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Stanford Medicine

Medicine and Literature, Stanford News, Surgery

The operating room: long a woman’s domain

The operating room: long a woman’s domain

In my recent story for Stanford Medicine magazine on the transformational changes in surgery, I reported that “women were once personae non gratae in the operating room.” An alumna of the medical school, Judith Murphy, MD, took me to task for my choice of words, for as she points out, women have long been the backbone of the OR.

“In fact, for decades, women outnumbered men in the OR – circulating nurse, scrub nurse, overseeing nurse, etc.,” she wrote to me. “So it is not that there were no women in the OR, but there were no women surgeons. No Women Who Count, although everyone knows these nurses are essential to successful surgery.”

When she was a medical student at Stanford in the early 1970s, she says female students and faculty had to use bathrooms and lockers that were labeled “Nurses,” whereas the men’s room was labeled, “Doctors.”

“We all laughed about it, but it did reflect the unconscious assumptions that your language still perpetuates, all these years later and after so much progress,” she shared with me. “The women who came after us were a bit more empowered and did not think it was funny; they complained, and the doors were changed to Men and Women.”

Murphy, a practicing pediatrician in Palo Alto for decades, says she might not have made note of the issue were it not for a recent encounter with a male acquaintance who, on learning she was connected to Stanford Hospital, said, “I never knew you were a nurse.”

“When he said that, I thought, ‘Darn, I can’t believe this is still happening.’ I gave him my usual response: ‘I have great respect for nurses and could never have done as good a job without them, but in fact, I’m a doctor,’” said Murphy, who is now retired.

“The power of the cultural unconscious assumption remains strong, even here where we have come so far,” she wrote. “This has been happening to me occasionally for 40 years, less so lately. I had hoped it would become archaic.”

Murphy says her response may have been a bit testier than in the past. But she can be excused, for it is always good to be reminded of our unconscious biases about the role of women in health care, reflected both in our language and behavior.

Previously: Surgery: Up close and personal and Stanford Medicine magazine opens up the world of surgery

From August 11-25, Scope will be on a limited publishing schedule. During that time, you may also notice a delay in comment moderation. We’ll return to our regular schedule on August 25.

Genetics, Humor, Medicine and Society, Science, Stanford News

Using epigenetics to explain how Captain America and the Incredible Hulk gained their superpowers

Using epigenetics to explain how Captain America and the Incredible Hulk gained their superpowers

When I was kid I used to watch the Incredible Hulk on TV and wait for Bruce Banner to fly into a rage, his muscles inflating like balloons, pants torn to shreds while his entire body turns green as he transforms into the Hulk. As I grew up, and learned more about the advances in genetics, it never occurred to me that cutting-edge genome-editing techniques could explain the scientific principles behind the Hulk’s metamorphosis or his fellow Marvel Comics star-spangled hero Captain America. In a recent Stanford Report story,  Sebastian Alvarado, a postdoctoral research fellow in biology, creatively applies the concepts of epigenetics to illuminate the process by which average Joes become superheroes.

As Alvarado notes in the piece and above video,  over the past  70 years scientists have developed tools for selectively activating and deactivating individual genes through chemical reactions, a process termed epigenetics. Similar to flipping on a light, switch gene expression can be “turned on” or “turned off. “We have a lot of genome-editing tools – like zinc finger nucleases, or CRISPR/Cas9 systems – that could theoretically allow you to epigenetically seek out and turn on genes that make your muscles physically large, make you strategically minded, incredibly fast, or increase your stamina,” he said.

In the case of Captain America, the process of deliberately switching on and off genes could offer a real-world explanation as to how scrawny Steve Rodgers gained extraordinary, strength, stamina and intelligence after being injected with “Super Solider Serum” and then blasted with  “Vita-Rays.” When it comes to Bruce Banner, a little more creative license is required. Alvarado’s theory is:

First, when gamma radiation hits DNA, it breaks the molecule’s double-stranded, ladder-like helix, a process known as chromothripsis. Your body can repair a few breaks without significant loss of function.

If many breaks occur – say, if you were caught in a giant gamma explosion – the repairs can become sloppy, and new instructions can be keyed into the genetic code. Alvarado suggested that it’s possible that when Banner’s DNA reassembled after the initial blast, it now included a handful of epigenetic switches. Instead of the switches being activated by light, however, the hormones produced when Banner is angry might flip the genetic switches to reconfigure his DNA to transform him into the big, green Hulk.

