As a kid growing up in Veracruz, Mexico, Michelle Armenta heard a lot about medicine from her parents. Her anesthesiologist father would describe finicky surgeries over dinner; her dentist mother would scour her mouth for cavities and chipped fillings. Back then, she didn’t have the exact words to describe the kind of scientist she hoped to become.

What she couldn’t have predicted was that her postdoc at Caltech would rely on a patient having exactly the right words to describe how Armenta’s science was affecting him. The patient in question had recently injured his spinal cord, losing both movement and feeling from his shoulders down. She and her labmates —including fellow Wunderkind Luke Bashford — wanted to see if they could, through wires surgically implanted in the patient’s brain, use electrical currents to create sensations that he’d lost.

After the electrodes were inserted in the operating room and the patient had recovered, they began trying to create feelings in his arm with nothing more than signals inside his skull.

“His injury was 1 1/2 years or two years out, but he was able to recall what it felt like prior to his injury,” Armenta said. “He used natural expressions of someone pressing on a specific part of his forearm, or a small tap, or a slight vibration, and also feelings of movement what we usually call proprioception: He felt like what we would feel like when you would move your elbow or your arm to the right or the left.”

Armenta has since moved on to the visual prosthetics company Second Sight Medical Products, but the lab hopes to use this research alongside a robotic arm, so that a patient could manipulate the artificial limb and “feel” how it’s coming into contact with the world.

— Eric Boodman

The Caltech lab, before Luke Bashford’s arrival as a postdoc, had already shown that a patient could learn to control a cursor on a screen or a prosthesis with his or her brain: It was a question of putting electrodes in the right spots so a computer could read the person’s intention.

But our movements aren’t quite that simple. When you move your hand, you feel its position shift in space. Close your eyes and you still know where it is.

Not so for someone who’s had a spinal cord injury and lost all movement and sensation from the shoulders down. Even if that person can control a robotic prosthetic, their movement will be choppy if they aren’t getting that kind of spatial feedback.

So Bashford — along with fellow Wunderkind Michelle Armenta — wanted to figure out if there was a way to mimic such sensations in an artificial limb. That also meant surgically implanting electrodes into a person’s brain — but instead of recording certain natural patterns of electricity, these electrodes would be emitting their own jolts. When the team was finally ready to try it on a patient, a buzz in the brain often resulted in a sensation in his paralyzed arm.

“He would describe the feeling of a squeeze, or a tapping, or movement to the right, and then he would give the duration and the location,” said Bashford. “The participant has a memory of his life before his injury, he’s able to recall these sensations not as anything particularly strange. … They’re naturalistic, but obviously they’re not produced in a natural way.”

Bashford is originally from London, and on top of California’s biomedical engineering charms, he’s also been enjoying its mountain biking trails. There is still also plenty of work to be done in the lab. The team’s hope is to bring these two branches of their work together, so that a person is not only able to move a prosthetic, but also get sensations from it.

— Eric Boodman

When not in a cognitive neuroscience lab, Christopher Berger heads to the beach to relax; surfing is his “zen time,” he said.

But a beach isn’t necessarily a relaxing place for the brains that Berger studies. If a wave is coming in, a person will see it coming, hear it breaking, smell the salt in the water, and feel the sand underfoot. The brain must pull all of those sensations together in the brain to make a complete and coherent picture.

But what if you can’t see or hear or feel something? Could that experience still be replicated for people whose perception is different — like deaf people or people whose vision or nerves are compromised?

Maybe. That’s what Berger, a postdoctoral scholar at Caltech, is trying to figure out.

Berger studies how brains integrate all the sensory information they receive. It’s not always straightforward. Think of a ventriloquist — the voice isn’t coming from the puppet, of course, but because our brains hear the voice and see the puppet, the two get connected.

The same thing can happen with things we imagine. “If you imagine seeing that object, you will also misperceive the sound as coming from the place you’ve imagined it coming from,” Berger explained.

Understanding how our brains process sensory information could have very concrete uses. “The more we understand about basic foundations of perception, the more we can do to restore it to individuals who lack perception,” Berger said.

That could mean better prostheses that can “restore” a person’s sense of touch or sense of sight after a stroke or an injury.

— Kate Sheridan

We usually don’t associate bacteria with cancer cells, but research performed by Susan Bullman, a postdoctoral fellow at the Dana-Farber Cancer Institute, hints that the two go together.

In particular, Bullman showed that fusobacterium — a species normally found in the mouth — associate and travel with colon cancer tumors.

“We were absolutely surprised by that,” Bullman said. Her results suggest that bacteria are linked to particular types of cancer rather than their anatomical location.

Even more promising, antibiotics targeting fusobacterium slowed the growth of patient tumors that had been transplanted into mice. Although researchers still don’t know how the microbes are abetting cancer cells, they hope that using drugs to target specific bacteria within tumors could help halt disease progression in human patients.

Bullman first became interested in the power of bacteria when her brother was born with cystic fibrosis — a disease involving a buildup of mucus in the lungs that increases the risk of infection. Still just a kindergartner, Bullman absorbed her parents’ lessons on how microbes could be transmitted from one person to the next and decided to become a scientist.

While becoming an expert in medical microbiology, Bullman realized that studying cystic fibrosis “hit a little too close to home.” She decided to focus instead on colorectal cancer, one of the most common causes of cancer-related deaths in the U.S. Her plan is to use initial startup funds from a prestigious K99 grant from the National Institutes of Health to open her own lab focusing on the connection between microbiota and cancer progression.

