Four National Cancer Institute-designated cancer centers – Dana-Farber Cancer Institute, Fred Hutch Cancer Center, Memorial Sloan Kettering Cancer Center, and The Sidney Kimmel Comprehensive Cancer Center and Whiting School of Engineering at Johns Hopkins – have joined forces and secured funding from AI technology leaders AWS, Deloitte, Microsoft and NVIDIA, to create the Cancer AI Alliance (CAIA). The alliance will apply responsible AI to the collective power of the participating cancer centers’ data to unlock insights while protecting data security, all to identify more ways to transform cancer research and care.

Fred Hutch Cancer Center, which spearheaded the formation of CAIA and secured its initial funding, will serve as the alliance’s coordinating center.

“Collectively, the data held by the nation’s leading cancer centers has been an untapped source of new cancer discoveries that has been out of reach. This alliance helps solve the key technical challenges that will enable us to securely use both AI and massive computational power to find these breakthrough insights and save more lives,” said Thomas J. Lynch Jr., MD, Fred Hutch president and director and holder of the Raisbeck Endowed Chair.

The alliance will serve as a collaboration center by providing shared infrastructure and shaping industry standards, which will not only shift researchers from solving problems in isolation to solving them together but support greater health outcomes by exposing data trends for rare cancers and small populations that can result in more meaningful and broadly impactful discoveries.

CAIA is supported by more than $40 million in funding and the best and latest AI technology and expertise from AWS, Deloitte, Microsoft, NVIDIA and Slalom to launch the coordination and computation capacity needed to securely bring cancer research and data together at rapid speed using responsible AI.

“AWS is proud to support the Cancer AI Alliance and help deliver on its critical mission of transforming cancer research and care. Together, we will accelerate innovation in cancer discovery and treatments, deploy generative AI at scale, and leverage the power, agility, and security of cloud computing to revolutionize health and patient outcomes,” said Matt Garman, CEO, Amazon Web Services.

“Our collaboration with the Cancer AI Alliance underscores Deloitte’s long-standing commitment to help transform the life sciences and healthcare industry,” said Jason Girzadas, CEO of Deloitte US. “We are proud to be investing our talent, resources, and innovative AI, cyber security and health equity technologies to help enhance cancer research, improve treatments and address one of the most pressing health challenges of our time.”

“We are at a breakthrough moment for finding cancer cures thanks to rapid advancement in AI. With leading AI capabilities, diverse data types and standards, and modern cloud infrastructure in place, thoughtful collaboration across leading cancer research centers can help accelerate progress. The Cancer AI Alliance will be integral in this lifesaving work, and we are proud to be supporters,” said Juan Lavista Ferres, Corporate Vice President & Chief Data Scientist, Microsoft.

“The convergence of AI, multimodal healthcare data and federated learning will usher in a new era for cancer research,” said Jensen Huang, founder and CEO of NVIDIA. “We are delighted to partner with Cancer AI Alliance to help researchers transform cancer care.”

Currently, cancer researchers face two challenges to using AI modeling: accessing the computational resources to analyze large volumes of data at speed, and remaining compliant with the regulatory and privacy requirements associated with sharing data from multiple cancer centers.

CAIA will serve an enabling role, providing the computing infrastructure to members of the alliance to process high volumes of cancer data generated during routine cancer care, such as electronic health records, pathology images, medical images and genome sequencing. This data, when paired with AI, could lead to novel insights in tumor biology, treatment resistance, and identification of new therapeutic targets.

All of this will be developed while maintaining data security, privacy and alignment with regulatory and ethical standards. Paired with strict governance, CAIA will use a federated AI learning framework in which each cancer center maintains its independent data and AI models are sent to the data to produce results. Those results are then aggregated across participating members to uncover insights, all without sharing or exposing any of the raw data behind it.

While CAIA is launching with four inaugural cancer center members, four foundational partners and one enabling partner, additional members are expected to be added. The governing committee, comprised of representatives from cancer centers, will determine membership criteria in the months ahead. The alliance’s aspirational goal is to support cancer innovation with $1 billion in resources over time.