As for the Hulk’s skin turning green, anyone who has suffered a nasty bruise has firsthand knowledge of the process that might be behind this transformation. When you bruise, red blood cells at the point of injury die and the oxygen-carrying molecule on their surface, hemoglobin, begins to break up. One of hemoglobin’s metabolites, Alvarado said, is a molecule called biliverdin, which can make the blood appear green and is responsible for the avocado hue at the edge of a bruise.

Giant gamma explosion and epigenetics aside, there’s one question that has scientifically stumped Alvarado: How do the Hulk’s pants stay on after every transformation?

From August 11-25, Scope will be on a limited publishing schedule. During that time, you may also notice a delay in comment moderation. We’ll return to our regular schedule on August 25.

Aging, Mental Health, Research, Sleep, Stanford News

Stanford researcher examines link between sleep troubles and suicide in older adults

Stanford researcher examines link between sleep troubles and suicide in older adults

Chassériau painting - smallAfter nights spent tossing and turning, I’m grumpy. The world becomes darker, slower and smaller.

That’s why I wasn’t terribly surprised to learn that sleep-deprived older adults are more likely to kill themselves, the results of a study published Aug. 13 in JAMA Psychiatry. Lead author Rebecca Bernert, PhD, instructor of psychiatry and behavioral science and her team examined data from a pool of 14,456 adults older than 65 between 1981 and 1991. They then probed the sleep patterns of 20 people who died by suicide with those of 400 similar individuals.

They found that participants with impaired sleep had a 1.4 percent greater chance of death by suicide than participants who slept well. “This is important because sleep disturbances are highly treatable and arguably less stigmatizing than other suicide risk factors,” Bernert commented in a press release.

Bernert and her team plan to work to develop potential interventions through two ongoing clinical trials.

What did surprise me about the findings was the prevalence of suicide deaths in older adults, particularly among older men: In fact, white men over 65 have a rate of 31 deaths by suicide per 100,000, much higher than the general population rate of 13 or so per 100,000.

Regardless, any number of suicides is too high, a belief Bernert reiterates emphatically.

“Suicide is preventable,” Bernert said. “But the interventions for suicide prevention are alarmingly scarce.”

That’s why for Bernert, the suicide net recently approved for the Golden Gate Bridge is a no-brainer. She recently joined the board of directors of the Bridge Rail Foundation, the nonprofit formed to advocate for the net. “This is a very effective way to prevent suicides,” she said.

More than 1,600 people have died by suicide at the bridge; a similar number of deaths due to any other reason would have necessitated public intervention decades ago, she said.  She attributed the delay, in part, to the powerful stigma that surrounds suicide.

Bernert urged others to learn about suicide by visiting the American Foundation for Suicide Prevention, or, if in crisis, to call 1-800-273-TALK to reach a 24-hour help line.

Becky Bach is a former park ranger who now spends her time writing, exploring, or practicing yoga. She’s currently a science writing intern in the medical school’s Office of Communication & Public Affairs.

Previously: Stanford’s Keith Humphreys on Golden Gate Bridge suicide prevention: Get the nets, CDC report highlights the dangers of sleep deprivation and Sleep deprivation may increase young adults’ risk of mental distress, obesity
Painting by Théodore Chassériau via Wikipedia Commons

From August 11-25, Scope will be on a limited publishing schedule. During that time, you may also notice a delay in comment moderation. We’ll return to our regular schedule on August 25.

Medical Education, Medical Schools, SMS Unplugged

Buzzwords in medical school

Buzzwords in medical school

SMS (“Stanford Medical School”) Unplugged was recently launched as a forum for students to chronicle their experiences in medical school. The student-penned entries appear on Scope once a week; the entire blog series can be found in the SMS Unplugged category.

Learning in medical school often feels like learning a completely new language. There are numerous acronyms (OPQRST, CAGE, etc.) and molecules (IL-1, TGF-beta, etc.) and more. But most striking to me are two particularly ubiquitous buzzwords: “high-yield” and “protected time.”

