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Summer 2025
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Precision Oncology
Giving that feels ‘beyond meaningful’: The Steinberg Family
The Steinberg family honors the memory of loved ones by celebrating and supporting a profession that takes caring to another level
Fred Hutch Associate Chief Nursing Officer Suni Elgar speaks during the Nurses Week Town Hall meeting on May 7, 2025 at Fred Hutch Cancer Center. Photo by Robert Hood / Fred Hutch News Service.
In 2017, Suni Elgar, MPH, RN, hadn’t yet become associate chief nursing officer at Fred Hutch Cancer Center, but change was coming. Her supervisor, Rosemary Ford, BSN, RN, was wrapping up a 40-year career. Ford had led the way in standardizing patient-centered care in bone marrow transplant nursing and knew Elgar could continue her legacy.
This would mean more schooling for Elgar, but she had three young children and felt overwhelmed, especially knowing the cost of an advanced degree.
“Thinking of your children’s future and saving for their college, it’s hard to prioritize yourself,” she said.
But then in 2018 Elgar was awarded the Harold and John Steinberg Memorial Nursing Scholarship. She was among a half-dozen annual recipients nominated by peers. The award opened the way for a career-altering opportunity for her.
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“Receiving that scholarship helped relieve a burden on my family,” she said, “and the recognition affirmed that my colleagues wanted to invest time and energy into me, grow me as a leader and keep me at the institution.”
Howard and Cynthia Steinberg aimed for this kind of impact when they imagined the scholarship fund more than three decades ago. They made their first contribution in 1995 and later decided to establish it as an endowment, meaning that the principal is invested, and the earnings can be spent annually to help provide sustained support in perpetuity.
Continual and ongoing contributions from the Steinbergs and their friends and family have made it possible for nearly 130 nurses to receive more than $315,000 in continuing education experiences, with recipients bringing back knowledge and new skills to their teams. The Steinbergs have also been open to the evolving needs of recipients, with initial funds being used more for conferences and later funds being used more for degree programs, like the one Elgar chose.
Continuing to work full time, Elgar got her master’s degree in public health from the University of Washington, coupling prior international experience in democracy and human rights to her current commitment to oncology nursing.
Looking back, her twins now just a year from starting college, she feels incredibly grateful.
“I came to nursing a little bit older than some folks after being out and working in the world, and I feel like one of the most miraculous parts of this job is how continuing education expands our horizons,” she said.
Howard and Cynthia Steinberg with Nancy Greenwood Vehrs, left, a member of Fred Hutch’s Philanthropy team, at a 2019 visit during the 25th anniversary of the Harold and John Steinberg Memorial Nursing Scholarship awards.Fred Hutch file photo
The Steinbergs’ journey through unexpected hardships
The Steinbergs’ generosity is rooted in support they received many years ago and a desire to help other families avoid the heartache they experienced. The story begins in 1963 in Kansas City, Missouri. Howard Steinberg was 3 years old and his brother, John Steinberg, 2, when their father, Harold Steinberg, opened a Budget Rent a Car franchise.
“He took great care of his family, loved to play golf and never stopped working,” Howard Steinberg said. By the late 1970s, the company had grown from 13 cars to a fleet of 400 and was generating more than $3 million in revenue.
Then, disaster struck the family. In 1980, when Howard and John Steinberg were both in college, 55-year-old Harold Steinberg was diagnosed with multiple myeloma, a cancer of plasma cells, a type of white blood cell found in the bone marrow. In 1981, on a trip to purchase another Budget franchise, he died suddenly of a cerebral hemorrhage, a complication from chemotherapy.
The family was in shock.
“We were privileged, upper-middle-class, but our mother was suddenly on her own. And although we were already young adults, we still grew up fast,” Howard Steinberg said.
His mother, Sondra Steinberg, sold their business interest. However, a few years later, her sons had an opportunity to repurchase it.
“Two young guys convinced the bank in Kansas City to lend us a heck of a lot more money than they ever should have,” Howard Steinberg said.