“There’s a ton more research that we really need to do,” she said. “This is what fuels me and motivates me to think about novel approaches to treating and preventing cancer.”

— Justin Chen

As early as his freshman year at Harvard, Tyler Clites knew he wanted to build better prosthetics. He didn’t know that would mean designing better amputations, too.

“In a traditional amputation, muscles are tied down within the residual limb so they can’t move, and muscles like to be able to move,” said the postdoc. Instead, he and the team led by Hugh Herr, head of biomechatronics at the MIT Media Lab, envisioned a surgery in which muscles would be tied to each other, agonist to antagonist, so that when one contracts the other stretches. “That replicates the mechanisms that the body naturally uses, and that the brain expects to see for joint movement,” Clites explained.

By allowing those muscle pairs to continue to move in tandem, the team could, with sticker-like sensors, read exactly how the person wanted to move the leg that’s no longer there, and transmit that intention to a robot prosthetic. But perhaps the craziest part is that in retaining those upstream muscular relationships, the patient also retains much of the ability to feel how their missing extremity is moving through space. “Our patients have an intuitive sense of where their prosthetic toe is,” said Clites.

Four years ago, this was an idea on a whiteboard. Now, it’s been tried out in 10 humans. They don’t just have meticulous control over their artificial limb; they also feel like it’s a part of their body.

Clites likes to tinker with other, less high-tech projects when he’s outside of the lab — he and his wife recently rebuilt a piano together. But there’s also still plenty of work to do on these prosthetics. They’re now collecting data on their first above-the-knee surgery, and they’ve tweaked the prosthetic so it’s no longer confined to the lab. For their next experiments, Clites said, he’s going to take the patients off-roading.

— Eric Boodman

Bone marrow transplants cure leukemia and lymphoma with what’s inside them — stem cells that make blood cells.

Those stem cells are also why scientists think they might be able to harness bone marrow to treat diseases like sickle cell anemia. But despite decades of research, creating these hematopoietic stem cells in the lab is currently impossible.

Enter Erich Damm and his zebrafish.

Zebrafish and humans make blood cells in similar ways, but seeing it happen in zebrafish is easier, Damm explained. The embryos are transparent, so if he sticks them under the microscope, he can see the fish develop and watch blood cells flow.

“We’re trying to figure out how the embryo does it, so it can teach us how to do that in the lab,” said Damm, a fourth-year postdoctoral research associate at St. Jude Children’s Research Hospital.

What Damm discovered — and recently published in Nature Cell Biology — is that neural crest cells might influence how and when these stem cells are created. (A fish embryo’s neural crest cells eventually become brain cells and nerve cells.)

In theory, understanding the signals that these neural crest cells are sending might help scientists create blood cells by mimicking the environment into which they are born.

Damm is a transplant himself. He arrived in Memphis four years ago from Toronto, where he did his graduate work, and speaks highly of his new city’s vibrant live music scene and mild climate.

“It’s a city where you can run outside all year round,” he said — and he does, running the Memphis marathon once and the half-marathon other years.

“I’m not fast enough to be competitive with these crazy 20-year-olds who are running at warp speed,” he said. “As long as I complete it, I’m happy with that.”

— Kate Sheridan

Over billions of years, evolution has enabled birds to fly and chameleons to change color.

Cesar de la Fuente-Nunez is harnessing this ingenuity to design new medicines faster and cheaper than traditional methods. As a postdoctoral fellow at the Massachusetts Institute of Technology, he has created a computer algorithm that mimics the natural process of evolution to develop small proteins, called peptides, with powerful antimicrobial properties.

De la Fuente-Nunez said that his goal is to “go beyond what nature has explored and design new [peptides] unlike anything we see in the biological world.”

Using his algorithm, he increased the power of Pg-AMP1 — a peptide from the guava plant with weak antimicrobial activity. Through many virtual cycles of evolution, the peptide mutated into thousands of variants — the strongest of which cleared bacterial infections in mice.

In the future, de la Fuente-Nunez will test computer-generated peptides in humans to demonstrate how artificial evolution can be a critical tool in combating the growing danger of antibiotic-resistant bacteria.

Like evolution’s winding path, de la Fuente-Nunez’s career trajectory has taken him through laboratories in Spain, Canada, and the United States. Meeting scientists with different backgrounds has inspired him to set up science hubs in Brazil and Colombia — online collaborations in which de la Fuente-Nunez shares ideas and mentors more junior scientists.

“Having done science in different places has really enriched me as a person and as a scientist,” de la Fuente-Nunez said. "The future of science really lies in this huge diversity of people who are interested in solving scientific problems.”

— Justin Chen

Shekinah Elmore is a resident in the Harvard Radiation Oncology Program who has her own experiences with cancer. She was diagnosed with Li-Fraumeni syndrome, a rare genetic disorder that predisposes her to some of the same cancers she treats.

"Will knowledge about our personal genomes deliver us, or be our undoing?" she asked in a New England Journal of Medicine piece. "My knowledge has both empowered and broken me — I don’t know which it’s done more. Flying between fatalism and denial, I eventually decided that I had to live, normally.”

But Elmore has done more than live “normally.” Not only does she care for patients in Boston, she also works to bring cancer care to sub-Saharan Africa.

Armed with a master’s degree in global health and biostatistics from Columbia and several years of experience implementing HIV/AIDS programs in sub-Saharan Africa, Elmore began medical school knowing that she would continue her global health advocacy, research, and on-the-ground efforts.