I feel like I heard both these terms – and particularly the former – thrown around every single week of this past school year. “High-yield” has been used to refer to, as you might guess, the material that yields the highest amount of gain – i.e. for us students, it’s the material that’s going to show up on our tests. This term pervades not only conversations among classmates but also study materials. First Aid – one of the main Step 1 book resources – takes pains to highlight “high-yield” concepts, and Pathoma – another Step 1 resource – goes even further, identifying ideas that are not just “high-yield” but also “highEST-yield.”

This idea of focusing on “high-yield’ concepts bothered me at first and continues to bother me a little bit today, largely because my classmates and I often determine for ourselves what is “high-yield” and what is “low-yield,” dedicating our study time to the former and ignoring the latter. The worst part is that we may be ignoring information that may be “low-yield” in the context of exams but actually “high-yield” in the context of patient care. The flip side of this is that we only have a certain number of hours in the day; perhaps it makes sense for us to be judicious about what we focus our attention on?

Another phrase that has been widespread in medical school is the term “protected time.” I started hearing this during the very first week of medical school, when we had part of our afternoon off for “protected study time.” Later in the year, I attended a panel featuring five pediatricians. The question of work-life balance came up, and one of the doctors mentioned that she carved out “protected time” to be with her 2-year-old daughter every evening between 5 and 7 PM. This statement was met with general appreciation but also minor panic. There are so many aspects of our life that deserve “protected time” – family, friends, time for creativity, and more – and yet, again, there are only 24 hours in a day. Where does “protected time” start and end? And what does it include? And is it really reasonable to expect “protected time” when there are so many patient -care demands for physicians to navigate?

As I’m about to enter my second year of medical school, some of my questions remain unanswered. How can my classmates and I make sure to learn medicine well enough and thoroughly enough that we can both meet and exceed expectations in patient care? Is identifying “high-yield” material an ineffective, shortsighted approach? And how do we identify what falls under “protected time”? Here’s hoping I figure out this tentative balance during this upcoming year!

Hamsika Chandrasekar just finished her first year at Stanford’s medical school. She has an interest in medical education and pediatrics.

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From August 11-25, Scope will be on a limited publishing schedule. During that time, you may also notice a delay in comment moderation. We’ll return to our regular schedule on August 25.)

Global Health, Infectious Disease, Public Health, Public Safety, Stanford News

Biosecurity experts discuss Ebola and related public health concerns and policy implications

Biosecurity experts discuss Ebola and related public health concerns and policy implications

ebola_081214

More than 1,800 people in the West African nations of Liberia, Sierra Leone and Guinea have contracted the Ebola virus since March and the death toll has surpassed 1,000, according to the latest figures from the World Health Organization. As the number of cases and death continue to climb many are concerned about what can be done to curtail the outbreak and the likelihood of it spreading to the United States.

In a Q&A recently published by the Center for International Security and Cooperation and The Freeman Spogli Institute for International Studies, Stanford biosecurity experts David Relman, MD, and Megan Palmer jointly answer these questions and others related to the public health concerns and policy implications if the outbreak. On the topic of broader lessons about the dynamics and ecology of emerging infectious diseases that can help prevent or respond to outbreaks now and in the future, they respond:

These latest outbreaks remind us that potential pathogens are circulating, replicating and evolving in the environment all the time, and human action can have an immense impact on the emergence and spread of infectious disease.

We are starting to see common factors that may be contributing to the frequency and severity of outbreaks. Increasing human intrusion into zoonotic disease reservoir habitats and natural ecosystems, increasing imbalance and instability at the human-animal-vector interface, and more human population displacement all are likely to increase the chance of outbreaks like Ebola.

The epicenter of this latest outbreak was Guéckédou, a village near the Guinean Forest Region. The forest there has been routinely exploited, logged, and neglected over the years, leading to an abysmal ecological status quo. This, in combination with the influx of refugees from conflicts in Guinea, Liberia, Sierra Leone, and Cote d’Ivoire, has compounded the ecological issues in the area, potentially facilitating the spread of Ebola. There seems to be a strong relationship between ecological health and the spread of disease, and this latest outbreak is no exception.

While forensic analyses are ongoing, unregulated food and animal trade in general is also a key factor in the spread of infectious diseases across large geographic regions. Some studies suggest that trade of primates, including great apes, and other animals such as bats, may be responsible for transit of this Ebola strain from Central to Western Africa.

