the child’s life.

The parents were uniformly grateful for the sequencing technology that made it possible to understand what was causing their baby’s illness, even in cases where the child didn’t survive long after diagnosis. One mother mentioned that realizing some of the best doctors in the country didn’t know what was ailing her daughter made the experience even more frightening. After months of worried confusion about their young children’s deteriorating health, for these parents to have an answer was a relief.

But because the technique is so new, several ethical details still need clarification – which the NIH study hopes to answer. From the Nature news story:

Misha Angrist, a genomic-policy expert at Duke University in Durham, North Carolina, says that although the 24-hour genome process is impressive, it is not clear whether genomic sequencing of newborns will soon become standard practice. Many questions remain about who will pay for sequencing, who should have access to the data and how far clinicians should go in extracting genome information that is unrelated to the disease at hand. Then there is the question of how informative the process is. “I think it’s really important that we do these experiments so that we start to see what that yield is,” Angrist says.

All four teams will include an ethicist who will be responsible for dealing with questions like the ones Angrist raises. The other three trials at Boston Children’s Hospital, the University of North Carolina in Chapel Hill, and at the University of California, San Francisco are still awaiting approval from the Federal Drug Adminstration.

Previously: Stanford patient on having her genome sequenced: “This is the right thing to do for our family” When ten days = a lifetime: Rapid whole-genome sequencing helps critically ill newborn Assessing the challenges and opportunities when bringing whole-genome sequencing to the bedside Whole genome sequencing: The known knowns and the unknown unknowns
Photo by kqedquest

Cancer, Genetics, Stanford News, Videos, Women's Health

Despite genetic advances, detection still key in breast cancer

Despite genetic advances, detection still key in breast cancer

Just a few years before the launch of the first national breast cancer awareness month, I found a small lump in my left breast. I still remember the cold chill that ran through me – and stayed with me until several days later when a surgeon discovered that the lump was not a tumor. His parting words have never left me: “Remember how you’ve been feeling.” He wanted to make sure I would go on to have regular mammograms.

Spreading the word about the disease and the importance of detecting it in its early stages was – and is – the point of the national awareness campaign. In the almost 30 years since that first campaign, advances in imaging technology have enabled earlier detection of breast cancer, genome sequencing has identified some of the mysteries behind the development risk, and selecting the most effective surgery and chemotherapy is more and more of an individualized choice.

Stanford has a powerful team of physicians addressing all aspects of breast cancer science and care. On Oct. 16, breast-imaging specialist Jafi Lipson, MD, assistant professor of radiology, and breast cancer surgeon Amanda Wheeler, MD, clinical assistant professor of surgery, will give a free lecture, “The Latest Advancements in Screening and Treatment for Breast Cancer,” at the Sheraton Palo Alto. And throughout the month, Stanford Health Care will post short educational videos and infographics on a variety of breast-cancer topics, including types of breast cancer, options in surgical reconstruction, and why enduring the pain of compression in mammography is worth the effort. Today, Stanford Health Care kicks off the month with a video featuring Stanford breast cancer expert Alison Kurian, MD, explaining the role that genetics play in disease development (above).

Because one in eight women will develop breast cancer in her lifetime, I would urge all of us to keep in mind the reality of this disease – and to honor those we know who have survived, or not, by paying attention.

Previously: NIH Director highlights Stanford research on breast cancer surgery choicesBreast cancer patients are getting more bilateral mastectomies —  but not any survival benefitBreast cancer awareness: Beneath the pink packaging and At Stanford event, cancer advocate Susan Love talks about “a future with no breast cancer”

Applied Biotechnology, Genetics, In the News, Nutrition, Public Health, Research

“Frankenfoods” just like natural counterparts, health-wise (at least if you’re a farm animal)

"Frankenfoods" just like natural counterparts, health-wise (at least if you're a farm animal)

cow2More than a hundred billion farm animals have voted with their feet (or their hoofs, as the case may be). And the returns are in: Genetically modified meals are causing them zero health problems.

Many a word has been spilled in connection with the scientific investigation of crops variously referred to as “transgenic,” “bioengineered,” “genetically engineered” or “genetically modified.” In every case, what’s being referred to is an otherwise ordinary fruit, vegetable, or fiber source into which genetic material from a foreign species has been inserted for the purpose of making that crop, say, sturdier or  more drought- or herbicide- or pest-resistant.