CAIA is expected to be operating by the end of 2024 and producing its first insights by the end of 2025.

Articles

The Cancer AI Alliance (CAIA) is a collaboration between four leading cancer centers and AI technology leaders AWS, Deloitte, Microsoft, and NVIDIA. It aims to harness AI to transform cancer research and care by securely utilizing vast data resources. Fred Hutch Cancer Center leads the initiative, which is supported by over $40 million in funding. CAIA will provide shared infrastructure and industry standards, enabling researchers to address challenges collaboratively. The alliance will maintain data security and privacy while using federated AI learning to generate insights without sharing raw data.

AWS, Deloitte, Microsoft and NVIDIA bring the latest in AI technology, coordination, and compute to the alliance and back with initial funding.

Cancer Centers Launch Cancer AI Alliance to Unlock Discoveries, Transform Care Using Cancer Data and Applied AI

Tumors often get a lot of help in their efforts to survive and grow. Non-cancerous cells around a tumor can help it avoid attacks by the immune system, resist therapies that target them, and allow it to spread to other parts of the body. Researchers are now finding that some of these helpful neighbors aren’t even human cells — they’re bacteria.

The role that bacteria may play in promoting cancer is receiving more scientific attention. Two new studies from investigators at Fred Hutchinson Cancer Center reveal how bacteria infiltrate tumors and how they could be helping tumors progress and spread. The team also showed that the different microbial players in a tumor’s microbiota (the full collection of microbes it carries) could influence how a cancer responds to treatment. The two papers, 

, which has been linked to colorectal cancer.

“What we’re showing is that there are regions of the tumor that are heavily colonized by bacteria — micro-niche regions — and they differ functionally from regions that do not harbor bacteri

,” said Fred Hutch cancer microbiome researcher and study co-lead, 

, of the work outlined in the Nature study. “And these bacteria-rich regions have increased metastatic potential.”

Bullman and her collaborator, Fred Hutch molecular microbiologist 

, combined observations from tumors with lab-based experiments and small-molecule drug screens to show that 

 may shape conditions in tumors to keep them safe from immune attack and help them spread through the body. They discovered that some cancer therapeutics may work because they not only target tumor cells, but also the bacteria that are helping them.

The collaborators also found that other microbes — including the intestinal bug 

 — may render an anti-microbial and chemotherapeutic drug ineffective, which could shield both the tumor and 

 from treatment. These findings could help researchers develop new strategies to take down cancer by tackling its microbiome.

“This work is at the intersection of cancer and microbiome research,” Bullman said. “There’s compelling emerging data to suggest that nearly all major cancer types harbor an intra-tumoral microbiota.”

And it’s not just in colorectal cancer tumors, where the association with bacteria may seem logical. Breast, pancreatic and lung tumors are also among the cancers shown to harbor microbial communities. More and more studies suggest that the tumor microbiota may shape tumor development, progression and response to treatment.

“When we think about a patient’s cancer, we usually think about the malignant cells,” Bullman said. “What are the mutations driving the cancer, and how can we target them? But what is underappreciated is that within these patient tumors there is a microbial ecosystem that can support cancer progression.”

Bullman and Johnston wanted to better understand the intimate connections between bacteria and the tumor microenvironment, and how these connections influence cancer-cell behavior. To do this, they adapted spatial transcriptomics, a leading-edge technology that allows researchers to detect where genes are turned on and off in slices of tumor tissue.

The investigators saw that a range of bacterial species, including 

, live within oral cancer and colorectal cancers. But they also found that the bugs aren’t evenly distributed across the tumors.

“We observed bacterial hotspots, or micro-niches, which opened up a number of questions as to how these formed and might be impacting cancer biology,” Johnston said.

Bacteria influence tumor-cell behavior, immune microenvironment

Led by Jorge Galeano Niño, MD, PhD, the postdoctoral fellow who spearheaded the work, the team compared regions of oral and colorectal tumors that were rich in bacteria to those that lacked bacteria. They saw distinct differences.