During medical school, at Harvard, she conducted research on palliative care needs in Malawi, worked with Partners in Health in Haiti, and investigated patient experiences with cancer in Rwanda on a Fulbright award. Now, as a fourth-year resident, she’s shifted her attention to improving global radiotherapy delivery and cancer care — currently, in Zimbabwe.

“It seems like this great but impossible challenge to think about how we actually develop cancer systems that have radiation as a part of them,” she said.

For Elmore, this research fits into her philosophy on medicine. Having been a patient herself, she said that she always tries to ask questions from the patient perspective. But she goes one step further: “What questions can I ask to help move the needle on health equity?”

— Orly Nadell Farber

For scientists trying to treat neurodegenerative disease, the process can feel like building a car while driving it. No one’s exactly sure what fuels the brain-destroying effects of Parkinson’s and Alzheimer’s disease, so each new treatment is a shot in the near-dark, based on incomplete science and subject to a high risk of failure.

Jessica Flynn, a postdoc at the National Institutes of Health, is hoping to change that by exploring the microscopic mechanisms that lead to neurodegeneration.

Her work involves using super-sensitive microscopes to unravel just how the body produces a protein called amyloid, which plays a role in Parkinson’s and Alzheimer’s. Scientists have long known that different forms of the protein contribute to different diseases, but Flynn’s intensive work has showed that the process by which amyloid folds into its final shape might explain particular symptoms of neurodegenerative disease, a finding that could one day affect how Parkinson’s and Alzheimer’s are diagnosed and treated.

Flynn’s interest in neurodegeneration began with a tragedy: In her freshman year of college, her grandfather died of Parkinson’s disease.

“Watching him change from this very lively, strong man into someone who was greatly hindered by his disease, it was a terrible experience for my family,” Flynn said. “I thought, if I could use my love of science to solve this problem so many people experience, I would do that.”

She first planned a career in medicine, majoring in pre-med before realizing “it wasn’t my jam,” she said. “But then I took a chemistry class and it was like, ‘These are my people.’”

Now, years later, Flynn is chipping away at the fundamental mysterious of neurodegeneration, shining a light in the dark that first attracted her to biomedical science.

— Damian Garde

Nicole Gaudelli set out to find new antibiotics and ended up at the cutting edge of the quest to rewrite human life.

She showed up at David Liu’s Harvard University lab in 2014 with the intention of studying how evolution can give birth to new enzymes that might prove useful in treating infections. But she began to get distracted by her colleagues’ work in editing DNA. A year and a half later, when Liu’s lab came up with a brand-new way to correct errors in the human genome, her head was completely turned.

That technology is called base editing, and it functions like a pencil alongside CRISPR-Cas9’s famous scissors. Where other editing techniques work by snipping out errant code and pasting in a correction, base editing allows scientists to change individual letters of the genome without breaking the double helix.

“Basically it goes directly from the thing you don’t want to the thing you do want without cutting the DNA,” Gaudelli said.

To that point, Gaudelli had focused on basic research, but in base editing, she saw a technology that might one day help people with devastating conditions and potentially cure some inherited diseases.

Gaudelli’s quest to forge a career in science began in the fifth grade, when she was tasked with drawing a picture of what she wanted to be when she grew up. Science was already her passion, but textbooks spoke of Louis Pasteur and Francis Crick while offering few female role models. But after some encouragement from her father, she drew a scientist in a lab coat, adding “a disproportionately large pink bow” to leave no question about gender, and turned it in.

Now Beam Therapeutics, founded earlier this year, is pressing forward in hopes of bringing base editing to patients, and Gaudelli is leading a team of scientists.

— Damian Garde

Lin Guo, a research associate at the Perelman School of Medicine within the University of Pennsylvania, studies the bizarre and deadly process of protein misfolding that occurs in amyotrophic lateral sclerosis.

When they are folded properly, Guo said, proteins are “little machines that live in your body and do all the work" of keeping you alive.

When proteins misfold and become oddly shaped, they no longer perform their jobs. Even worse, in some instances, contorted proteins can recruit normal proteins to misfold as well, creating a chain reaction where abnormal proteins clump together and disrupt the inner workings of the cell.

Such is the case with the untreatable neurodegenerative disease ALS — an illness in which neurons that control voluntary muscles required for speaking, swallowing, and breathing die. Sometimes called Lou Gehrig’s disease for the famous ballplayer who had it, the disease also affected Stephen Hawking.

Guo’s research has identified a possible solution relying on nuclear-import receptors — a type of protein best known for shuttling other proteins in and out of the nucleus. In a surprising finding, Guo showed that these import receptors could untangle clumps of proteins responsible for ALS in test tubes, yeast cells, and flies. Boosting the amount of import receptors in fly models of ALS doubled the diseased animals’ lifespan.

In the future, Guo imagines combating neurodegeneration in human patients by using drugs that increase the activity or amount of nuclear-import receptors in the cell.

“If we could achieve the same extension of patient life, that would be remarkable,” said Guo, “Right now the only drugs available for ALS can extend patients’ life for three months.”

— Justin Chen

Dennis Jones, an enthusiastic traveler himself, studies movement — through lymphatic vessels. His research follows the course of both infections and cancer.

“Answering new questions that no one has studied before” feels more like a hobby than a job, he said.

On the infection side, Jones examines how methicillin-resistant Staphylococcus aureus (also known as MRSA) releases toxins that can damage lymphatic muscle cells. The damage impedes flow and can cause lymphedema, or chronic swelling, in patients.

