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Top cancer groups team up to take on health disparities

Four national organizations push for richer data, more inclusive research to better serve the underserved

July 24, 2017 | By Diane Mapes / Fred Hutch News Service

Wellness Festival Health Fair

Volunteers work the information table at the Cierra Sisters' Community Wellness Festival and Health Fair at the Holy Temple Evangelistic Center in unincorporated King County, a "medical desert" and "food desert" south of Seattle, on Saturday. Volunteers provided health information, tips on cancer prevention and gave away fresh fruits and vegetables during the fair.

Photo by Robert Hood / Fred Hutch News Service

It’s no surprise that there are health haves and have-nots in our country, particularly when it comes to cancer.

The health haves have money, insurance, socioeconomic and even geographical advantages on their side.

The health have-nots? 

They may reside in rural or suburban areas with few doctors, much less a cancer treatment center with all the latest therapies. They may live in “food deserts” where fruits and vegetables are inaccessible or “food swamps” where junk food — and obesity and all of its related diseases — are the norm. Maybe they’re afraid to go to the doctor because they mistakenly believe all cancer is a death sentence or they’ve experienced racial bias from their health care providers. Maybe they don't speak English so can't decipher crucial cancer prevention messages.

No, the surprise isn’t that health disparities are so prevalent that our most vulnerable populations — the poor, the elderly, ethnic minorities and such — are more likely to die after a cancer diagnosis than, say, middle-income whites. The surprise is that these well-documented health disparities have gone on for as long as they have.

But change is afoot. Four leading cancer organizations have joined forces to decry these longstanding disparities and call for a collaborative effort to ensure cancer research benefits all patients, regardless of race, ethnicity, age, gender, income, education or the communities in which they live.

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6 things to know about glioblastoma

Following Sen. John McCain’s diagnosis, Fred Hutch experts offer ‘the long view’ on brain cancer research

July 21, 2017 | By Mary Engel / Fred Hutch News Service

Sens. Edward M. Kennedy, Joe Lieberman, John McCain

Sen. John McCain, right, said of his old friend and favorite sparring partner, Sen. Edward M. Kennedy, left, "He took the long view. He never gave up." Kennedy, shown here along with Sen. Joe Lieberman, center, died of glioblastoma in 2009.

File photo by Rex / Shutterstock via AP

There was something especially poignant about the news that John McCain, the Republican senator who has represented Arizona in Congress for more than 30 years, has been diagnosed with the same aggressive brain cancer that felled another Senate giant, his long-time friend and favorite Democratic sparring partner, Edward M. Kennedy of Massachusetts. Cancer really is bipartisan.

Late Wednesday, McCain’s office released a statement that the former Navy pilot who survived five years as a prisoner of war during Vietnam and twice ran as his party’s candidate for president had glioblastoma. McCain is now reviewing treatment options with his family and care team at Mayo Clinic Hospital in Phoenix, Arizona.

Colleagues from both sides of the aisle, world leaders and ordinary people reacted with an outpouring of supportive emails, tweets, Facebook postings and prayers. McCain’s daughter, Meghan McCain, captured the public mood in her moving personal tribute. “The cruelest enemy could not break him,” she wrote. “The aggressions of political life could not bend him. So he is meeting this challenge as he has every other. Cancer may afflict him in many ways: But it will not make him surrender. Nothing ever has.” 

Glioblastoma is a particularly cruel enemy. Kennedy lived for 15 months after his diagnosis, which is about the median survival time for glioblastoma with treatment. He died in August 2009 at age 77.

McCain, who is now 80, spoke at the funeral. In words that could also describe himself, he praised Kennedy’s “bellowing laughter” and “uncanny sense for when differences could be bridged.” Noting his old friend’s passion for legislating — and life — McCain said, “He took the long view. He never gave up.”

Drawing on experts at Fred Hutchinson Cancer Research Center, here is the long view on glioblastoma diagnosis, treatment and research:

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Good News at Fred Hutch

Celebrating faculty and staff achievements

July 20, 2017

CBS correspondent Susan Spencer interviews Dr. Jim Olson in his Fred Hutch lab earlier this year.