“We saw that the regions colonized by bacteria were highly immunosuppressive,” Bullman said.

These areas had more of a kind of immune cell that can help tumors avoid attack by T cells, a type of immune cell that can kill cancer cells. (T cells are targeted by several 

.) The team also saw that fewer T cells had made their way into bacteria-rich regions.

“And when there were T cells [near bacteria-rich regions], there was upregulation of immune checkpoint proteins,” Bullman said.

Immune checkpoint proteins restrain T cells from attacking cancer cells, and are targeted by checkpoint inhibitors, a type of 

. Although several checkpoint inhibitors are 

, patients often see only limited effects against their tumors. Bullman and Johnston’s study might offer an explanation as to how a patient’s microbiota could influence whether their cancer responds to a checkpoint inhibitor.

The team also saw that regions with bacteria were more likely to be necrotic, with fewer dividing cells. It might sound like bad news for the tumor, but other research has shown that the tumor cells that spread and metastasize through the body often break away from necrotic areas. Cells can’t migrate while they’re rapidly dividing, so conditions that encourage cells to stop growing and start moving are conditions that can promote metastasis.

 could be encouraging tumor progression and immune evasion, but the data was correlative and couldn’t rule out the possibility that the microbes are just attracted to necrotic, already-immunosuppressed areas. To examine how bacteria may influence tumors, the team used tumor spheroids, which are tumor cells grown in 3D clusters in the laboratory.

To assess whether bacteria may promote an immunosuppressive environment, the scientists grew colorectal cancer spheroids with immune cells called neutrophils. Neutrophils crawled around and through tumor spheroids without bacteria. But when the investigators added 

 to the spheroids, they saw that neutrophils stopped moving and clustered within spheroids.

“The neutrophils migrated inside the spheroid and appeared trapped,” Galeano Niño said. “It supported what we saw in the patient spatial data: That there were neutrophils in the regions colonized by bacteria. That's interesting because neutrophils negatively impact T-cell activity. This could perhaps explain what we’re seeing with the T-cell exclusion in those regions colonized by bacteria.”

The team also saw that tumor cells in the spheroids moved differently when bacteria were present. In spheroids without bacteria, the tumor cells moved 

, which helped the spheroids grow larger, but didn’t help them release single cells capable of seeding new metastases.

“When bacteria were present, the cancer epithelial cells migrated as single cells — and they brought bacteria with them,” Bullman said.

 often travels with colorectal cancer metastases.

But how exactly are bacteria interacting with and influencing cells? To learn more, the team adapted single-cell transcriptome sequencing technologies for bacteria, developing an approach they called INVADEseq 

Using INVADEseq, the team saw that tumor cells infected with bacteria ramped up genes associated with cancer progression and metastasis. In oral tumor samples, the investigators saw that bacteria preferentially infected cancer epithelial cells and specific immune cell types within patients’ tumors. Infected tumor cells were more likely to have turned on genes involved in responding to DNA damage, which is a hallmark of cancer.

“The functional work supports [the idea] that the bacteria have a direct role in shaping these micro-niche regions,” Bullman said.

Tumor microbiome influences drug efficacy

If bacteria are promoting tumor progression, treating bacteria seems like an obvious way of also treating the tumor. Bullman’s previous study supported this idea: when she treated mice engrafted with human tumor tissue with antibiotics, 

this slowed the growth of colorectal cancers

“This raises the possibility of targeting specific members of the microbiota for patient cancer treatment,” Bullman said.

But that proof-of-principle work relied on metronidazole, a drug that kills off a wide range of bacteria, even those that benefit us.

“You don’t want to knock out all the beneficial microbes within a patients microbiota — this needs to be very targeted,” she said. “So, we designed a small-molecule screen of over 1,800 compounds to try and identify narrow-spectrum inhibitors of 

Surprisingly, about 15% of the antimicrobials that meet this criterion were also chemotherapeutics — including 5-fluorouracil, or 5-FU, which is already routinely used to treat colorectal cancer.