Derided as “Frankenfoods” by critics, these crops have been accused of everything from being responsible for a very real global uptick in allergic diseases to causing cancer and autoimmune disease. But (flying in the face of the first accusation) allergic disorders are also rising in Europe, where genetically modified, or GM, crops’ usage is far less widespread than in North America. It’s the same story with autoimmune disease. And claims of a link between genetically modified crops and tumor formation have been backed by scant if any evidence; one paper making such a claim  got all the way through peer review and received a fair amount of Internet buzz before it was ignominiously retracted last year.

But a huge natural experiment to test GM crops’ safety has been underway for some time. Globally, between 70 and 90 percent of all GM foods are consumed by domesticated animals grown by farmers and ranchers. More than 95 percent of such animals – close to 10 billion of them – in the United States alone consume feed containing GM  components.

This was, of course, not the case before the advent of commercially available GM feeds in the 1990s. And U.S. law has long required scrupulous record-keeping concerning the health of animals grown for food production. This makes possible a before-and-after comparison.

In a just-published article in the Journal of Animal Science, University of California-Davis scientists performed a massive review of data available on performance and health of animals consuming feed containing GM ingredients and  products derived from them. The researchers conclude that there’s no evidence of GM products exerting negative health effects on livestock. From the study’s abstract:

Numerous experimental studies have consistently revealed that the performance and health of GE-fed animals are comparable with those fed [otherwise identical] non-[GM] crop lines. Data on livestock productivity and health were collated from publicly available sources from 1983, before the introduction of [GM] crops in 1996, and subsequently through 2011, a period with high levels of predominately [GM] animal feed. These field data sets representing over 100 billion animals following the introduction of [GM]crops did not reveal unfavorable or perturbed trends in livestock health and productivity. No study has revealed any differences in the nutritional profile of animal products derived from[GM]-fed animals.

In other words, the 100 billion GM-fed animals didn’t get sick any more frequently, or in different ways. No noticeable difference at all.

Should that surprise us? We humans are, in fact, pretty transgenic ourselves. About 5 percent of our own DNA can be traced to viruses who deposited their  genes in our genomes, leaving them behind as reminders of the viral visitations. I suppose that’s a great case against cannibalism if you fear GM foods. But I can think of other far more valid arguments to be made along those lines.

Previously: Ask Stanford Medicine: Pediatric immunologist answers your questions about food allergy research, Research shows little evidence that organic foods are more nutritional than conventional ones and Stanford study on the health benefits of organic food: What people are saying
Photo by David B. Gleason

Cardiovascular Medicine, Genetics, Research, Science, Stanford News, Stem Cells

Stem cell study explains how mutation common in Asians affects heart health

Stem cell study explains how mutation common in Asians affects heart health

10011881004_d5ab6d7cd9_zMany Asians carry a mutation that causes their faces to flush when they drink alcohol. The affected gene is called ALDH2, and it also plays a role in cardiovascular health. Carriers are more susceptible to coronary artery disease and tend to recover more poorly than non-carriers from the damage caused by a heart attack. Now Stanford cardiologist Joseph Wu, MD, PhD, and postdoctoral scholar Antje Ebert, PhD, have learned why.

The researchers used a type of stem cell called an induced pluripotent stem cell, or iPS cell, to conduct the study. The stem cells are made from easily obtained tissue like skin, and they can be coaxed in the laboratory to become other types of tissue, like heart muscle cells. It’s one of the first times iPS cells have been used to examine ethnic-specific differences among populations. The research was published yesterday in Science Translational Medicine.

From our release:

The study showed that the ALDH2 mutation affects heart health by controlling the survival decisions cells make during times of stress. It is the first time ALDH2, which is involved in many common metabolic processes in cells of all types, has been shown to play a role in cell survival. In particular, ALDH2 activity, or the lack of it, influences whether a cell enters a state of programmed cell death called apoptosis in response to stressful growing conditions. [...]

The use of heart muscle cells derived from iPS cells has opened important doors for scientists because tissue samples can be easily obtained and maintained in the laboratory for study. Until recently, researchers had to confine their studies to genetically engineered mice or to human heart cells obtained through a heart biopsy, an invasive procedure that yields cells which are difficult to keep alive long term in the laboratory.