Photo by Molly McElroy / Fred Hutch News Service

CBS ‘Sunday Morning’ to feature Dr. Jim Olson’s Tumor Paint research this weekend

CBS “Sunday Morning” this weekend will take viewers into the Fred Hutchinson Cancer Research Center lab of Dr. Jim Olson to show how Tumor Paint, a “molecular flashlight” he discovered that’s derived from scorpion venom, distinguishes cancer from healthy tissue. The show will air in the Seattle area from 7 to 8:30 a.m. Sunday on KIRO-TV.

During his interview with CBS correspondent Susan Spencer, Olson said that if Tumor Paint is approved by the U.S. Food and Drug Administration, “I think this will potentially be the biggest improvement in cancer surgery, maybe, in 50 years.”

The award-winning newsmagazine, a Sunday morning staple for many, first aired in 1979 and is hosted by journalist Jane Pauley. The program reaches about 6 million viewers across the nation each week.

Fred Hutch has licensed the technologies relating to Tumor Paint to Blaze Bioscience and has an ownership interest in Blaze. Olson has an ownership interest in Blaze Bioscience. Both Fred Hutch and Olson may financially benefit from their interests if the company is successful in marketing this product. The terms of the financial arrangements with Blaze Bioscience have been reviewed and approved by Fred Hutch in accordance with its conflict of interest policies.

Tumor Paint is an investigational product and has not been approved for commercial marketing by the U.S. Food and Drug Administration or any other regulatory authority.  No conclusions should be drawn from the information in this story about the safety, efficacy, or likelihood of regulatory approval of this investigational product.

— Kristen Woodward / Fred Hutch News Service

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From student to scientist to mentor

A science education program helped launch Louisa Pendergast’s research career. Now she’s helping mentor more science teachers at Fred Hutch.

July 20, 2017 | By Rachel Tompa / Fred Hutch News Service

Louisa Pendergast and Kathryn Wallace

Research technician Louisa Pendergast (right) is mentoring Northwest School biology teacher Kathryn Wallace in a research project at Fred Hutch through the Science Education Partnership program.

Photo courtesy of Caren Brinkema / SEP

You’ve probably heard that adage about giving someone a fish versus teaching them to fish. But how many more people could you feed if you taught a teacher to fish?

That’s the educational paradigm Fred Hutchinson Cancer Research Center’s Science Education Partnership has been leading for the past 26 years. With the goal of bringing modern, real-life science and technologies to more students in Washington state, the educators at SEP are looking not to the students — but to their teachers.

Every summer, two dozen or so middle school and high school science teachers convene at the Hutch and plunge into an intensive, two-week science boot camp. Each teacher participating in the program learns new techniques in a teaching lab, and then is paired with a scientist to participate in an ongoing research project in that researcher’s laboratory.

“We’re uniquely positioned because working with teachers, there’s such a great multiplier effect. We can reach so many students through providing professional development and support to teachers,” said SEP’s director, Jeanne Chowning.

The program also loans out molecular biology kits and lesson plans for classroom use. Once a teacher has been through SEP, they’re members for life — and many of them borrow kits or benefit from other Hutch resources year after year.

The program aims to improve overall science literacy in the state, as well as to attract more people into science careers, Chowning said. And sometimes those students-turned-scientists decide to give back.

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How cancer fools healthy neighboring cells

‘Tumor microenvironment’ research underscores why we need cancer immunotherapy — and how to make it work for more patients

July 18, 2017 | By Rachel Tompa / Fred Hutch News Service

Illustration of a stylized cancer cell making friends with neighboring cells

Like tiny con men, cancer cells have numerous tricks to fool healthy cells in their neighborhood to help the tumors grow. Research in this area is leading to improved cancer treatments.

When we think of a tumor, we tend to think of the cancerous cells themselves, rogue agents fueled by a mindless collection of mutations that spur uncontrolled growth and division.

But cancer is not just the cancer itself. It turns out that the tumor’s neighbors can be just as important to the disease.

