On September 26, 1963, Salt Lake City’s population was only 189,000. Yet more than 100,000 people gathered along North Temple to welcome President John F. Kennedy to Utah.

In his speech at the Salt Lake Tabernacle, Kennedy used the words “black and white,” but he was not referring to the 200,000 strong March on Washington a month earlier or to the killing of four African American girls attending Sunday school 10 days earlier. Black and white referred to positions on foreign policy. Communism was the threat.

With the Salt Lake metro area only 1.4 percent non-white (Latinos were counted as white), it was easy for many residents to ignore the tumult occurring across the nation. Not so on college campuses. The Daily Utah Chronicle reported regularly on student civil rights activism around the country. One article stated that U student Stephen Holbrook, “active in the Republican Party and the NAACP, ” had participated in the Freedom March on Washington.

Two months after Kennedy’s visit to Utah, he was assassinated. For many, it was the end of innocence.

University of Utah Professor Mark Matheson MA’85, who grew up in Salt Lake City, remembers “watching the aftermath of sorrow on black and white TV. By elementary school, we were writing essays on integration, which sparked a developing interest in the civil rights movement.”

Since Matheson began teaching, after receiving his master’s degree in English from the U and his doctorate from the University of Oxford, he has included Dr. King’s “Letter from Birmingham Jail” in his curriculum.

MUSE

Matheson now heads up the U’s MUSE Project (My U Signature Experience), which aims to provide undergraduate students with transformative educational opportunities. Each year, the MUSE staff chooses a theme for campuswide discussion, with the centerpiece being a text by a distinguished national guest. MUSE then organizes events including lunchtime lectures, book groups, and student dinners with professors and community leaders.

The 2014-15 theme was justice; its book was My Beloved World, by U.S. Supreme Court Justice Sonia Sotomayor. Her visit to campus drew more than 7,000 people from the campus and well beyond. How do you follow that? Matheson learned that an icon in the civil rights movement, U.S. Congressman John Lewis from Georgia, had written a book—a graphic novel inspired by a 1956 comic book telling Martin Luther King, Jr.’s story. Congressman Lewis created March—which became a trilogy of books— with co-author Andrew Aydin and illustrator Nate Powell. Matheson, a humanities professor, saw the graphic novel style as “a fresh genre that students are drawn to and excited about and find accessible.”

The theme was perfect: Community. “At the heart of all Lewis’s activism is the concept of the ‘Beloved Community,’ which implies growth and development and change in every person who works toward that goal,” says Matheson.

MARCH

Eight U professors incorporated March into their classes for 2015-16, and more than 1,000 students received copies of March: Book One (and in some cases, Book Two) donated by the O.C. Tanner Company. (Book Three comes out this August.)

March provided Matheson the opportunity to teach the role of texts in the civil rights movement. “Dr. King invoked Western cultural traditions—including the Bible, the Declaration of Independence, and the U.S. Constitution—i n the service of a profound message of justice for African Americans,” he says.

Matheson’s prediction that students would connect with March was correct.

“There are some books that just touch you right in the heart…. For me this was that book,” says Said Abdirahman Samatar, a chemical engineering/pre-law major. “It put a spotlight on some topics that I was unaware of.”

Students Said Samatar and Jessica Ramirez discuss the powerful impact of Lewis’s story.

Finance major Jessica Ramirez, who had learned little about civil rights in school, said the book was very informative, yet not intimidating. “It was the perfect way to tell a story of the civil rights movement,” she says. “This book is a good way to get people’s interest, and now those who have read the graphic novel can go and read more about the movement.”

Tyrell Pack, who studies chemical engineering, already had a deep knowledge of the civil rights movement. Still, he found March “very powerful.” Its graphic format “helped make stories and situations relatable and easy to visualize,” he says. Pack had written an essay on John Lewis in elementary school. He was excited for this “once in a lifetime” opportunity to hear him speak in person.

GOOD TROUBLE

On November 11, 2015, to a capacity crowd of more than 800 at the U, Lewis shared his story of growing up one of 10 children of sharecroppers in highly segregated rural Alabama. As a child, he saw “whites only” signs and asked why. When he had to sit in the balcony of movie theaters, he asked why. Lewis was told, “That’s the way it is. Don’t get in the way, don’t get in trouble.”