You’ve likely read about Wu’s previous work with heart muscle cells derived from iPS cells. Now he’s shown iPS cells are also a good way to compare the effect of genetic differences among populations, and he has big plans. More details about his plans from our release:

Wu is working to start a biobank at the Stanford Cardiovascular Institute of iPS cells from about 1,000 people of many different ethnic backgrounds and health histories. “This is one of my main priorities,” he said. “For example, in California, we boast one of the most diverse populations on Earth. We’d like to include male and female patients of major representative ethnicities, age ranges and cardiovascular histories. This will allow us to conduct ‘clinical trials in a dish’ on these cells, a very powerful new approach, to learn which therapies work best for each group. This would help physicians to understand for the first time disease process at a population level through observing these cells as surrogates.”

Previously: Induced pluripotent stem cell mysteries explored by Stanford researchers, A new era for stem cells in cardiac medicine? A simple, effective way to generate patient-specific heart muscle cells and “Clinical trial in a dish” may make common medicines safer, say Stanford scientists

Photo by Nicholas Raymond

Genetics, Pediatrics, Stanford News, Surgery, Transplants

Double kidney transplants leave Hawaii siblings raring to go

Double kidney transplants leave Hawaii siblings raring to go

kidney patients

Two kids; two cases of a rare, often fatal disease; and now, thanks to the work of Lucile Packard Children’s Hospital doctors, two growing kids.

Both Julia Faisca, nearly 10, and Dominic Faisca, 8, suffer from cystinosis, a genetic disease that causes an amino acid — cystine — to build up in the kidney, eye and other places in the body.

The condition retarded the siblings’ growth, and damaged their kidneys. And by May 2013, Julia’s kidneys needed to be replaced. Fortunately, just three months later, she had a new kidney. And the Faisca family received the good news that a kidney was waiting for Dominic while they were flying to California from their home in Hawaii for a routine checkup for Julia.

“We’ve been busy — two kidney transplants in less than a year,” the kids’ mom, Natasha, said in a recent Inside Stanford Medicine story:

“Since their transplants, they aren’t picky eaters anymore,” Natasha said. “I joke with the doctors that the kids are eating me out of the house now. But it’s well worth it.”

Although they’ll always be on medication to protect their new kidneys and will need to return for twice-yearly checkups at Stanford, there’s finally a sparkle in their eyes, Natasha said.

“Dominic and Julia are growing like weeds and it’s really fun to watch them turn into regular kids,” said pediatric transplant specialist Paul Grimm, MD.

Both transplants were conducted by Waldo Concepcion, MD, a specialist in multi-organ transplantation.

Becky Bach is a science-writing intern with the Office of Communications and Public Affairs.

Previously: Baby born with rare, often-fatal kidney disease “doing well” at Packard Children’s Hospital, Contact sports OK for kids with one kidney, new study says and “Delivering hope” at Packard Children’s Hospital
Photo by Norbert von der Groeben

Applied Biotechnology, Bioengineering, Genetics, Research, Stanford News

A computer kit could lead to better way to design synthetic molecules

A computer kit could lead to better way to design synthetic molecules

SmolkeSlipping something small into cells to regulate gene expression has long been a goal of biomedical researchers. And there have been many efforts to do just that. Usually researchers concoct a teeny strip of microRNA, or miRNA, and hope it does the trick.

But now, researchers at Stanford’s Department of Bioengineering have developed a computer model to take the guesswork out of designing miRNA. The model determines how to assemble a molecule so it will measure the level of a certain compound in a cell and then use that information to regulate the expression of a gene.

The research is featured in the current edition of Nature Methods, and senior author Christina Smolke, PhD, describes the process in a release issued this week:

“You start with an idea of what you want to do in the cell, and then you build and iterate on a design over and over until you reach something close to what you want,” Smolke said. “As we design and build more sophisticated systems, we will want the ability to efficiently achieve precise quantitative behaviors, and being able to accurately predict relationships between the system inputs and outputs are important to achieving this goal.”

She and Smolke’s team — which includes former graduate student Ryan Bloom and former undergraduate Sally Winkler —tested the model on the well-known Wnt signaling pathway, which plays a key role in embryonic development, stem cell production and cancer. The synthesized miRNA correctly monitored the protein produced by the pathway, validating their model.