Overall, Relman and Palmer remind the public, “It’s important that we not lose sight of more chronic, but less headline-grabbing diseases that will be pervasive, insidious long-standing challenges for Africa and elsewhere.”

Previously: Stanford global health chief launches campaign to help contain Ebola outbreak in Liberia and Health workers use crowdsourced maps to respond to Ebola outbreak in Guinea
Photo by European Commission DG ECHO

From August 11-25, Scope will be on a limited publishing schedule. During that time, you may also notice a delay in comment moderation. We’ll return to our regular schedule on August 25.

Neuroscience, Parenting, Pediatrics

Can musical training help close the achievement gap between high and low-income children?

Can musical training help close the achievement gap between high and low-income children?

scope Music and kids

Drawing data from hundreds of students from low-income urban communities, a recent study offers new insights into understanding the academic gap between children from varying socioeconomic backgrounds and demonstrates the impact of musical training in helping low-income youth improve their language and reading comprehension skills.

The research (.pdf) was presented at the American Psychological Association’s annual convention and involved elementary and high school-aged students who participated in two separate projects measuring neural responses along with language and cognitive evaluations over a two-year period. Younger participants were part of Los Angeles-based nonprofit Harmony Project and older subjects attended three public high schools in Chicago. As explained in a press release:

[Researchers] studied children beginning when they were in first and second grade. Half participated in musical training and the other half were randomly selected from the program’s lengthy waiting list and received no musical training during the first year of the study. Children who had no musical training had diminished reading scores while Harmony Project participants’ reading scores remained unchanged over the same time span.

Over two years, half of the [Chicago] students participated in either band or choir during each school day while the other half were enrolled in Junior Reserve Officer’s Training Corps classes, which teaches character education, achievement, wellness, leadership and diversity. All participants had comparable reading ability and IQs at the start of the study. The researchers recorded the children’s brain waves as they listened to a repeated syllable against soft background sound, which made it harder for the brain to process. The researchers repeated measures after one year and again at the two-year mark. They found music students’ neural responses had strengthened while the JROTC students’ responses had remained the same. Interestingly, the differences in the music students’ brain waves in response to sounds as described above occurred after two years but not at one year, which showed that these programs cannot be used as quick fixes, [Northwestern neurobiologist Nina Kraus, PhD] said. This is the strongest evidence to date that public school music education in lower-income students can lead to better sound processing in the brain when compared to other types of enrichment education, she added.

“Research has shown that there are differences in the brains of children raised in impoverished environments that affect their ability to learn,” Kraus further explained in the release. “While more affluent students do better in school than children from lower income backgrounds, we are finding that musical training can alter the nervous system to create a better learner and help offset this academic gap.”

Previously: Pump up the bass, not the volume, to feel more powerful, Denver rappers’ music motivates kids (of all ages) to eat better and Brains of different people listening to the same piece of music actually respond in the same way.
Photo By: CherryPoint

From August 11-25, Scope will be on a limited publishing schedule. During that time, you may also notice a delay in comment moderation. We’ll return to our regular schedule on August 25.

Ethics, Genetics, Medicine and Society

Film documents rise and fall of a genome matching service – and poses tough ethical questions

Film documents rise and fall of a genome matching service - and poses tough ethical questions

Jesse_01When I think of “science fiction,” I picture three-eyed aliens with purple-and-gold tentacles — not the disturbing demise of a man, and a company, depicted in the film “The Perfect 46.”

Nor do I expect to ponder the ethics of a company that strives to produce genetically “pure” children.

Yet this is precisely the type of science fiction filmmaker Brett Ryan Bonowicz dished up to a sold-out Stanford crowd last week. Following the film, an all-star panel of genetics experts fielded questions.

The film’s premise is simple, and alluring. People can send their sequenced genome, along with their partner’s,  in to a company called The Perfect 46 and allow its proprietary algorithm to figure out if their children will be born genetic-defect free — or not.

“Jesse [Darden, the company’s CEO] wasn’t going to cure the diseases, he would just breed them out. It made a lot of people uncomfortable,” said one of the characters in the film.

So uncomfortable, in fact, that the company, and its leader Jesse Darden, played with a standout performance by actor Whit Hertford, unravels quite thoroughly – with Darden’s painful personal and professional demise forming the meat of “The Perfect 46’s” somewhat-tortured plot.