At age 15, he heard a radio show about Rosa Parks, who refused to sit in the “colored” section of a bus, and about Dr. Martin Luther King, Jr. “The actions of Rosa Parks and the words of [Dr.] King inspired me to find a way to get in the way, to get in trouble,” he told the crowd. “And that’s what I did, I got in trouble. Good trouble, necessary trouble.”

Lewis’s first act of civil disobedience, at age 16, was to request a library card.

Inspired by Dr. King, Lewis began “studying the way of peace, the way of love, the way of nonviolence. ” Lewis joined students and adults of all ages who bravely challenged the segregation laws of the South.

U.S. Congressman John Lewis speaking passionately about civil rights to a capacity crowd at the U last November.

Sitting at “whites only” lunch counters in Nashville, they suffered attacks. People “spit on us. Put a lit cigarette out in our hair or down our backs,” he said. As soon as one group of students was knocked unconscious or thrown in jail, another group arrived to request to be served. Then came the Freedom Rides, in which blacks and whites rode together on segregated buses. In town after town, they suffered assaults, firebombs, and beatings.

Lewis was one of six people who organized the August 28, 1963, march on Washington. He spoke just prior to Dr. King’s “I Have a Dream” speech. It was one of the actions that spurred the passage of the 1964 Civil Rights Act. The following year, Lewis led a march from Selma to Montgomery, Alabama, to demand voting rights. The bloody attack on the marchers, broadcast nationwide, hastened the passage of the Voting Rights Act of 1965.

In 1986, after more than 40 arrests, Lewis entered political life. “If you would have told me that some day I would be a U.S. Congressman and that an African American would be the president of the United States…,”

Lewis said to an impassioned round of applause near the end of his speech. Lewis urged students to become involved in the political process. “There are forces in America today that are trying to take us back to the time when it was impossible or difficult for students, young people, people of color, and seniors to participate in the democratic process,” he said. “In the final analysis, it doesn’t matter if we are black or white or Latino or Asian American. We’re one family. We live in the same house.”

INSPIRATION

Pack was impressed by Lewis’s message that “if there is a problem within our society, the best way to fix it is to organize a method of altering the obstruction.” As citizens, he says, “we have the ability to elect officials who can implement change on a government level.”

However, Pack is skeptical that activists today will tolerate the violent attacks that characterized the civil rights era. He sees protests, fueled by social media, as a more viable way of drawing attention to the need for social change. “Social media can introduce younger generations to ideas about injustices around the world, which is powerful enough to lead to change if enough people follow the movement,” he says.

A finance major and MUSE intern, Ramirez already knew the power of MUSE speakers. She had first learned about the MUSE program when she heard that Sonia Sotomayor was coming to campus in 2014. She immediately wanted to invite Latino students from her high school, Cyprus High, in Magna. “I thought it would be a great opportunity for them to be inspired by a successful Latina woman,” she says. The program gave her the green light and copies of Sotomayor’s books (Ramirez led a book discussion). She anticipated 30–40 students attending the speech, but more than 100 came.

“Race relations will remain stagnant if no action is taken and people do not speak about injustices,” says student Tyrell Pack.

Ramirez found the timing of Lewis’s talk propitious. “His speech was inspiring,” she says, “especially with everything going on in the country today. It definitely made me think more about how to approach things with peace, not violence or hate. I already believed we still have a long way to go regarding civil rights and equality, and meeting the congressman only made me want to be more involved and informed.”

Samatar’s first experience with MUSE and the U was when he was “lucky enough to miss school for a day,” at West High School, to hear 2013 MUSE keynote speaker Wes Moore, a black combat veteran and author. While on campus, Samatar learned more about MUSE. And later when he was trying to decide which university he wanted to attend, he came back to campus to help run the MUSE table at Red, White, and U day. “That night, I applied to be a MUSE Scholar and was accepted,” he says. “The MUSE program is one of the reasons I am at the University of Utah.”