On the cancer side, Jones has shown that as cancer cells move through the lymphatic system, they wrap around existing blood vessels and co-opt their nutrient supplies — a finding that has extensive implications for cancer therapy. Going forward, Jones plans to study how cancer cells evade the immune system in lymph nodes, a site rich with patrolling immune cells.

Now a postdoctoral fellow at Massachusetts General Hospital and soon to kickstart his own lab at Boston University, Jones has come a long way from his hometown of Collins, Miss. With a population just shy of 2,600, many people from Collins don’t go to college let alone graduate school, Jones said. He completed his B.S. at Morehouse College and his Ph.D. at Yale.

But his Mississippi roots run deep. His four siblings remain there, and his twin sister just completed her registered nursing degree. “I think I’m more proud of her than I am myself,” he said.

Jones is surrounded by people with a passion for health and science. He met his wife in graduate school, and said they lean on one another for both “emotional and scientific support.” As for their nearly 4-year-old daughter, she may catch the science bug in the future: “She’s curious about a lot of things, so maybe that’s the start of being a good scientist.”

— Orly Nadell Farber

Viruses have been around for millions of years, shaping the course of our planet and doing mysterious work within us every day. To Kellie Jurado, nothing could be more fascinating.

The Yale University postdoc first gazed into the abyss of virology as a curious undergrad at New Mexico State University, finding that every morsel of information on those ubiquitous and sometimes ancient infections led her down a deeper path of interest and discovery.

“These are evolutionarily perfected machines,” Jurado said. “What could be cooler than that?”

She landed her current post at Yale University just as the Zika virus emerged in the Americas, the outbreak of a poorly understood virus that gained global attention. And her enduring curiosity came in handy.

Jurado’s work helped elucidate Zika’s pathology, explaining the many ways it can spread among people and get passed on to fetuses in the womb. Her most recent discovery, published in Nature Microbiology earlier this year, offered clues to Zika’s devastating effects on the brain. Studying the brains of mice infected with the virus, Jurado and her colleagues observed that the body’s natural defenses, while trying to fight off Zika, were inflicting unintended damage on the brain.

That discovery widened Jurado’s aperture by exposing her to the many outstanding questions around the immune system’s role in the central nervous system. Now she’s digging into how immune cells police just which molecules get access to the brain, probing a system that has deep importance both in preventing infection and in potentially sneaking therapeutic antibodies past the body’s gatekeepers.

It’s a pursuit that will undoubtedly bring up questions that only lead to more questions, which, to Jurado, is a reminder of why she wanted to be a scientist in the first place.

“I really loved the idea of being curious for a career,” she said. “We’re lucky that even exists.”

— Damian Garde

When it came time to think about his residency, Dr. Abraar Karan decided he wanted to take a page from Dr. Paul Farmer's book.

Farmer, like Karan, works at Brigham and Women's Hospital in Boston and is best known for his work treating and advocating for people around the world who are sick and living in poverty, through the nonprofit he co-founded, Partners in Health.

Karan — who earned a medical degree at the University of California, Los Angeles, and a master's degree in public health at Harvard — had a passion for global health ever since he was a medical translator and assistant in the mountains of the Dominican Republic during a service trip as an undergraduate student at Yale. He's traveled to Uganda, Nicaragua, Thailand, Mozambique, and his home country, India, for research and clinical work.

Karan quickly realized that to make a long-term impact, he and others would need to address the conditions that contribute to sickness in the first place.

Now, the second-year resident zeroed in on one way to do that: prevent mosquito bites. Karan co-founded a company called Hour72+ that's producing an insect repellant he hopes will last longer and be more effective than others on the market.

The key ingredient: a special polymer first developed more than a decade ago. The father of Karan's co-founder — one of his college roommates and a student at Harvard Business School — had created the polymer for surgical adhesives. The idea never took off, but the patent still existed.

“The characteristics of the polymer allows for long-term adhesion to the skin without absorbing through the skin,” Karan explained. The company won this year's Harvard Business School New Venture Competition. Karan and his business partner are hoping to launch the Hour72+ spray in the U.S. next year and are also partnering with health officials to provide the repellant to people in Nigeria and Brazil.

Karan's work has fueled his love of travel. He's gone whitewater rafting in almost every country he's worked in. He’ll keep traveling: In addition to being a second-year resident, he’s also one of a handful of global health fellows, able to spend half the year in both 2019 and 2020 working abroad.

— Megan Thielking

Medication adherence is a notoriously difficult problem to tackle. Ameya Kirtane thinks it might help patients if they didn’t have to take pills so often — and he hopes to find a way to make that happen.

“There’s a significant amount of pill fatigue that sets in, and it results in millions of dollars in avoidable health care costs,” said Kirtane, a postdoctoral researcher at Massachusetts Institute of Technology who works with chemical engineer and MIT professor Bob Langer.

Kirtane wanted to find a way to deliver a drug for a whole week, rather than just for a day. The central challenge: Anything that’s ingested doesn’t stick around in the digestive tract for that long.

So Kirtane and his colleagues designed a capsule made of a star-shaped structure, with a dose loaded on each point and folded inward. Once the capsule is swallowed, the points unfold and gradually release the doses over a week. In studies on pigs, the capsules stuck in the stomach, released three HIV drugs over a week, and then disintegrated to pass through the gastrointestinal tract. Their work, published in Nature Communications, has been licensed to a company for use in humans.

“We are planning to try this with other drugs that could benefit from these kinds of therapies and trying to prolong the administration of these drugs,” Kirtane said.