It was supposed to be a family affair, with the two brothers complementing each other and continuing their father’s legacy. But after overcoming one all-encompassing challenge, they soon faced another. In 1992, at age 30 and newly married, John Steinberg was diagnosed with acute myeloid leukemia. Their physician in Kansas City recommended he go to “the best place in the world to have a bone marrow transplant,” and that’s when the family’s story intersected with Fred Hutch.
Finding a family of nurses far from home
Fred Hutch, where E. Donnall Thomas, MD, had recently received the Nobel Prize for developing bone marrow transplantation, had already performed more than 1,000 transplant procedures. The family felt hopeful — and overwhelmed.
“We didn’t know anything about Fred Hutch, and Seattle seemed like the end of the earth,” Howard Steinberg said.
John Steinberg received two bone marrow transplants in two years, one in 1993 and the next in 1994. Howard Steinberg was the donor both times. In an uncertain situation far from home, Fred Hutch nurses gave the steady, comforting and knowledgeable support that the Steinbergs needed until John’s death in 1994 from an infection.
“The nurses knew everything that was going on and took care of John — they felt like family,” Howard Steinberg said.
Celebratory Giving
Howard and Cynthia Steinberg continue to remember their loved ones and celebrate life, something John Steinberg especially would have wanted.
How do they know? Because he was always thinking of others and because their twins, Halle and John, were born one year to the day after his death.
The family is Jewish, and observing a Yahrzeit, or the anniversary of a death, is deeply significant as a time for remembrance, honoring and mourning. Cynthia Steinberg believes that their children’s birth date was no coincidence. “John got involved in that,” she said.
“My brother would prefer us to be having a party rather than mourning,” said Howard Steinberg. So, every year, they light candles and celebrate. The couple often gives in honor of their birthdays and other milestones, an approach that also moves others to donate.
Their friends and family have contributed over $75,000 to Fred Hutch’s Harold and John Steinberg Memorial Nursing Scholarship Fund.
Challenging experiences made easier
When he and his wife established the scholarship fund, Howard Steinberg wrote a letter to Fred Hutch. In it, he said:
“Out of all bad things come some good. We went to the Hutch under difficult circumstances, but you all made things bearable. My family would like to recognize all of you for your outstanding work in the treatment of cancer patients and especially those of you that are receiving scholarships. We can think of no better way to honor the memory of my father and brother than by naming this scholarship fund after them and by paying tribute to you and your efforts.”
Over the years, the Steinbergs have received notes from nursing recipients about their experiences, like 2020 scholarship recipient Hailey Fantozzi, BSN, RN, who went to the International Symposium on Late Complications After Childhood Cancer, sharing that, “It served as a beneficial reminder that the mental, emotional, and physical effects of cancer remain for a lifetime, and it is of monumental importance to continue to advocate for survivorship care.”
For 2018 awardee Julia Majovski, DNP, ARNP, the fund allowed her to get her doctorate in nursing practice.
“Going back to school full time as an adult is hard when you have a family to support,” she wrote. “Your substantial gift allowed me to work less so that I could focus on my studies more.”
Registered nurse Hailey Fantozzi, left, and nurse practitioner Julia Majovski are both past recipients of the Harold and John Steinberg Memorial Nursing ScholarshipPhoto courtesy of Hailey Fantozzi and Fred Hutch file photo
“After my brother and I bought the business back, we’d work late washing cars together because we were so short-staffed back then,” he said.
Fred Hutch was a different place back then, too. Being a bone marrow transplant donor was much more invasive, for instance.
“They did it the old-fashioned way, taking [the donated cells] out of the hip,” Howard Steinberg said. “I even had to get an epidural.”
The Steinbergs also can’t forget how new and challenging the treatments were for John Steinberg, bringing into focus all the progress they’ve seen — and contributed to — since then.
In addition to the Harold and John Steinberg Memorial Nursing Scholarship Fund, the Steinbergs have supported Fred Hutch’s Center for Metastasis Research eXcellence, or MET-X, to better understand, detect and prevent the spread of cancer; invested in the work of leukemia biology expert Soheil Meshinchi, MD, PhD, through Project Stella, and established the Sondra Steinberg Prosterman Endowment for Ovarian Cancer in memory of Howard Steinberg’s mother to advance ovarian cancer research.
