It’s one thing to feel connected to your work. But it’s a whole other thing to be working with the goal of hopefully finding a cure someday for a disease or condition that has directly impacted you or a loved one.
Johnson & Johnson has long been a trailblazer when it comes to developing innovative treatments for diseases and conditions as diverse as cancer, acne and respiratory infections. Today, Janssen Pharmaceuticals, part of the Johnson & Johnson family of companies, is also on a mission to create a world without disease through prevention, interception and possible cures.
Behind this groundbreaking work are researchers across the company who have made it their guiding purpose, and who’ve worked laboriously for years, to pinpoint potentially lifesaving therapies. Scientists like Gus, Kimberly and Julian, who take their jobs very personally—because they’ve battled the very condition or disease they’re studying.
We take a look at how they all hope to help get us closer to a world without disease in 2018.
Gus Zeiner
“When I first started experiencing symptoms of fatigue six years ago, I brushed them off as being due to sleep deprivation—after all, I was a busy working dad with a 4-year-old and an 8-month-old.
But then I noticed that when I did my normal after-work mountain bike trail loop, it was taking longer and longer to finish. And after being late for day care pickup a few times, my wife and I decided it was time for me to see my doctor.
He took some blood and told me I was anemic, and that I probably had a vitamin B12 deficiency. The treatment for this was high-dose vitamin therapy. Six months later, when I wasn’t feeling any better, he sent me for a bone marrow biopsy. The results were frightening: I was diagnosed with an aggressive form of myelodysplastic syndrome (MDS), a rare blood disorder that about a third of the time develops into acute myeloid leukemia (AML).
I was in total shock. I was 39, and diagnosed with a type of cancer that typically hits people in their 60s or 70s. My first thought was for my kids, who might have to grow up without a dad. My father passed away when I was 13, and I remember wondering if it was some sort of generational curse.
My doctors warned me that this type of MDS wasn’t likely to respond to the standard of care, chemotherapy, and the only hope I had was a bone marrow transplant. Since I didn’t have any siblings who could provide a match, my only option was the bone marrow registry.
Thankfully, we found a match within a couple of months and I had the transplant in July 2012. Still, my prognosis was grim: Even with a bone marrow transplant, I didn’t expect to live for more than a couple of years. For my type of MDS, the literature reported zero survivors five years after a transplant. Everyone in those studies who didn’t die of the transplant relapsed and died of MDS.
Yet I’ve made it through the five-year mark, which I ascribe mostly to luck, and somewhat to the fact that I was young and in relatively good shape when I had the transplant. Most people who have MDS have comorbidities like heart disease or type 2 diabetes.
The whole experience impacted me profoundly. I’m a molecular biologist, and was working on ways to improve gene expression measurement research at the time.
Prior to my diagnosis, I had actively avoided directly working on cancer during my career because I felt that, in such a crowded field, my contributions were likely to be incremental.
This view changed after my transplant. I now felt there was real value in being a patient because that lens would enable me to see and weigh problems differently than everyone else. I decided to refocus my career to make new cancer therapies that could restore dignity to patients.
In 2013, a friend introduced me to Ben Wang, a scientist and entrepreneur whose wife, Kim, had AML. Kim had a transplant as well, but she wasn’t as lucky as I was and passed away a year later. Ben and I decided to put our wonder twin powers together and also joined forces with Stanford biologist Christina Smolke, Ph.D., to create Chimera, a company dedicated to building next-generation cellular therapies for cancer.
Johnson & Johnson believed in our vision, and invested in us as a start-up in their JLABS program in 2015.
We’re trying to build technology that will allow CAR-T—a particular type of cell that has shown tremendous results for cancer patients who haven’t responded to standard therapy—to be used safely and effectively to treat all cancers.
We are still relatively small, with a staff of about 10, but we have a big vision: In 10 years, I’d love to see our CAR-T technology in clinical trials on cancers that would be otherwise terminal.
When I was going through my bone marrow transplant, one of the hardest things for me was to see the impact of my treatment on my wife and two small sons. I could tell they felt helpless and unable to do anything except talk to me and try to get me to laugh.
It’s those memories that get me out of bed every morning and into the laboratory.”
But then I noticed that when I did my normal after-work mountain bike trail loop, it was taking longer and longer to finish. And after being late for day care pickup a few times, my wife and I decided it was time for me to see my doctor.
He took some blood and told me I was anemic, and that I probably had a vitamin B12 deficiency. The treatment for this was high-dose vitamin therapy. Six months later, when I wasn’t feeling any better, he sent me for a bone marrow biopsy. The results were frightening: I was diagnosed with an aggressive form of myelodysplastic syndrome (MDS), a rare blood disorder that about a third of the time develops into acute myeloid leukemia (AML).
I was in total shock. I was 39, and diagnosed with a type of cancer that typically hits people in their 60s or 70s. My first thought was for my kids, who might have to grow up without a dad. My father passed away when I was 13, and I remember wondering if it was some sort of generational curse.