“That was really surprising to us,” Bullman said. “It raises the possibility that part of 5-FU’s treatment efficacy could be due to its antimicrobial activity.”

But for many patients, 5-FU treatment doesn’t prevent tumor growth. Could the tumor microbiota be contributing to this? When the team tested 5-FU against other bacterial strains taken from colorectal cancer samples, they saw that several, including a strain of 

, resisted its inhibitory effects. Growing this strain of 

 from 5-FU. (Another tumor-derived bacterial species they tested was unable to rescue 

 protected colorectal cancer cells from 5-FU as well. The 

 appeared to have a way of metabolizing the drug and minimizing its exposure to cancer cells or other bacteria.

“The findings show that intra-tumoral microbes are not innocent bystanders during disease progression, and suggest that the microbiota should be taken into consideration when thinking about optimal cancer treatments,” Johnston said.

The work further supports the idea that a tumor’s microbiota is an under-appreciated vulnerability and a potential treatment target. It appears that for some cancers, bacteria are important contributors to almost every step of tumor development and can even help shield it against treatment. Therapeutics that effectively modulate a tumor’s microbiota could help slow its growth as well as stave off metastasis or hobble cancer cells that have already spread.

The detailed analysis of bacterial species in both colorectal and oral tumors may also point to good oral health as an important way to help reduce cancer risk.

 is linked to periodontal disease — and it wasn’t the only oral bacteria the team saw inside tumor cells from patients. Another oral bacterial genus linked to gum disease, called 

, also made its way inside tumor cells. These bacteria have also been linked to oral cancer, though the associations are less strong than 

“There is a trend emerging of microbes that are traditionally associated with oral inflammatory disease being found in association with extra-oral and gastrointestinal cancers — which highlights the oral cavity as a breeding ground for pathogenic onco-microbes,” Johnston said.

In addition to allowing pathogens to spread to new areas of the body, it is possible that inflammation in the mouth, in the form of periodontal or endodontic disease, could be selecting for and encouraging the outgrowth of bacteria that are more specialized for growth in adverse conditions and capable of evading immune attack, he said.

Whether other tumors also harbor distinct bacterial micro-niches, and how these regions differ from non-colonized regions, are further questions Bullman and Johnston hope to answer. The team is exploring whether they can make tumors more responsive to immunotherapy or chemotherapy by manipulating their microbiomes. The first challenge will be developing strategies that are able to reach bacteria inside tumors. Further down the line, they hope to capitalize on the underlying biology of these tumor-homing microbes to develop novel therapeutic interventions, a strategy dubbed “bugs as drugs.”


By showing that microbes cluster in hard-to-reach areas of tumors, the same areas that are recalcitrant to current therapeutic regimens, the work clarified some hurdles that the team need to overcome in the development of new therapeutics.

“This holistic approach to assessing the tumor microenvironment, which is a multi-species ecosystem, will advance our understanding of cancer biology, and I believe will reveal new therapeutic vulnerabilities in cancer,” Bullman said.

This work was supported by the National Institutes of Health, the National Institute of Dental and Craniofacial Research, the National Cancer Institute, an Irvington Postdoctoral Fellowship from the Cancer Research Institute and a Washington Research Foundation Fellowship.

Two new studies show how bugs could help tumors progress and resist treatment.

How Bacteria Give Cancer a Helping Hand

Dr E. Donnall Thomas put newly founded Fred Hutchinson Cancer Center on the map in the 1970’s through his Nobel Prize-winning work developing bone marrow transplantation as a curative therapy for leukemia.

Last week, leading researchers from around the globe visited Seattle 

 and to discuss the future of transplantation, gene and cellular therapies at the inaugural 

Thomas, who passed away in 2012 at the age of 92, led research that has been transformative for generations. Among the participants celebrating his legacy was 

, one of the original Fred Hutch scientists who worked with Thomas and still heads the Transplantation Biology Program; and graduate student David Granadier, whose poster about regeneration of the thymus gland — a source of disease-fighting T cells — was awarded top prize by conference organizers.