“As meaningful as this is, we would prefer that all three of them, Harold, John and Sondra, were still with us,” said Cynthia Steinberg. “Since we can’t have that, it’s beyond meaningful to us that our giving is helping others — it makes you feel that they are still touching people, even after they’re gone.”
Mission Possible
Fred Hutch study finds genetic driver of drug resistance in small cell lung cancer
Researchers use CRISPR-Cas9 gene-editing tool on tumor cells grown in mice to better model how tumors that initially respond to chemotherapy become resistant
Fred Hutch lung cancer researcher Dr. David MacPherson. Photo by Robert Hood / Fred Hutch News Service.
Small cell lung cancer, or SCLC, is aggressive, lethal and particularly cruel because chemotherapy initially works so well.
But within just a few months, SCLC becomes resistant to drugs and dashes hopes.
“What is seen in the clinic is often quite remarkable responses to chemotherapy initially, but these are just transient responses and tumors come back,” said David MacPherson, PhD, a Fred Hutch Cancer Center scientist who specializes in small cell lung cancer. “The vast majority of patients — despite having striking initial responses — do extremely poorly.”
The five-year survival rate for SCLC is less than 6%.
MacPherson’s lab in the Human Biology Division investigates what causes this rapid switch from hope to despair in SCLC, which accounts for about 15% of lung cancers.
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Researchers at Fred Hutchinson Cancer Research Center have made an important discovery in understanding how this resistance develops. By studying both human patients and mouse models of SCLC, they found that a gene called KEAP1 plays a crucial role in chemotherapy resistance.
When the team knocked out KEAP1 in tumor cells, they saw a remarkable change: cells that were once vulnerable to chemotherapy became resistant. This suggests that KEAP1 is a key driverA study from the lab published recently in the journal Science Advances, describes a new way to screen for the genes that matter in chemotherapy resistance by using human tumor cells implanted in mice.
The study identifies a gene that is well understood in other cancer types — but poorly characterized in SCLC — that drives drug resistance when it gets turned off, which could lead to new therapies and improved odds for SCLC patients.
PDX mice aren’t from Portland
Researchers often manipulate genes in cancer cells grown in laboratories under controlled conditions to understand what role they play in disease, but those cell lines only partly mimic how cancer behaves in a living organism.
SCLC cell lines grown on plastic and exposed to drugs in experiments don’t reliably re-enact the rapid switch to chemotherapy resistance observed in patients, which limits their value in understanding the genetic mechanisms driving that lethal transition.
However, mice implanted with human tumor cells that have not been grown on plastic — patient derived xenograft (PDX) models of the disease — show the same response to chemotherapy as the patients from whom the samples were collected.
MacPherson, who holds the Vinh Bui and Tram Le Endowed Chair for Lung Cancer, uses SCLC cells floating in patients’ blood to set up PDX mouse models for experiments that provide a more authentic environment than a lab dish.
For example, MacPherson’s lab has previously shown that when they altered (scientists say “perturbed”) the MCYN gene, causing it to produce more of its product than usual in PDX models of SCLC, they observed the switch to chemotherapy resistance.
“What we wanted to do with this study is move from single-gene perturbations to querying hundreds or thousands of genetic perturbations to identify which ones of those are important,” MacPherson said.
One way to perturb genes is to knock them out of commission and see what happens in their absence.
Making a screen with guides and scissors
The team used a molecular tool called CRISPR-Cas9 to knock out genes researchers believe could play a role in making tumors resistant to chemotherapy.
This versatile, Nobel Prize-winning tool has two parts: an enzyme called Cas9 that snips DNA at precise locations and CRISPR guide molecules that deliver the Cas9 snippers to the gene that researchers want to knock out.
When the cell repairs the break, it’s usually not good enough to restore the gene’s function, which knocks it out.
The CRISPR guides can be combined in a library of gene knockouts that can be applied to a population of cells in a single experiment.
MacPhersons’ team built a library of CRISPR guides for 400 genes that might play a role in making tumors resistant to chemotherapy.