My doctors warned me that this type of MDS wasn’t likely to respond to the standard of care, chemotherapy, and the only hope I had was a bone marrow transplant. Since I didn’t have any siblings who could provide a match, my only option was the bone marrow registry.
Thankfully, we found a match within a couple of months and I had the transplant in July 2012. Still, my prognosis was grim: Even with a bone marrow transplant, I didn’t expect to live for more than a couple of years. For my type of MDS, the literature reported zero survivors five years after a transplant. Everyone in those studies who didn’t die of the transplant relapsed and died of MDS.
Yet I’ve made it through the five-year mark, which I ascribe mostly to luck, and somewhat to the fact that I was young and in relatively good shape when I had the transplant. Most people who have MDS have comorbidities like heart disease or type 2 diabetes.
The whole experience impacted me profoundly. I’m a molecular biologist, and was working on ways to improve gene expression measurement research at the time.
Prior to my diagnosis, I had actively avoided directly working on cancer during my career because I felt that, in such a crowded field, my contributions were likely to be incremental.
This view changed after my transplant. I now felt there was real value in being a patient because that lens would enable me to see and weigh problems differently than everyone else. I decided to refocus my career to make new cancer therapies that could restore dignity to patients.
In 2013, a friend introduced me to Ben Wang, a scientist and entrepreneur whose wife, Kim, had AML. Kim had a transplant as well, but she wasn’t as lucky as I was and passed away a year later. Ben and I decided to put our wonder twin powers together and also joined forces with Stanford biologist Christina Smolke, Ph.D., to create Chimera, a company dedicated to building next-generation cellular therapies for cancer.
Johnson & Johnson believed in our vision, and invested in us as a start-up in their JLABS program in 2015.
We’re trying to build technology that will allow CAR-T—a particular type of cell that has shown tremendous results for cancer patients who haven’t responded to standard therapy—to be used safely and effectively to treat all cancers.
We are still relatively small, with a staff of about 10, but we have a big vision: In 10 years, I’d love to see our CAR-T technology in clinical trials on cancers that would be otherwise terminal.
When I was going through my bone marrow transplant, one of the hardest things for me was to see the impact of my treatment on my wife and two small sons. I could tell they felt helpless and unable to do anything except talk to me and try to get me to laugh.
It’s those memories that get me out of bed every morning and into the laboratory.”
Julian Symons
“I’ve been trying to find a cure for respiratory syncytial virus (RSV) for almost a decade. Why am I so motivated? I’ve seen the impact of the virus on my own elderly father—and I know how deadly it can be.
My father came down with RSV in 2000, at age 75. My wife and I had gone to visit my parents over Christmas, and we both had a mild cold, which didn’t seem like anything serious. In hindsight, it must have been RSV. My father, a former lifelong smoker, had chronic obstructive pulmonary disease (COPD), a condition that makes you more vulnerable to complications of RSV because it affects your breathing.
He got sick with what seemed like the same cold a couple days later, but it spiraled out of control very rapidly. He got up in the morning with a runny nose, and by the afternoon, was gasping for air and struggling to breathe.
He was rushed to the ER, where they put him on oxygen to help him breathe. He stayed in the hospital for two weeks.
Most healthy adults get several RSV infections throughout their lifetime and it’s not a big deal. But if you’re over age 65 and have chronic heart or lung problems or are immunocompromised, the infection can quickly turn life-threatening. Seeing my father lying on a hospital bed, surrounded by tubes and monitors, drove home how deadly this disease really is.
I didn’t start researching a drug for RSV until a decade later, when I began working for Alios BioPharma, which Johnson & Johnson acquired in 2014. We had created a broad acting antiviral drug, which we imagined would be used for many different types of viruses. We were about to start testing it against RSV when we realized that another class of drugs that we were developing might be even more effective. We tested about 200 compounds, and found that one of them prevented RSV from replicating. That was the first precursor for an RSV treatment we are currently studying.
Both of my parents died in 2004, but I often think of my father and wonder if a drug like this would have helped relieve his symptoms and shorten his hospital stay. What also haunts me is the image of infants suffering with RSV. I’ve visited pediatric hospitals and seen children as young as 3 weeks infected with RSV lying in an incubator with feeding tubes and oxygen monitors, struggling to survive.
No one that little should be in that sort of pain. It is very motivating to see patients at both ends of the spectrum—the very young and the frail elderly—that your work could help.”
My father came down with RSV in 2000, at age 75. My wife and I had gone to visit my parents over Christmas, and we both had a mild cold, which didn’t seem like anything serious. In hindsight, it must have been RSV. My father, a former lifelong smoker, had chronic obstructive pulmonary disease (COPD), a condition that makes you more vulnerable to complications of RSV because it affects your breathing.
He got sick with what seemed like the same cold a couple days later, but it spiraled out of control very rapidly. He got up in the morning with a runny nose, and by the afternoon, was gasping for air and struggling to breathe.