Like tiny con men, cancer cells are adept at tricking healthy parts of the body into doing their dirty work for them. Some tumors build physical walls around themselves by recruiting healthy cells or molecules to do their bidding. Many can trigger the growth of new blood vessels to supply them with energy for their expansion. In some cancers, like certain lung cancers, tumors can actually contain more noncancerous cells than cancer cells.

This “tumor microenvironment” — the noncancerous cells and molecules that are nevertheless an integral part of cancer — also heavily influences whether a treatment will work. Especially, researchers are finding, in the case of immunotherapies.

When it comes to this burgeoning class of cancer treatments that harness the body’s own immune system to attack tumor cells, the microenvironment is king. In fact, some recently developed cancer immunotherapies ignore the cancerous cells entirely, focusing instead on enabling neighboring healthy cells to slip out of the tumors’ grasp and realize their natural cancer-killing abilities. The tumor’s local milieu is so complex, however, it remains a major roadblock standing in the way of applying immunotherapies’ early successes in blood cancers to solid tumors like breast, lung, colon, liver and pancreatic cancers, which are the top five deadliest cancers in the U.S., according to the American Cancer Society.

“Tumor microenvironment issues come hand-in-hand with working on solid tumors,” said Fred Hutchinson Cancer Research Center’s Dr. Kristin Anderson, who is part of a team working to develop immunotherapies for ovarian cancer and other solid tumors.

That’s why cancer researchers need to understand it.

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Promising results in trial of engineered T cells in high-risk leukemia

High response rates to experimental immunotherapy in patients with treatment-resistant chronic lymphocytic leukemia

July 17, 2017 | By Susan Keown / Fred Hutch News Service

Dr. Cameron Turtle

Dr. Cameron Turtle presented findings regarding CAR T-cell therapies in leukemia and lymphoma patients at the annual meeting of the American Society of Clinical Oncology last June in Chicago.

ASCO file photo

Editor's note: This story was first published in Dec. 2016, when the results of this study were presented at the American Society of Hematology's annual meeting. It has been updated to reflect the researchers' publication on Monday of their results in the Journal of Clinical Oncology.

The published paper shows that about 70 percent of patients with the most common adult leukemia had their tumors shrink or disappear following an experimental immunotherapy based on chimeric antigen receptor (CAR) T cells. The researchers also found that measuring genetic traces of cancer cells taken from bone marrow biopsies might be a better indicator of prognosis than the standard lymph node scan.

The 24 patients had undergone most standard therapies available to them and yet their chronic lymphocytic leukemia had come back strong. Almost all of them had been treated with a newly approved, targeted drug called ibrutinib; data from other studies show that most patients whose disease progresses after ibrutinib treatment do not survive long. The majority of the 24 had chromosomal markers in their leukemia cells serve as “predictors of a bad response to most standard therapies,” said Dr. Cameron Turtle of Fred Hutchinson Cancer Research Center.

But most of these patients, who were enrolled in a small, early-phase trial, saw their advanced tumors shrink or even disappear after an infusion of genetically engineered immune cells. Turtle, one of the study’s leaders, first presented these results in December at the annual meeting of the American Society of Hematology in San Diego.

In the trial, participants’ disease-fighting T cells were removed from their blood and genetically engineered in a lab at Fred Hutch to produce an artificial receptor, called a CAR, or chimeric antigen receptor, that empowered them to recognize and destroy cancer cells bearing a target molecule called CD19. After patients received chemotherapy, the CAR T cells were infused back into their bloodstream to kill their CD19-positive cancers.

While all 24 patients with chronic lymphocytic leukemia, or CLL, received the experimental therapy, the study authors focused on the results in a subgroup of 19 patients who received particular chemotherapy regimens and doses of CAR T cells the researchers now prefer, based on recent data in other groups of patients on the trial.

Fourteen of 19 experienced a partial or complete regression of their disease in their lymph nodes. And of the 17 who had leukemia in their bone marrow when they enrolled on the trial, the marrow became cancer-free in 15 after they received CAR T cells. 

“It’s very pleasing to see patients with refractory disease respond like this,” Turtle said. The research team “had seen very good responses [to the same CAR T-cell therapy] in acute lymphoblastic leukemia and non-Hodgkin lymphoma, so we hoped responses would be good in CLL too.”

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