, president and director of Fred Hutch and holder of the Raisbeck Endowed Chair, told the gathered experts that their field, which sprang from bone marrow 

, has made it possible today to turn the human immune system on to fight specific cancers.

“It has made a huge difference in the lives of our patients,” he said.

Bone marrow transplantation a foundation of immunotherapy

The explosive growth of immunotherapy was highlighted in a keynote presentation by renowned University of Pennsylvania immunologist 

, who treated the first patients with CAR T-cell therapy — blood cells genetically engineered to attack leukemia — in 2010.

June traced his interest in the field to 

 in bone marrow transplantation under Dr Thomas, beginning in 1983. Thomas and his team proved that immune cells transplanted from donors were preventing relapse of cancer in recipients through an effect known as “graft-vs.-leukemia.” From that insight, that the immune system could be harnessed to control cancer, came the idea of modifying a patient’s own immune cells with enhanced tumor-fighting capabilities.

June reflected on the years since those first CAR-T cell transplants, and how a pharmaceutical industry has blossomed around the development of these living drugs. Since his 

 were treated a decade ago, more than 15,000 patients have undergone T-cell therapy using commercial drugs or products in development by academic medical centers.

June noted that researchers have gone beyond the modification of T cells and are now exploring the benefits of engineering other blood cells such as macrophages, fibroblasts and natural killer cells. He discussed studies showing that combinations of these different engineered blood cells might work better.

“I think we are going to see virtually every hematopoietic cell (immature forms of varied blood cells) be synthetically engineered,” he said.

June added that the field’s current challenge is to scale up manufacturing and rein in costs — by reducing the “vein-to-vein” time it takes between removing a patient’s cells, genetically altering them and returning them.

Key to future success of immunotherapy is exploration of ways to tackle solid tumors, which embed themselves behind physical barriers and within a hostile biochemical microenvironment to fend off immune assaults.

The symposium was organized by the Hutch’s 

, or IIRC, a cross-disciplinary organization designed to pool the talents of researchers who work at the lab bench with those who treat patients in clinical trials. While this is the first meeting of its kind, the IIRC plans to hold a Thomas symposium every two years on the Hutch campus.

, scientific director for the IIRC and holder of the José Carreras/E. Donnall Thomas Endowed Chair for Cancer Research, said the cross-disciplinary immunotherapy team was created at a time when immunotherapy research was progressing well beyond blood cancers, tackling the difficult challenges of solid tumors.

“It has served an incredible role in bringing science together across the divisions,” he said. “We are way outside of liquid cancers in this field now.”

In more than a dozen technical presentations, invited speakers discussed their latest work in the field. It was a deep dive into experiments tackling old problems like graft-vs-host disease — where immune cells from a donor attack as foreign the healthy tissues of a transplant recipient; and studies of newly appreciated issues such as how the microbiome — communities of bacteria in our gut — can affect responses to cancer therapies.

Dr Alexander Marson, of the University of California at San Francisco, described how the new gene-editing technology known as CRISPR could be used to systematically catalog thousands of genetic switches within T cells. The precision of CRISPR gene-editing allowed his laboratory researchers to knock out these switches, known as transcription factors, and infer their function by seeing what happens to the T cells in their absence. Their method allowed them to build a library of 10,000 different switches.

Equipped with this library, their hope is to rev up precisely those T cells involved in immune defenses against cancer.

“We’re trying to understand the genetic circuitry of T cells well enough that we can actually rewrite these to improve T-cell therapy outcomes,” he said.

 director of the Hutch’s stem cell and gene therapy program, said the conference also highlighted that gene therapy itself — the effort to cure disease by replacing missing or faulty segments of DNA — grew out of bone marrow transplantation. Holder of the Stephanus Family Endowed Chair for Cell and Gene Therapy, Kiem noted that 41 years ago, Fred Hutch doctors were the first to treat the inherited blood disorder 

“Several speakers, including Dr John Tisdale of the National Heart, Lung, and Blood Institute, showed how we can now use a patient’s own cells, and correct them using gene-editing technologies, to cure diseases like thalassemia, sickle cell disease or other immunodeficiencies,” he said.