Kirtane, who grew up in India, spends a good amount of his free time going to concerts. He’s loved Bollywood music since he was a kid — and still loves it — but has branched out thanks to members of his wife’s family, who studied classical music.

But he doesn’t totally tune out science once he leaves the lab. A personal favorite: A PBS documentary from earlier this year on the hunt for the Higgs boson.

“It taught me a lot about patience in science. Even if you don’t see the implications of your work right then and there, someone is going to benefit from it,” Kirtane said. “That’s what gets me out of bed every single day.”

— Megan Thielking

Ruiting Lin is a cancer biologist whose work spans an array of cellular pathways and metabolites. One of her projects examines how dietary supplements influence cancer development.

Chondroitin sulfate is among them. Lin’s work has shown that the supplement, frequently taken for osteoarthritis, may promote the growth of melanoma cells harboring a specific — and common — mutated oncogene. This finding is part of a larger body of work aiming to arrive at “precision diets,” which would be designed based on a person’s genetic profile.

In addition to her dietary research, Lin is interested in studying cancer drug resistance and lung cancer in particular. Her aunt, who she said helped raise her, passed away from lung cancer.

“She triggered my motivation,” said Lin. “I want to challenge myself to see if I could make a contribution” in the fight against cancer.

Born in Shandong, China, Lin completed her bachelor's degree there, but moved to Shanghai to pursue a doctorate at Fudan University. She came to the U.S. for a postdoctoral fellowship at the Winship Cancer Institute at Emory.

Lin publishes her research, but rarely shows off her other work: drawings and watercolor paintings. “Art balances my science side,” she said. She envisions the two sides merging in the future, using her artistic skills to help educate the public about cancer biology. “I really want to make my talent in art contribute to science,” said Lin.

— Orly Nadell Farber

Drew Linsley’s work might make some pathologists nervous. As a postdoc at Brown, Linsley is working on a way to make computer vision good enough to automatically distinguish a healthy cell from a diseased one.

“Biomedical imaging is a field where, really, machine vision hasn’t made a huge impact yet,” Linsley said. “What I do every day is try to, in effect, reverse-engineer the visual system and develop a computer visual system that can see the world like we do.”

Linsley was doing his Ph.D. in 2012 — which, he said, was “an important year for nerds like me.” That year, an artificial intelligence researcher at the University of Toronto named Geoffrey Hinton and his group published a paper about an algorithm called a convolutional neural network. Basically, this algorithm was way, way better at sorting things into categories than previous computer vision systems — which is the whole point of artificial intelligence.

But these models have limits. If you show these algorithms a kind of dog it has never seen before, it might struggle to categorize it. A human would not — we can extrapolate based on our past experience to categorize something new.

The perceptual-grouping-type algorithms that Linsley is developing, could push the field forward — which might explain why his life is “hectic” right now, Linsley said. But he and his wife, a writer, still find time to see their friends and walk their border collie.

“Eventually, I’ll get to that work-life balance,” he said. “I’m working on it.”

— Kate Sheridan

As a child, Shawn Liu was introduced to medicine as he watched his physician parents treat patients. But the experience led him to some deeper questions: Why does a disease develop in the first place? And could answering that question open up new avenues for treating it?

“I saw that understanding the mechanism, for me, it was more attractive,” Liu said.

Liu, 33, who grew up in China, is now a postdoc at the MIT-affiliated Whitehead Institute, where he is at work uncovering epigenetic factors in disease. He has focused on the role of methyl groups in turning genes on and off, and how errant methylation can lead to a disease.

In one of his key discoveries, Liu figured out how to apply CRISPR genome-editing technology to methyl groups. By tweaking them, Liu showed that it was possible to change gene expression and influence, for example, cell fate. He then turned his approach to a model of Fragile X syndrome, a neurological condition. The disease occurs when one group shows “hypermethylation,” in turn silencing a key gene. Liu and his colleagues reported that they could reduce the methylation, which then allowed for normal gene expression.

“This result suggests epigenetic editing could be a treatment for Fragile X syndrome and maybe other diseases,” Liu said.

Liu, who enjoys photography and playing badminton outside the lab, is now studying another neurologic condition to see how widely the technology could be applied. And even if his research doesn’t immediately point to new treatment approaches, it could uncork a greater understanding of the mechanisms behind diseases.

— Andrew Joseph

Initially, the discovery looked like a mistake. Dr. Caroline Maloney, a surgical resident and postdoc at Northwell Health, was trying to figure out if gefitinib, a drug approved for other cancers, would work on osteosarcoma. She knew the medication acted on a specific protein in these other kinds of tumor cells. It seemed to work on the cancer she was studying, too. But the protein it should have been acting on was nowhere to be found.

Maloney found the results frustrating, but her mentor urged her to see where they led. It turned out the drug had another, unknown protein target. Cancer cells don’t just proliferate uncontrollably — they also co-opt their surroundings into helping them — and it looked like gefitinib was helping to reverse that. “We are changing the way that the immune cells are reacting to the cancer so that they are acting in an anti-cancer way, rather than being hijacked by the cancer,” Maloney explained.

After testing it on mice during her Ph.D., she’s planning on moving into clinical trials, hoping to get the drug into children as soon as possible. Her hope is that this drug will help those kids whose cancers pop up elsewhere after their original osteosarcoma has been removed.

This was hardly the future she’d imagined for herself as a kid. She’d always wanted to be a dancer. But in some ways, the two jobs aren’t so different.