For me, the ethical quandary is a no-brainer: perfect – what fun is that? My husband and I are both far from perfect, and if we had a perfect child, it certainly wouldn’t be anything like us.

More seriously, however, the film poses thorny questions about the future of consumer genetics, a boom-and-bust field that’s both promising and terrifying. “The Perfect 46” doesn’t answer these questions, but the post-screening panelists delved into some of them.

During the talk, the experts made  it clear the technology featured in the film isn’t there – yet. Right now, if scientists sequence a genome , they don’t know the meaning of the many versions, or allele , of the gene that pop up. “Often, we don’t know if it’s disease-causing or not,” said panel member Michael Snyder, PhD, Stanford professor and chair of genetics.

Although the film takes place in the “near future,” corporations that provide basic genetic screening are already available, the experts said. And corporations may not be providing adequate counseling for potential parents, panel member Sandra Lee, PhD, a senior researcher at the Stanford Center for Biomedical Ethics, pointed out.

The Stanford-heavy audience seemed to dig the movie, but I thought the film would be more effective if its lessons were a little subtler and its pace a bit quicker.

Still, the questions it asks are real, even pressing, and not science-fictiony at all.

Becky Bach is a former park ranger who now spends her time writing, exploring, or practicing yoga. She’s currently a science writing intern in the medical school’s Office of Communication & Public Affairs.

Previously:Stanford patient on having her genome sequenced: “This is the right thing to do for our family”, Stanford geneticist discusses genomics and medicine in TEDMED talk, New recommendations for genetic disclosure released and A conversation about the benefits and limitations of direct-to-consumer genetic tests
Screenshot of movie courtesy of Clindar

From August 11-25, Scope will be on a limited publishing schedule. During that time, you may also notice a delay in comment moderation. We’ll return to our regular schedule on August 25.

Cancer, Men's Health

Managing a prostate cancer diagnosis: From leader to follower, and back again

We’ve partnered with Inspire, a company that builds and manages online support communities for patients and caregivers, to launch a patient-focused series here on Scope. Once a month, patients affected by serious and often rare diseases share their unique stories; this month’s bonus column comes from patient advocate Jim Rieder.

Caring for others has always been part of my approach to life. I built my career in health care serving as the CEO of a statewide non-profit foundation, in addition to being the CEO of seven diverse types of hospitals. Naturally, I was intimately familiar with the steps necessary for a person to become an empowered patient. But when I was forced into the role of being the patient, the initial transformation was surprisingly more intense and unsettling than I had imagined it would be.

Managing prostate cancer is a battle. Recognize it as such. Invest the time and energy necessary to empower yourself with the knowledge you’ll need to make informed choices about your path of treatment

When a person is diagnosed with any type of cancer, the obvious objective is to get rid of it completely as quickly as possible. After being diagnosed with prostate cancer in 2002 and doing my due diligence, I ultimately decided that a radical prostatectomy was the best course of treatment for me. I had the surgery in 2003, and I’m very happy to report that I’ve been cancer-free ever since. However, it’s important to recognize that there’s not a one-size-fits-all solution for treating prostate cancer.

In response to prostate cancer diagnosis, it’s critical to take a step back, take a few deep breaths, and try to approach the situation calmly and logically. Don’t let anyone rush you. There’s ALWAYS time to evaluate the medical options and get a second opinion from another medical expert who ideally is not affiliated with the same practice as the physician who provided the initial diagnosis or treatment recommendations. Know that watchful waiting or active surveillance can be viable options. Every treatment has side effects, which typically include erectile dysfunction and/or incontinence. The skill of the physician and the amount of experience specific to the procedure being performed are very important in minimizing the presence and ongoing impact of these side effects.

Some guys pursue their treatment and quietly return to business as usual without ever talking about their prostate cancer or its side effects. While I respect the option of maintaining privacy, I encourage anyone who’s facing a diagnosis of prostate cancer to reach out for help from others who have already traveled the same path, and to reciprocate down the line by helping others who will be grappling with the voluntary transition into joining the prostate cancer community. Also recognize that prostate cancer affects spouses or partners, as well as family members. Their support is also very important.