The scope of immunotherapies discussed at the symposium included cancer vaccines. Dr Catherine Wu, who heads stem cell transplantation and cellular therapies at the Dana-Farber Cancer institute in Boston, said a goal of therapeutic cancer vaccines is to “drive T cells into the site of tumors, because you need the right soldier at the site of activity to do the work.”

Her team is conducting clinical trials of vaccines against several solid tumors, including melanoma, renal cell carcinoma and ovarian cancer. The targets are neoantigens, proteins that appear on the surface of tumor cells that may be highly specific to each individual patient. The idea is to tailor a vaccine to target their particular set of tumor neoantigens.

“Vaccines, if you have the right set of antigens, have the potential to increase the depth and diversity of T-cell responses,” she said.

Although these trials are cutting-edge research, Wu said the vaccine work is also rooted in the immunological insights required for successful transplantation.

“I’ve had a chance to reflect on the large footprint that Don Thomas and the Hutch have had on the field of cancer immunotherapy,” she said. “It laid down the foundations for modern immunotherapy in many ways.”

Indeed, for many of the attendees, the most inspiring talk of the symposium was that of Thomas’ longtime collaborator Storb, who gave an evening keynote talk about his early years when he and his mentor were among a handful of scientists struggling to achieve safe and effective bone marrow transplants.

In 25 minutes, Storb summarized 57 years of his research, which began in 1965 when he came on a Fulbright grant from a research laboratory in Paris to work with Thomas in Seattle.

“I felt more and more removed from clinical activities,” Storb said. “I wanted to do something that actually had meaning for patients.”

It was a depressing time, working with rats and mice that continually rejected transplanted marrow.

“Most investigators had left the field,” Storb said. “It was a really discouraging state of affairs.”

Yet Thomas and his small team persisted in the tedious work, gradually uncovering the need to condition the recipients before transplant with radiation or chemicals to destroy the existing marrow, to find compatible matches of donor to recipient, and to find immunosuppressant drugs to prevent rejection of the graft after the transplant.

In 1971, they transplanted bone marrow into their first patient. “He recovered fully,” Storb said. “He is still alive today, 51 years later.”

Worldwide, 1.5 million transplants for cancer

Over the course of years, the group expanded, becoming part of the founding team of Fred Hutch in 1975. After several relocations, they moved with Fred Hutch to its current campus in South Lake Union. All the time, they were continuing to refine their procedures, developing tissue typing technologies to match donor and recipient, finding the right drug and radiation regimens to prepare the patient for transplant, minimizing graft-vs.-host disease and fighting infections. Drug combinations they developed became standards of care in a procedure now performed on more than 22,000 patients in the U.S. annually. Worldwide, an estimated 

 have received transplants for cancer and other blood disorders.

While the work was painstaking and often tedious, the team was always creative. Early on, Storb needed to test an antibody serum as a drug to prevent graft-vs.-host disease. Known as anti-thymocyte globulin, it could only be grown by injecting immune cells from the human thymus into horses, goats or rabbits. He found a farmer who kept all three animals, on farmland in Redmond that would one day become the site of Microsoft’s headquarters.

Storb repeatedly credited Thomas for his leadership and vision.

“Don had this incredible backbone. He always believed in it,” he said.

Dr Judith Shizuru, a transplant physician at Stanford, told Storb at the close of his presentation that his influence extends well beyond Seattle, and she thanked him for the care, passion and insight he has brought to the field.

“You are always there to answer questions for us,” she said. “You are a hero.”

Leading researchers from around the globe visited Fred Hutchinson Cancer Center to honor Dr E. Donnall Thomas and to discuss the future of transplantation, gene, and cellular therapies at the inaugural Dr E. Donnall Thomas Symposium.

Fred Hutch Hosts Inaugural Dr E. Donnall Thomas Symposium

Growing up in Oxford, England, Fred Hutchinson Cancer Center postdoctoral researcher Dr. Nick Salisbury became fascinated with understanding "why things are" from a scientific lens.