“Our goal was to identify genes that were important for this switch from small cell lung cancer being exquisitely chemo-sensitive to rapidly becoming chemo-resistant,” MacPherson said.
They converted the library into viral particles capable of infecting cells so that each cell receives just one CRISPR guide directing Cas9 where to snip, which knocks out one — and only one — gene per cell.
By dripping the viral knockout brew on tumor cells, they could perform experiments to see which cells live and which cells die under drug treatment conditions, screening out irrelevant genes to identify the genes that matter most for survival.
Modeling knockouts in mice
CRISPR screens often are applied to tumor cells grown outside of their native environments in plastic dishes.
But that’s the approach that hasn’t worked so well for SCLC because the cells don’t mimic how tumors behave in living organisms when they receive chemotherapy.
So instead, MacPherson’s team tested their library of knockouts on tumor tissue growing in PDX mice.
First, they removed tumor cells from the mice and exposed them to their viral library of CRISPR guides.
They reserved some of the transformed cells to represent conditions at the beginning of the experiment. Then they re-implanted the rest of the transformed cells (about a million cells per mouse).
Once the mice developed tumors, they were exposed to one of two conditions.
Some mice received chemotherapy and others received only saline. The mice that received chemotherapy showed a similar response as the human patients: tumors shrank, but then they came back.
The team removed tumors from both groups and analyzed the tissue with genomic sequencing to see which of the knocked-out genes mattered in the tumors that came back.
Their screen turned up some of the usual suspects in SCLC, but it also spotlighted a new driver of chemotherapy resistance: a gene called KEAP1.
When they knocked out KEAP1, tumor cells that had been vulnerable to chemotherapy became resistant.
Dr. Lauren Brumage investigated why small cell lung cancer tumors become resistant to chemotherapy while at Fred Hutch. Photo courtesy of Lauren Brumage
Clinical relevance
Cells turn off KEAP1 when they respond to stress caused by substances called oxidants that snatch electrons from other molecules and damage cells. Turning off KEAP1 activates other molecules in an antioxidant signaling pathway that repairs the damage.
It’s an essential cellular process for survival, but if that pathway stays activated too long, it can fuel tumor growth.
When KEAP1 popped up in the screen, it got the researchers’ attention because KEAP1 dysregulation is also known to confer chemotherapy resistance in the most common type of lung cancer, though its role in SCLC has not been well characterized.
Tumors linked to KEAP1 mutations in other cancers also are known to depend on a process that breaks down an amino acid called glutamine to produce energy supporting rapid growth and proliferation.
Co-first author, Lauren Brumage, PhD, performed an experiment to see if that dependence on glutamine metabolism also exists in SCLC tumors when KEAP1 is knocked out.
Her experiment confirmed that loss of KEAP1 creates the same vulnerability and potential for a drug that would inhibit something the tumor needs to grow.
“This mutation on the one hand causes this dramatic chemoresistance, but it also allows for a therapeutic vulnerability that could be exploited in the clinic, potentially,” MacPherson said.
Brumage, then a student in the Molecular & Cellular Biology Graduate Program jointly offered by the University of Washington and Fred Hutch, did much of her doctoral work in the MacPherson lab. Co-first author, Scott Best, also is a student in the same program.
Brumage earned her PhD last year and is now a scientist working for the Seattle-based biotech company Omeros, which develops small-molecule and antibody therapeutics.
The MacPherson team received further confirmation that they were on to something clinically relevant when they collaborated with Barzin Nabet, PhD, a scientist with the South San Francisco-based biotech company Genentech.
He analyzed data from a Phase III clinical drug trial for patients with extensive stage SCLC and found that 6% of the patients had mutations to KEAP1 in their tumors, and the tumors in other patients found different ways to activate the same program caused by KEAP1 mutation. Activation of this program correlated with worse responses to treatment and worse overall survival.
“It speaks to the real-world relevance of what we’re doing in these mouse models,” Brumage said. “I was just glad to see that there is actual clinical significance to this because that’s really what got me into science and research in the first place.”
This work was supported by grants from the National Institutes of Health and Fred Hutch Cancer Center Support Grants.
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