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Cardiovascular Medicine, Research, Stanford News

Study highlights increased risk of death among patients with atrial fibrillation who take digoxin

Study highlights increased risk of death among patients with atrial fibrillation who take digoxin

After a decade of focusing on treatments for heart failure and heart attacks, it’s atrial fibrillation’s turn in the spotlight, said Mintu Turakhia, MD, MAS,  assistant professor of cardiology and director of cardiac electrophysiology for Palo Alto VA Health Care System.

“It’s a huge cost to society and one of the most common inpatient diagnoses,” Turakhia said.

Atrial fibrillation is an irregular and rapid heart rate — caused by spasms of the heart’s upper chambers — that afflicts more than 3 million Americans, increasing their risk of stroke and heart failure. Turakhia and his team planned to dig beneath the surface of atrial fibrillation using data from more than 122,000 patients with recent atrial fibrillation diagnoses in the U.S. Department of Veterans Affairs (VA) health-care system.

They started by examining the efficacy of digoxin, a generic drug derived from the plant foxglove. The results were striking: Patients who received digoxin were 3 percent more likely to die than similar patients.

“The take-home point is to question whether people should really be on this drug,” Turakhia said in a release. “These data challenge the current guidelines.”

Both doctors and patients assumed digoxin was safe because derivatives of foxglove had been used for centuries, not because it had been proven safe or effective, Turakhia said. He said there are many other preferable treatments for atrial fibrillation and he plans to work to standardize treatment for atrial fibrillation in coming years.

“Can we be smarter about how we deliver atrial fibrillation care so it’s delivered efficiently with less variation?” Turakhia asked.

The study will be published in the Aug. 19 issue of the Journal of the American College of Cardiology, which appears online today.

Becky Bach is a former park ranger who now spends her time writing, exploring, or practicing yoga. She’s currently a science writing intern in the medical school’s Office of Communication & Public Affairs.

Previously: Hybrid procedure helps treat difficult cases of atrial fibrillation and Newly approved drug appears to provide more cost-effective stroke prevention than warfarin

From August 11-25, Scope will be on a limited publishing schedule. During that time, you may also notice a delay in comment moderation. We’ll return to our regular schedule on August 25.

Cancer, Genetics, Research, Science, Stanford News

Unraveling the secrets of a common cancer-causing gene

Unraveling the secrets of a common cancer-causing gene

The Myc protein can cause a lot of trouble when it’s mutated or expressed incorrectly. Under those condition it’s called an oncogene, and it’s associated with the development of more than half of all human cancers. But because its cellular influence is vast (it controls the expression of thousands of genes and regulatory molecules), it’s been tough for scientists to learn which of its many effects are cancer-causing.

Now oncologist Dean Felsher, MD, PhD, and his colleagues have found that just a handful of genes are responsible for the Myc oncogene’s devastating outcomes. Their work was published today in Cancer Cell. As I wrote in our release:

The genes identified by the researchers produce proteins that govern whether a cell self-renews by dividing, enters a resting state called senescence or takes itself permanently out of commission through programmed cell suicide. Exquisite control of these processes is necessary to control or eliminate potentially dangerous tumor cells.

In particular, the researchers found that Myc works through a family of regulatory RNA molecules that govern how (and when) tightly packaged genes in the DNA/protein complex called chromatin are made available for transcription into proteins that do much of the work of the cell. Understanding this process might help researchers find ways to throw a molecular wrench into the Myc mechanism.

“One of the biggest unanswered questions in oncology is how oncogenes cause cancer, and whether you can replace an oncogene with another gene product,” Felsher told me. “These experiments begin to reveal how Myc affects the self-renewal decisions of cells. They may also help us target those aspects of Myc overexpression that contribute to the cancer phenotype.”

The reliance of many cancer cells on oncogenes like Myc is called oncogene addiction. In many cases, blocking the expression of an oncogene, or tinkering with its activity, causes cancer cells to stop growing and tumors in animals to regress. Recently Felsher and his colleagues published an article in the Proceedings of the National Academy of Sciences describing how inactivating two oncogenes at once can work better to fight cancer in animal models by making it more difficult for the cancer cells to develop resistance to therapy.

Previously: Tool to identify the origin of certain types of cancer could be a “boon to doctors prescribing therapies” and  Smoking gun or hit-and-run? How oncogenes make good cells go bad

From August 11-25, Scope will be on a limited publishing schedule. During that time, you may also notice a delay in comment moderation. We’ll return to our regular schedule on August 25.

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