“They’re both meticulous forms of art — surgery is very artistic, they’re both athletic in their own way … they’re very precise and demanding fields,” she said. “I’ve been trained to put up with the world of surgery and how hierarchical and how strict it is from my ballet training. There’s no one more demanding in the world than a ballet teacher.”

— Eric Boodman

Dr. Jennifer Manne's public health research spans the globe: She's studied access to Chagas disease treatment in the Americas, collected data on diabetes care in South Africa, and analyzed the impact of mandatory STD testing policies for female entertainers in South Korea.

As a Ph.D. student at the Harvard T.H. Chan School of Public Health, Manne concentrated on global health, where she founded a research project examining access to cardiometabolic care.

Manne went on to earn a medical degree from Boston University and stayed in the city for an internal medicine residency at Beth Israel Deaconess Medical Center. There, she scored a grant to study diabetes diagnosis and care among people with and without HIV in rural South Africa. She looked at everything from the drugs a patient was taking to control her diabetes to whether a patient had ever been formally diagnosed with the disease.

“If you don’t know you have a condition, you can’t implement lifestyle changes or take medicines,” Manne said.

Manne and her colleagues found that only about one-fifth of overweight or obese people at high risk of diabetes remembered ever being offered glucose testing. Among people with diabetes, the findings were equally troubling: Only one-third remembered having a glucose test, and only one-quarter were on medication.

Manne has scrutinized similar issues across the globe. She contributed to a sweeping study of hypertension and diabetes prevalence and India and recently wrapped up an empirical study of health system performance when it comes to treating diabetes in 29 low- and middle-income countries. Manne — who completed her residency in June — wants to continue her research on health system performance in her new role as a clinical and research fellow focused on infectious diseases at Massachusetts General Hospital and Brigham and Women's Hospital.

Manne loves being able to travel for her work. But when she’s in Boston, she sticks to her other favorite hobby: long-distance running. She’s completed more than a half-dozen marathons, many more half-marathons, and often jogs with her husband and 2-year-old daughter.

— Megan Thielking

The idea sounded like waking up from one nightmare into another. The U.S. military, in the grips of Cold War hysteria, wondered how to save the personnel manning submarines if something went wrong leagues under the sea. The solution that scientists proposed was to fill their lungs with fluid.

“It’s like drowning them without drowning them,” said Diane Nelson, a presidential postdoctoral fellow at Carnegie Mellon University.

Five decades after those liquid-breathing experiments began, Nelson is trying to figure out how to use the technique so solve a very different problem. Patients with lung diseases like cystic fibrosis are often given aerosolized drugs to inhale, but their illnesses prevent them from properly breathing them in.

When she first arrived at Carnegie Mellon for her Ph.D., the absurd-sounding idea of delivering oxygen to the lungs through a liquid had been shown to work back in the 1960s: When submerged in a heavy kind of liquid called a perfluorocarbon, cats could breathe and survive for weeks. But when, in the 1990s, researchers had tried to ventilate near-death human babies with an oxygenated version of the stuff, all of the infants eventually died, although the researchers did see some lung improvement before they did.

So Nelson set about showing that an antibiotic delivered to rodent lungs with a drip of this kind of liquid could, in fact, kill bacteria. Now that she’s shown this might be a useful method for delivering drugs, she’s sidled into the chemical engineering department to figure out how best to suspend medications in perfluorocarbons, so that the technique works better.

She’d always thought she would end up a physician. But an undergraduate course on the engineering that underlies our own bodies convinced her she’d rather be tinkering in the lab. “In the hospital, you don’t get to see how an EKG works, you just stick it on a patient, get the readout, and give them a drug,” she said.

— Eric Boodman

When Lindsey Plasschaert was on her way to making a discovery that shook up our understanding of cystic fibrosis, she didn’t initially think what she had found could be that big of a deal. She was making a roster of all the cell types in our lungs, and when she uncovered a new cell type, there were so few of them that she thought they couldn’t be that special.

“I wasn’t as excited as maybe I think I should have been from the beginning,” she said. “I thought that maybe they weren’t that important.”

It turned out, though, that that small group of cells — which Plasschaert and her colleagues dubbed pulmonary ionocytes — are home to much of the activity of a gene that, when mutated, causes CF. The finding could help guide researchers as they work to develop CF therapies.

As a postdoc at Novartis Institutes for BioMedical Research in Cambridge, Mass., Plasschaert has found a sweet spot pursuing basic research and discovery while working in industry.

But Plasschaert was not always on the path to research. In college, she was interested in engineering and thought she might become a veterinarian. Toward the end of her time as an undergraduate, she started working in a biology lab because she liked the professor.

“I thought it was much more exciting than working at the animal hospital where I was volunteering,” she said.

Plasschaert, whose husband is also a scientist (they talk science as they walk to work together), is interested in how cells in a tissue communicate and interact. But her broader passion for science is tied to something more foundational.

“I like solving problems,” she said. “I think I’m someone who could go into different fields in biology. To me it’s sort of like a puzzle. There are these pieces and you can try to connect them, and you do the experiment and figure it out.”

— Andrew Joseph

Lesbian, gay, and bisexual individuals are more likely than their heterosexual peers to experience depression, anxiety, and substance use disorder. Epidemiologist Travis Salway wants to close those gaps by finding ways that communities can better meet their mental health needs.

Salway, a postdoctoral research fellow at the University of British Columbia, wants to answer two critical questions: “What are the barriers that sexual minorities face in getting prompt, affirming health care that they need? And how as a health care system do we reorganize, retrain, or reallocate our resources?”