Becky Bach is a former park ranger who now spends her time writing about science or practicing yoga. She’s a science writing intern in the Office of Communications and Public Affairs. 

Previously: A non-surgical test for brain cancer?, From plant to pill: Bioengineers aim to produce opium-based medicines without using poppies, Researchers engineer biological “devices” to program cells
Photo of Smolke by L.A. Cicero

Autoimmune Disease, Genetics, NIH, Research, Science

Tiny hitchhikers, big health impact: Studying the microbiome to learn about disease

Tiny hitchhikers, big health impact: Studying the microbiome to learn about disease

I don’t know about you, but I’m fascinated with the idea of the “microbiome.” If you’re unfamiliar with the term, it describes the millions upon millions of tiny, non-human hitchhikers that live on and in you (think bacteria, viruses, fungi and other microscopic life). Although the exact composition of these molecular roommates can vary from person to person, they aren’t freeloaders. Many are vitally important to your metabolism and health.

We’ve reported here on the Human Microbiome Project, launched in 2007 and supported by the National Institutes of Health’s Common Fund. Phase 2 of the project started last fall, with grants to three groups around the country to study how the composition of a person’s microbiome might affect the onset of diseases such as type 2 diabetes and inflammatory bowel disease, as well as its role in pregnancy and preterm birth. Now the researchers, which include Stanford geneticist Michael Snyder, PhD, have published an article in Cell Host & Microbe detailing what data will be gathered and how it will be shared.

As explained in a release by the National Human Genome Research Institute:

“We’re producing an incredibly rich array of data for the community from the microbiomes and hosts in these cohorts, so that scientists can evaluate for themselves with these freely available data which properties are the most relevant for understanding the role of the microbiome in the human host,” said Lita M. Proctor, Ph.D., program director of the Human Microbiome Project at NIH’s National Human Genome Research Institute (NHGRI).

“The members of the Consortium can take advantage of each other’s expertise in dealing with some very complex science in these projects,” she said. “We’re generating these data as a community resource and we want to describe this resource in enough detail so people can anticipate the data that will be produced, where they can find it and the analyses that will come out of the Consortium’s efforts.”

As I’ve recently blogged, data-sharing among researchers and groups is particularly important for research efficiency and reproducibility. And I’m excited to hear what the project will discover. More from the release:

For years the number of microbial cells on or in each human was thought to outnumber human cells by 10 to 1. This now seems a huge understatement. Dr. Proctor noted that the 10-to-1 estimate was based only on bacterial cells, but the microbiome also includes viruses, protozoa, fungi and other forms of microscopic life. “So if you really look at the entire microbial community, you’re probably looking at more like a 100-to-1 ratio,” she said.

Although thousands of bacterial species may make their homes with human beings, each individual person is host to only about 1,000 species at a time, according to the findings of the Human Microbiome Project’s first phase in 2012.

In addition, judging from the array of common functions of bacterial genes, if the bacteria are healthy, each individual’s particular suite of species appear to come together to perform roughly the same biological functions as another healthy individual. In fact, researchers found that certain bacterial metabolic pathways were always present in healthy people, and that many of those pathways were often lost or altered in people who were ill.

Stanford’s Snyder will join forces with researchers in the laboratory of George Weinstock, PhD, of the Jackson Laboratory for Genomic Medicine in Connecticut to investigate the effect of the microbiome on  the onset of Type 2 diabetes. Snyder may be uniquely positioned to investigate the causes of the condition. In 2012, he made headlines when he performed the first ever ‘omics’ profile of himself (an analysis that involves whole genome DNA sequencing with repeated measurements of the levels of RNA, proteins and metabolites in a person’s blood over time). During the process, he learned that he was on the cusp of developing type 2 diabetes. He was able to halt the progression of the disease with changes in exercise and diet.

Previously: Stanford team awarded NIH Human Microbiome Project grantElite rugby players may have more diverse gut microbiota, study shows and Could gut bacteria play a role in mental health?

Applied Biotechnology, Cancer, Genetics, Pediatrics, Research

Gene-sequencing rare tumors – and what it means for cancer research and treatment

Gene-sequencing rare tumors - and what it means for cancer research and treatment

Sequencing the genes of cancer patients’ tumors has the potential to surmount frustrating problems for those who work with rare cancers. Doctors who see patients with rare tumors are often unsure of which treatments will work. And, with few patients available, researchers are unable to assemble enough subjects to compare different therapies in gold-standard randomized clinical trials. But thanks to gene sequencing, that is about to change.

