Photo by Bill Wright / Fred Hutch News Service
Hutch United is seeking applicants for new fellowships created to support underrepresented scientists —and to broaden the attraction of top minds to Fred Hutchinson Cancer Research Center.
The program is the most inclusive of its kind among top cancer centers, organizers said. It welcomes applications from trainees identifying as racial and/or ethnic minorities, disabled, women, transgender, lesbian, gay, bisexual, veterans, non-U.S. citizens and individuals with low socioeconomic backgrounds.
"While several other institutions use buzzwords like 'diversity' in their marketing, the Hutch [United] fellowship tangibly shows that we are a national leader in diversity efforts and are ready to put our money where our mouth is," said Biswajit "Bish" Paul, a doctoral candidate in the Molecular and Cellular Biology Program at Fred Hutch. Paul identifies as a queer, immigrant, scientist of color from a low-income background.
The fellowships will fund one graduate student and one postdoctoral fellow for up to two years, providing $100,000 annually in direct costs. Applications are due May 15. Eligible candidates don't necessarily need to be employed at Fred Hutch but should have established relationships with a primary mentor based in one of the institution's five scientific divisions.
"This not only helps recruit a diverse pool of talented scientists, but it also helps create an environment that promotes their retention," said Paul, a member of the Hutch United fellowship committee and leader of the project. In that role, he worked with Fred Hutch President and Director Dr. Gary Gilliland to secure funding for the fellowships.
Hutch United is a Fred Hutch organization dedicated to promoting underrepresented and self-identified minority scientists at the center.
The fellowships were developed through a group effort among Hutch United members — all of them volunteers, said Erin dela Cruz, a graduate student in the Fredricks Lab and co-chair of Hutch United.
In addition to those photographed, other key contributors to the work included Hutch United members Drs. Dan Stone and David Boyd, and Dr. Oliver Fregoso (founding Hutch United core board member and former co-chair). Dr. Kiran Dhillon, a founding Hutch United board member and research associate in the Human Biology Division, first proposed the fellowships idea.
In researching the project, the group examined whether similar, wholly inclusive fellowships exist at any of the top 40 cancer institutes. None did, they found.
For more information, please contact HutchUnited@fredhutch.org.
Bill Briggs / Fred Hutch News Service
Photo by Bill Wright / Fred Hutch News Service
An April 28 ceremony honored Fred Hutch’s Dr. Oliver Press as the first Giuliani/Press Endowed Chair, funded by a gift from David and Patricia Giuliani. With his endowed chair, Press’ research on targeted therapies for blood cancers will be supported in perpetuity.
“Words cannot express my gratitude to the Giulianis for the generous gift of this endowed chair,” said Press, a lymphoma researcher and oncologist who is serving as interim head of Fred Hutch’s Clinical Research Division. “I will continue to use the generous contributions from the Giulianis to continue to try to cure B-cell lymphomas, with a focus on mantle cell lymphoma,” he said.
Dozens of colleagues and supporters offered Press handshakes, hugs and congratulations at the celebration, held in the lobby outside Press’ administrative office on the Fred Hutch campus.
Personally and through their family foundation, the Giulianis have supported Fred Hutch, and Press’ research in particular, for years. Press is one of the world’s experts in mantle cell lymphoma, a type of non-Hodgkin lymphoma that Patricia Giuliani was diagnosed with more than a decade ago. Press is known for his development of antibody-based, targeted therapies in mantle cell lymphoma and other blood diseases, particularly radioimmunotherapies, which deliver a precise, deadly dose of radiation straight to cancer cells. He is also developing an engineered T-cell therapy in mantle cell lymphoma and related cancers.
In recognition of their gift establishing the endowed chair, the Giulianis were presented with a small, intricately fashioned paper chair in a glass case.
“Today we’re here to celebrate the work you all do,” David Giuliani said. “Ollie is exceptional, but he’s exceptional among the exceptional people and facilities here at the Hutch.”
The Giulianis met Press long before Patricia developed lymphoma: The families’ sons played on the same high school football team. The story of the families’ friendship was among many shared at the celebration as the cloudy sky out the windows darkened over Lake Union. Press’ former adviser at the University of Washington, Dr. Cornelius Rosse, drew cheers and applause as he shared his memories of the athletic young man with the wild mop of blond hair who was his first graduate student.
“He became the best graduate student there can be anywhere,” Rosse said. What makes Press such an exceptional and motivated scientist, said Rosse, is his pursuit of failure. “He will keep going on until he finds something at which he can fail.”
Susan Keown / Fred Hutch News Service
Photo by Robert Hood / Fred Hutch News Service
A study published this week led by researchers at Fred Hutch and Memorial Sloan Kettering Cancer Center has found a possible chink in the armor of a large class of acute myeloid leukemias and the leukemia-like disorder myelodysplastic syndrome, or MDS. Previous work from the research teams, led by Fred Hutch molecular biologist Dr. Robert Bradley and MSK oncologist Dr. Omar Abdel-Wahab, showed that a certain class of mutations in genes essential for one of life’s most fundamental processes can trigger MDS in a mouse model.
The disease-linked mutations fall in genes involved in the process known as RNA splicing, a key step cells take when they translate genetic information from DNA to RNA to protein, cutting and stitching the RNA molecule to remove the parts not needed in the final protein. About 90 percent of humankind’s approximately 24,000 protein-coding genes are spliced and the disease-linked mutations change the splicing of hundreds of those genes.
In the researchers’ study, published Monday in the journal Nature Medicine, Bradley, Abdel-Wahab and their colleagues pinpointed a potential therapeutic avenue that could help the 60 percent of patients with MDS and the upwards of 25 percent of AML patients who carry splicing mutations. Such mutations also occur in many other cancer types — including chronic lymphocytic leukemia, a certain type of eye cancer, and breast, pancreatic and lung cancers.
The researchers found that a drug that blocks normal splicing, a small molecule known as E7107, boosted survival time by about 30 percent in a mouse model of splicing-linked leukemia — but not in mice with other types of leukemia. The researchers believe the drug works by specifically crippling cancerous cells — since the cells already have abnormal splicing due to their unique mutations, further attacking splicing hobbles the malignant cells completely.
This is the first example of a potential path to targeted therapies for splicing-linked leukemia or MDS, said Bradley, an associate member of the Basic Sciences and Public Health Sciences divisions at the Hutch. Identifying better treatments for patients with these disorders is important, he said — the three-year survival for all patients with MDS is 35 percent. The only curative therapy for the disease is bone-marrow transplantation, but most patients are not eligible for transplant because they tend to be older or otherwise in poor health. And patients carrying mutations in splicing gene SRSF2, which this study focused on, tend to fare even worse.
Although E7107 had been tested in an early-stage clinical trial for patients with solid tumors, 5 percent of patients reported vision problems and so this drug is unlikely to be tested again in patients, Bradley said. He and his colleagues are currently testing other compounds that affect splicing in the hopes of identifying potential therapies that act similarly to E7107 against cancerous cells but without side effects.
“There are a lot of people now trying to understand splicing factor mutations because they occur in many different cancers,” Bradley said. “If we — or anybody else — can find a way to kill cells that carry splicing- factor mutations, that could be a therapy that’s applicable in many different diseases.”
Rachel Tompa / Fred Hutch News Service