To figure that out, Salway is collaborating with public health doctors and nurses, mental health providers, business analysts, and ethicists. He wants to dig up the evidence on what will work best to better reach LGB individuals.

Salway has also taken his questions directly to the people he’s trying to help. He’s trained as a suicide crisis volunteer. And when he started his doctoral research on the burden of suicide in LGB communities, Salway realized he needed to ask people about their own experiences. So Salway conducted interview after interview with gay men who had attempted suicide. He wove their stories together with data in his dissertation.

“Even though I am moved by numbers, the stories are also compelling,” said Salway.

He's also particularly interested in digging into the underlying data on sexual minorities and health outcomes. Some people might be reluctant to disclose that they are lesbian, gay, or bisexual, Salway said — and that can have a significant impact on nationwide studies that measure health outcomes.

Outside the office, Salway is pushing to translate his research findings into tangible actions in his own community. In 2015, he founded the LGBTQ Mental Health Roundtable, a community-driven effort to create new suicide prevention programs that target LGBTQ communities in Vancouver, where he lives.

Whenever possible, Salway tries to get out of Vancouver on the weekends to take advantage of the mountains and lakes surrounding the city. He and his partner love swimming, paddleboarding, and hiking with their dog in tow.

— Megan Thielking

Ansuman Satpathy, a postdoctoral fellow at Stanford University, was inspired by his father, a physics professor, to pursue science.

“I saw from very early on that … you could spend your time asking questions that no one knew the answer to,” he said.

Satpathy, who specializes in immunotherapy — a treatment that rallies immune cells to attack cancer — is working to solve a medical mystery: Why do immunotherapies work in some patients but have no effect in others?

To find an answer, Satpathy has combined two techniques that had previously been performed only in isolation. The first isolates the specific T cells, a type of white blood cell, that recognize cancer from thousands of their companions that respond to other threats like bacteria or viruses. The second, through an adroit use of genome sequencing, analyzes genetic switches that turn genes on and off.

“[We can] look very precisely at … the cells that are doing a good job at fighting the tumor and what’s going on in cells or patients that are doing a bad job,” he said.

By understanding which genetic switches are turned on in cancer-responsive T cells, researchers hope to engineer more effective immunotherapies.

It’s a big undertaking, but Satpathy credits Howard Chang, who heads the lab that Satpathy works in, and Mark Davis, an expert in T cells, for providing guidance.

“My career up to this point has really benefited from a lot of good mentors and collaboration,” said Satpathy, who plans to run his own laboratory one day and has already mentored several undergraduate and graduate students.

“That’s a really rewarding part of being in academia,” he said. “You’re able to influence younger people and teach them how to think about science and how to ask interesting questions.”

— Justin Chen

Computer models of proteins — tiny molecular machines that keep us alive — look like dense and incomprehensible tangles of ribbons, but to Franziska Seeger, these models are the key to designing new drugs.

Seeger, a postdoctoral fellow at the University of Washington, studies how proteins break during certain diseases and how to fix them. Each groove or nook in the surface of the diseased protein could be a handhold for another corrective protein. Depending on the scenario, the additional partner could increase the activity of an underperforming protein or calm an overactive one.

Determining how proteins will interact is difficult, but Seeger has taught computer programs, through trial and error, to learn which variables best predict how two proteins will behave around each other.

Building on her success, Seeger plans to lead a startup designing custom protein-based medications targeting cytokine IL-17, a protein involved in autoimmune diseases like multiple sclerosis, as well as proteins from viruses like Ebola and influenza.

“I’m mostly motivated by making a product that has real-world application,” said Seeger.

Much of Seeger’s inspiration stems from her childhood when her mother was diagnosed with multiple sclerosis. The diagnosis spurred Seeger to pursue biology in order to understand the disease. She also began playing chess — over eight hours a day on the weekends — and became an internationally ranked player.

“I’ve alway been fascinated by logic puzzles,” said Seeger, explaining that chess was an outlet for her meticulous mind before she became an expert in protein structure.

“I don’t play as much chess anymore as I would like,” Seeger said. But "I have an app on my phone and I join local chess clubs once in a while if they let me.”

— Justin Chen

The quest to cure cancer has long had a chicken-and-egg problem. If you’re going to develop a treatment for people, you first have to test it in animals. But if you can’t accurately replicate human tumors in mice, there’s no telling whether your drug actually has a shot.

Felipe de Sousa e Melo, a postdoc at Genentech, has spent the last decade working to solve that problem in colon cancer.

When caught early, the disease can be swiftly treated with surgery, but for patients whose tumors spread, there are few options for treatment and dismal odds of survival. That’s in part because scientists have only a limited understanding of how colon cancer works on a biological level, and that uncertainty has made it exceedingly difficult to develop new therapies.

And so de Sousa e Melo set out to build a better mousetrap by building a better mouse. Poring over data from human colon cancer patients, he identified the molecular markers that seem to determine whether people respond to standard therapy. Those discoveries helped his lab develop a range of genetically engineered mice whose tumors behave like those found in people.

“It’s reverse translation: We take patient data, inform ourselves, and then model it as accurately as possible,” the Swiss-born de Sousa e Melo said. “Before that it was a one-size-fits-all.”

Now his mice have become a proving ground for new approaches to colon cancer. That provides a better toolkit for future discoveries, de Sousa e Melo said, one that will hopefully lead to effective treatments for a devastating disease.