He was rushed to the ER, where they put him on oxygen to help him breathe. He stayed in the hospital for two weeks.
Most healthy adults get several RSV infections throughout their lifetime and it’s not a big deal. But if you’re over age 65 and have chronic heart or lung problems or are immunocompromised, the infection can quickly turn life-threatening. Seeing my father lying on a hospital bed, surrounded by tubes and monitors, drove home how deadly this disease really is.
I didn’t start researching a drug for RSV until a decade later, when I began working for Alios BioPharma, which Johnson & Johnson acquired in 2014. We had created a broad acting antiviral drug, which we imagined would be used for many different types of viruses. We were about to start testing it against RSV when we realized that another class of drugs that we were developing might be even more effective. We tested about 200 compounds, and found that one of them prevented RSV from replicating. That was the first precursor for an RSV treatment we are currently studying.
Both of my parents died in 2004, but I often think of my father and wonder if a drug like this would have helped relieve his symptoms and shorten his hospital stay. What also haunts me is the image of infants suffering with RSV. I’ve visited pediatric hospitals and seen children as young as 3 weeks infected with RSV lying in an incubator with feeding tubes and oxygen monitors, struggling to survive.
No one that little should be in that sort of pain. It is very motivating to see patients at both ends of the spectrum—the very young and the frail elderly—that your work could help.”
Kimberly Capone
“I started to develop acne in my early 30s, likely due to hormonal changes, right around the time I started Johnson & Johnson’s Consumer Microbiome Research Program in 2009. It surprised me because I’d always had dry skin and had never suffered any bad breakouts, not even in my teens.
As a microbiologist specializing in acne research, it’s a little embarrassing to be sporting pimples when I’m giving a presentation to a group of people! But it also gives me an invaluable, uniquely personal perspective on my work. When I have a very bad flare-up, for example, I now swab my skin to see what types of bacteria are on it. It helps me with my research, which is focused on the skin’s microbiome.
Like other parts of your body, your skin contains a wide variety of organisms, including P. acne bacteria that induce zits. But while everyone has P. acnes, not everyone has bad breakouts. We think other factors—such as diet, stress, even antibiotic use—can all impact your skin’s microbiome, shifting the ratio of good to bad bacteria. We think that the more diverse bacteria you have on your skin, the more likely P. acnes is held in check.
My hope is that eventually, when we pinpoint microbiome changes that trigger an acne flare, we’ll then be able to develop treatments to target them.
It took some trial and error, but I’ve finally found a beauty routine that works well for me—and for my skin. I use a gentle cleanser, like Neutrogena® Ultra Gentle Daily Cleanser, twice a day, which doesn’t strip all the good oils away, as well as the NeoStrata® Smooth Surface Daily Peel, which contains exfoliating glycolic acid that helps remove rough, dry skin. I’m also constantly trying new topical products.
Every time, I approach it like a scientist, and it always gives me a rush of excitement as I analyze the results. How has the treatment affected my skin? Has it caused it to become redder? More sensitive? Did it improve my breakout, or worsen it? It’s time-consuming and hard to do, and sometimes it can be nerve-wracking as I don’t know how my skin will respond.
But it’s very exciting for me to be part of a research group that looks at how microorganisms on the skin contribute to acne and overall health, in general. Not every researcher can be their very own test subject!”
As a microbiologist specializing in acne research, it’s a little embarrassing to be sporting pimples when I’m giving a presentation to a group of people! But it also gives me an invaluable, uniquely personal perspective on my work. When I have a very bad flare-up, for example, I now swab my skin to see what types of bacteria are on it. It helps me with my research, which is focused on the skin’s microbiome.
Like other parts of your body, your skin contains a wide variety of organisms, including P. acne bacteria that induce zits. But while everyone has P. acnes, not everyone has bad breakouts. We think other factors—such as diet, stress, even antibiotic use—can all impact your skin’s microbiome, shifting the ratio of good to bad bacteria. We think that the more diverse bacteria you have on your skin, the more likely P. acnes is held in check.
My hope is that eventually, when we pinpoint microbiome changes that trigger an acne flare, we’ll then be able to develop treatments to target them.
It took some trial and error, but I’ve finally found a beauty routine that works well for me—and for my skin. I use a gentle cleanser, like Neutrogena® Ultra Gentle Daily Cleanser, twice a day, which doesn’t strip all the good oils away, as well as the NeoStrata® Smooth Surface Daily Peel, which contains exfoliating glycolic acid that helps remove rough, dry skin. I’m also constantly trying new topical products.
Every time, I approach it like a scientist, and it always gives me a rush of excitement as I analyze the results. How has the treatment affected my skin? Has it caused it to become redder? More sensitive? Did it improve my breakout, or worsen it? It’s time-consuming and hard to do, and sometimes it can be nerve-wracking as I don’t know how my skin will respond.
But it’s very exciting for me to be part of a research group that looks at how microorganisms on the skin contribute to acne and overall health, in general. Not every researcher can be their very own test subject!”
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