Though this specific research was not intended to shape the child’s treatment, similar sequencing could soon help doctors decide how to treat rare cancers in real time

That’s the take-away from a fascinating conversation about the implications of personalized tumor-gene sequencing that I had recently with two Stanford cancer experts. Cancer researcher Julien Sage, PhD, is the senior author of a recent scientific paper describing sequencing of a pediatric tumor that affects only one in every 5 million people. Alejandro Sweet-Cordero, MD, an oncologist who treats children with cancer at Lucile Packard Children’s Hospital Stanford, is leading one of Stanford’s several efforts to develop an efficient system for sequencing individual patients’ tumors.

In their paper, Sage’s team (led by medical student Lei Xu) analyzed the DNA and RNA of one child’s unusual liver tumor, a fibrolamellar hepatocellular carcinoma. The cause of this form of cancer has never been found. Curious about what genes drove the tumor’s proliferation, the scientists identified two genes that were likely culprits, both of which promoted cancer in petri dishes of cultured cells. One of the genes, encoding the enzyme protein kinase A, is a possible target for future cancer therapies.

Though this specific research was not intended to shape the child’s treatment, similar sequencing could soon help doctors decide how to treat rare cancers in real time. Sweet-Cordero is working to develop an efficient system for getting both the mechanics of sequencing and the labor-intensive analysis of the resulting genetic data completed in a few weeks, instead of the two to three months now required. “We’re trying to use this kind of technology  to really help patients,” Sage said. “If you’re dealing with a disease that may kill the patient very fast, you want to act on it as soon as possible.”

In addition to giving doctors clues about which chemotherapy drugs to try, gene sequencing gives them a new way to study tumors.

“What’s really important is that, instead of categorizing tumors based on how they look under a microscope, we’ll be able to categorize them based on their gene-mutation profile,” Sweet-Cordero said. Rather than setting up clinical trials based on a tumor’s histology, as doctors have done in the past, scientists will group patients for treatment trials on the basis of similar mutations in their tumors. “In my mind, as a clinical oncologist, this is the most transformative aspect of this technology,” he said. This is especially true for patients with rare tumors who might not otherwise benefit from clinical trials at all.

And for childhood cancers, knowing a tumor’s gene mutations could also help doctors avoid giving higher doses of toxic chemotherapy drugs than are truly needed.

“The way we’ve been successful in pediatric oncology is by being extremely aggressive,” Sweet-Cordero said. Oncologists take advantage of children’s natural resilience by giving extremely strong chemotherapy regimens, which beat back cancer but can also have damaging long-term side effects. “We end up over-treating significant groups of patients who could survive with less aggressive therapy,” Sweet-Cordero said. “If we can use genetic information to back off on really toxic therapies, we’ll have fewer pediatric cancer survivors with significant impairments.”

Meanwhile, Stanford cancer researchers are also tackling a related problem: the fact that not all malignant cells within a tumor may have the same genetic mutations, and they may not all be vulnerable to the same cancer drugs. Next month, the Stanford Cancer Institute is sponsoring a scientific symposium on the concept, known as tumor heterogeneity, and how it will affect the future of personalized cancer treatments.

Sage’s research was supported by the Lucile Packard Foundation for Children’s Health, Stanford NIH-NCATS-CTSA UL1 TR001085 and Child Health Research Institute of Stanford University. Sage and Sweet-Cordero are both members of the Stanford Cancer Institute, and the National Cancer Institute-designated Cancer Center.

Previously: Smoking gun or hit-and-run? How oncogenes make good cells go bad, Stanford researchers identify genes that cause disfiguring jaw tumor and Blood will tell: In Stanford study, tiny bits of circulating tumor DNA betray hidden cancers

Big data, Evolution, Genetics, In the News, Research, Science, Stanford News

Flies, worms and humans – and the modENCODE Project

Flies, worms and humans - and the modENCODE Project

It’s a big day in comparative biology. Researchers around the country, including Stanford geneticist Michael Snyder, PhD, are publishing the results of a massive collaboration meant to suss out the genomic similarities (and differences) among model organisms like the fruit fly and the laboratory roundworm. A package of four papers, which describe how these organisms control how, when and where they express certain genes to generate the cell types necessary for complex life, appears today in Nature.