— Damian Garde

Before she became a cancer researcher in the U.S., Omkara Veeranki was a veterinarian in India.

She loved caring for animals, but in vet school she realized that “in order to eradicate a disease, you need to know the etiology,” she said.

This realization led her to pivot her career toward basic science. She moved to New York to pursue a master's degree in biotechnology at the University of Buffalo, then went on to get her Ph.D. at their Roswell Park Comprehensive Cancer Center. Now a postdoctoral fellow at the University of Texas MD Anderson Cancer Center, Veeranki works on drug development, taking a novel approach to drug testing.

To understand gastric and esophageal cancers, Veeranki takes tumor cells from a patient and transplants them into a mouse’s gastro-esophageal junction, which provides a higher fidelity model of human disease. Using this model and others, she tests a promising drug that targets a molecule called CDK9, which is overexpressed in many cancers.

In the future, she hopes to continue working in academic medicine.

“From my strengths and from my training, what I can do is develop new drugs or explore the drugs that are already present in the market and repurpose them for certain types of cancers," she said. "My whole goal is to mitigate the problem of this disease.”

She also looks forward to helping trainees in academia succeed. She currently mentors high school students in science as well as biomedical researchers who belong to minority groups at UT Health.

— Orly Nadell Farber

Cells don’t just die. Their deaths are planned from the moment they are born, Vasanthi Viswanathan explained. “Just like cells have a program to grow and divide and move, they have a program to die,” she said.

That plan can go awry. When it does, we suffer the consequences — namely, cancer. But those plans may also be a way to kill cancer — which is what Viswanathan is working on as a postdoc at the Broad Institute of MIT and Harvard. Viswanathan studies ferroptosis — a cell death program that requires iron.

Ferroptosis is different than the usual cell death program, called apoptosis. It’s “like a molecular fire gets set off in the cell,” she said. The cell’s membrane oxidizes while the cell itself becomes a huge bubble and eventually explodes. Finding a way to force cancer cells to go through ferroptosis might lead to new treatments.

Viswanathan’s life is a far happier consequence of plans gone awry. “From a young age, I was very attracted to music and dance. I thought of myself as an artist,” she said. When it came time to pick a career, her family encouraged her to try her hand at medicine. That didn’t work out, and she went off to study science in grad school at Columbia instead.

She still performs — though it’s mostly nursery rhymes for her 3-year-old daughter. And she has made new plans for her future. Viswanathan will be applying for faculty positions this fall. Having mentored undergraduate students during her time as a postdoc, she hopes to find one where teaching will be important. (Her husband, a physician-scientist, is also on the job market.)

“Ending up in science was not the plan — was not even my desire,” she said. “but I genuinely do love what I do right now.”

— Kate Sheridan

Alan Williams wants to democratize the latest advance in cancer treatment.

Genetically engineered therapies called CAR-Ts have changed the game for certain advanced cancers, rewiring patients’ own immune cells to attack tumors. But what if, instead of going the costly and time-consuming route of extracting and editing those cells, you could dose cancer patients with an off-the-shelf CAR-T?

That’s the question that lured Williams away from studying immunology at Yale University and into the labs of Cellectis, a New York biotech company at work on a quicker route to cancer-killing cell therapies.

Williams’ work basically boils down to mimicking nature. Cellectis starts with immune cells from healthy donors and then engineers them to home in on cancer. But the process doesn’t end there. Unlike CAR-Ts derived from patients themselves, Cellectis’ donor cells would be received as foreign invaders rather than local law enforcement if they were injected right away. In order to do their tumor-killing jobs, the off-the-shelf CAR-Ts have to be put into deep cover.

And that’s where Williams comes in. He’s working with genome-editing technology to delete a key molecular marker that would expose the CAR-T cells to an immune system attack. But that’s not enough either, Williams explains, because removing that marker could expose the off-the-shelf treatments to a second line of bodily defenses. And so, in tandem, his group is in search of an add-on therapy that could chaperone the edited cells to the cancerous targets.

Williams’ career in science has pulled him into the daunting complexities of the human immune system, but his fascination with the field began with a song. Back in seventh grade, at St. Rita School and Parish in New Orleans, his science teacher Sister Pam helped students memorize the multisyllabic names for biological organisms with songs.

“Being from New Orleans, she knew music was in our blood,” Williams said. “That parlayed into, ‘OK, I’ll pay attention to the rest of her lecture as well.’ And then it ballooned from there.”

— Damian Garde

When Rong Zhang was a student in his native China, he and his classmates had to have their temperatures monitored during the 2003 SARS outbreak. Later, when he started studying animal diseases as an undergraduate, it made him look back at the response to the outbreak and question what he could do to improve such public health campaigns.

“This is something I need to pursue,” he remembers thinking.

Zhang, 35, hopes that by better understanding viruses — how they slip into cells and establish an infection — we can develop better strategies to combat them. As a postdoc at Washington University in St. Louis, he is studying the interplay between viruses and human cells to uncover what factors enable or inhibit infection.

“Viruses are very small, very simple, but also very, very smart,” Zhang said. “They have evolved multiple ways to invade different cell types and organs and even different species to cause diseases.”

In his research, Zhang has identified the receptor that chikungunya targets, and in turn shined a light on why people infected by the virus suffer from joint pain: The cells with these receptors, which help build cartilage and muscle, crowd into joints.

It’s the type of discovery he hopes to continue to make as he moves forward in his career as a scientist.

“I like doing research,” he said. “And I love viruses.”

— Andrew Joseph