“Science is about understanding the way the world is and trying to come up with explanations,” he said. “And then you can make predictions about what will happen in the future.”

Salisbury was just named the third recipient to receive the 

 at Fred Hutch. Funded by Brooks Running on behalf of the 

, the goal of the fellowship is to develop scientific leaders who will advocate for a diverse and inclusive biomedical research workforce focused on rare cancer research.

The fellowship will fund Salisbury’s research on Merkel cell carcinoma, a rare and aggressive form of skin cancer caused by the Merkel cell polyomavirus. A quick diagnosis and appropriate treatment are essential to help cure this disease.

We sat down with Salisbury, who works in the lab of 

, to learn more about his research, how he got his start in science and what it means to him to be a Brave Fellow. This transcript has been lightly edited for clarity.

Can you tell us about your research project?

My research focuses on Merkel cell carcinoma. It's a rare skin cancer that is caused by the Merkel cell polyomavirus. 

, a professor here at Fred Hutch and holder of the 

, is a world-renowned expert in viruses that cause cancer.

So, this is really one of the best places to try to understand how this virus — that was discovered just over 15 years ago — causes this rare skin cancer.

What challenges did you overcome to pursue a career in science?

The really big challenge that I encountered was moving from England to the U.S. I finished my Ph.D. in the U.K. and then I decided to do my postdoctoral training in America. I wanted to move abroad since I'd spent my whole life up until that point in the U.K.

I first moved to Boston and was in one lab for just two or three months before the professor I was working with decided to leave academia and take up another position in the biotech industry. He closed down his lab and of course, that was very unexpected and quite scary because when you're an immigrant or you’ve moved to a new country, your visa and your ability to remain in the country is completely dependent on having a job. So, at that point, I was without a job and I needed to find a new lab to continue my postdoctoral training. I was thousands of miles away from home, from my friends, my family and my support network.

I managed to find another lab in Boston and things were going really well for about a year. Then one day the lab just was very abruptly shut down because the institute was carrying out an investigation into previous research misconduct that had happened allegedly many years before I joined. I had walked into another situation blindly not knowing what was happening. And so, again, that lab got shut down. So, it was two years in Boston of like very unproductive research.

, who is a fantastic researcher and one of the leading medical doctors in the U.S. for treating Merkel cell carcinoma. Patients come from all over the country to be treated by his team at the UW and the Hutch. He recruited me here to Seattle and that's how my journey at Fred Hutch began.

What next steps in your science does your new Brave Fellowship make possible?

The project that is being funded by the Brave Fellowship was a project that I started just a few months ago looking at the role of a human gene called YAP. We have found that this gene is turned off in Merkel cell carcinoma, and we think that if we can turn it back on, this would be bad for the cancer. We're trying to understand how it works in Merkel cell carcinoma and if we can develop a drug that could have the same effect as turning YAP back on.

This fellowship focuses on two things, to fund research that is focused on rare cancers like Merkel cell carcinoma. It also supports scientists from underrepresented communities within the academic scientific world. I am gay. There are LGBTQ+ scientists, of course, but there aren't that many LGBTQ+ scientists in the higher levels within academic research. I’m grateful that this fellowship is supporting me and I’m hoping to increase representation for LGBTQ+ scientists in the academic world.

It's a really fantastic opportunity, and I hope that I can make great strides in understanding or developing new therapies to treat Merkel cell carcinoma.

Rare skin cancer is focus of work by Fred Hutch scientist who will receive support honoring runner Gabe Grunewald. 

Fred Hutch Cancer Center

Articles

Cancer Centers Launch Cancer AI Alliance to Unlock Discoveries, Transform Care Using Cancer Data and Applied AI

How Bacteria Give Cancer a Helping Hand

Fred Hutch Hosts Inaugural Dr E. Donnall Thomas Symposium

Merkel Cell Carcinoma Researcher Dr. Nick Salisbury named Brave Fellow