From our release:

The research is an extension of the ENCODE, or Encyclopedia of DNA Elements, project that was initiated in 2003. As part of the large collaborative project, which was sponsored by the National Human Genome Research Institute, researchers published more than 4 million regulatory elements found within the human genome in 2012. Known as binding sites, these regions of DNA serve as landing pads for proteins and other molecules known as regulatory factors that control when and how genes are used to make proteins.

The new effort, known as modENCODE, brings a similar analysis to key model organisms like the fly and the worm. Snyder is the senior author of two of the papers published today describing some aspects of the modENCODE project, which has led to the publication, or upcoming publication, of more than 20 papers in a variety of journals. The Nature papers, and the modENCODE project, are summarized in a News and Views article in the journal (subscription required to access all papers).

As Snyder said in our release, “We’re trying to understand the basic principles that govern how genes are turned on and off. The worm and the fly have been the premier model organisms in biology for decades, and have provided the foundation for much of what we’ve learned about human biology. If we can learn how the rules of gene expression evolved over time, we can apply that knowledge to better understand human biology and disease.”

The researchers found that, although the broad strokes of gene regulation are shared among species, there are also significant differences. These differences may help explain why humans walk, flies fly and worms slither, for example:

The wealth of data from the modENCODE project will fuel research projects for decades to come, according to Snyder.

“We now have one of the most complete pictures ever generated of the regulatory regions and factors in several genomes,” said Snyder. “This knowledge will be invaluable to researchers in the field.”

Previously: Scientists announce the completion of the ENCODE project, a massive genome encyclopedia

Genetics, Medicine and Society, Pain, Research, Science, Stanford News

From plant to pill: Bioengineers aim to produce opium-based medicines without using poppies

From plant to pill: Bioengineers aim to produce opium-based medicines without using poppies

Basic RGBStanford bioengineer Christina Smolke, PhD, and her team have been on a decade-long mission to replicate how nature produces opium in poppies by genetically engineering the DNA of yeast and then further refining the process to manufacture modern day opioid drugs such as morphine, codeine and the well-known painkiller Vicodin.

Smolke outlined the methods in a report  (subscription required) published in this week’s edition of Nature Chemical Biology, which details the latest stages in the process of manufacturing opium-based medicines, from start to finish, in fermentation vats, similar to the process for brewing beer.

An article published today in the Stanford Report offers more details:

It takes about 17 separate chemical steps to make the opioid compounds used in pills. Some of these steps occur naturally in poppies and the remaining via synthetic chemical processes in factories. Smolke’s team wanted all the steps to happen inside yeast cells within a single vat, including using yeast to carry out chemical processes that poppies never evolved to perform – such as refining opiates like thebaine into more valuable semi-synthetic opioids like oxycodone.

So Smolke programmed her bioengineered yeast to perform these final industrial steps as well. To do this she endowed the yeast with genes from a bacterium that feeds on dead poppy stalks. Since she wanted to produce several different opioids, her team hacked the yeast genome in slightly different ways to produce each of the slightly different opioid formulations, such as oxycodone or hydrocodone.

“We are now very close to replicating the entire opioid production process in a way that eliminates the need to grow poppies, allowing us to reliably manufacture essential medicines while mitigating the potential for diversion to illegal use,” Smolke added.

While it could take several more years to refine these last steps in the lab, bioengineering opioids would eventually lead to less dependence on legal poppy farming, which has numerous restrictions and international dependencies from other countries. It would also provide a reliable supply and secure process for manufacturing important pain killing drugs.

Jen Baxter is a freelance writer and photographer. After spending eight years working for Kaiser Permanente Health plan she took a self-imposed sabbatical to travel around South East Asia and become a blogger. She enjoys writing about nutrition, meditation, and mental health, and finding personal stories that inspire people to take responsibility for their own well-being. Her website and blog can be found at www.jenbaxter.com.

Previously: Blocking addiction risks of morphine without reducing its pain-killing effects, Do opium and opioids increase mortality risk? and Patients’ genetics may play a role in determining side effects of commonly prescribed painkillers 
Photo by Kate Thodey and Stephanie Galanie

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