Prior to Lewis’s speech, Samatar had been deeply concerned about racial injustices happening on campuses such as the University of Missouri. “A student went on a hunger strike and was willing to risk his life for justice,” Samatar explains. “This really made me question if I am doing enough to educate myself.” He says he learned from MUSE keynote speakers Wes Moore and Congressman John Lewis that he has to take responsibility to educate himself. “You can’t do something if you know nothing,” he adds.

BROADENING PERSPECTIVES

Ramirez, Samatar, and Pack share a common experience with MUSE. They all grew up in Utah. None has lived anywhere else except as small children. For them, the MUSE experience, especially the speakers, has opened their eyes and minds to the broader world and encouraged them to explore new possibilities. In Utah, says Samatar, it’s frightening to see “how comfortable” you can become. “You know there are injustices, but they don’t always affect you as much as they should.” Through his experience with MUSE, the Black Student Union, and Diversity Scholars, he is becoming more aware.

Pack agrees that “race relations will remain stagnant if no action is taken and people do not speak about injustices.” He says, “Both March and Lewis’s presentation helped me realize that I can get involved with programs focused on topics I am passionate about.”

Ramirez notes that in Utah, young people may not learn about all of the educational opportunities available to them, or may be discouraged from pursuing them. “At my high school,” she says “a speaker came to our class and told us ‘college isn’t for everyone.’ ” It was an AP class.

She sees the MUSE program as “helping students meet people in positions of power and see that these positions and the ability they offer to make change in the world are accessible to them.” Hearing the speakers, she says, “helps you realize they are very similar to you in a lot of ways and that you have the same opportunities.” Personally, she learned from Sotomayor and Lewis that “If I want something, I can fight for it. I can make a difference.”

Following Lewis’s lead, Ramirez is looking for a way to “get into ‘good trouble.’ ” She will apply to law school this fall.

—Susan Vogel is a freelance writer, publisher, and attorney based in Salt Lake City.

To learn more about the U’s MUSE program, see the 2011 Continuum feature here.

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JOSHUA SCHIFFMAN IS A LOVER OF ALL THINGS ELEPHANT. As a pediatric oncologist and a professor in the University of Utah’s Department of Pediatrics, he and his exceptional team from Primary Children’s Hospital, Huntsman Cancer Institute, and the University of Utah are working to expand the focus of childhood cancer research to include prevention— and elephants have become important partners in that work. Curious, we sat down with Dr. Schiffman to find out more.

CONTINUUM: Why are you and your research team turning your focus toward cancer risk prevention, and what do elephants have to do with it?

SCHIFFMAN: Cancer researchers have done a great job providing cures for cancer, but it’s still the leading cause of disease-related death in children. Childhood leukemia used to be a death sentence. Now the cure rate is over 90 percent—which is fantastic! But there is much more we need to do.

Medications are toxic, care is extremely expensive, and there seems to be an increase in the incidence of leukemia and brain tumors, and we aren’t quite sure why. Of the 350,000 childhood cancer survivors in the U.S. today, most of them have chronic disease—heart problems, pulmonary problems, hearing problems—all related to the treatment we give them.

While medical research shows that up to one in three childhood cancers may be caused by genetic risk, there has been little action by medical research in cancer prevention. By the time symptoms appear, it’s often too late. If we can find the cancer before symptoms are present, we have a much better shot at a good outcome—100 percent versus 20 percent survival in some situations. Cancer prevention is most important, and we are discovering that the p53 gene in elephants may play a pivotal role in it.

Schiffman with Eric Peterson, the elephant keeper at Hogle Zoo. (Photo by August Miller)

CONTINUUM: What is the p53 gene, and how does it help prevent cancer?

SCHIFFMAN: P53, also known as TP53, regulates the cell cycle and cell death, so it functions as a tumor suppressor. P53 is one of the most important genes to protect people from cancer. It’s called the Guardian of the Genome in the peer-reviewed literature and behaves much like a superhero. If there is DNA damage to a cell, p53 shows up on the scene to stop the cell from dividing and to help coordinate repair, or sometimes even to kill the cell. If p53 doesn’t work because it is missing or mutated, then the cell accumulates massive amounts of DNA mutations, keeps dividing, never dies, and that’s cancer. That’s why p53 is so important.

Most people have two copies of p53—one from mom, one from dad. However, it turns out that people with Li-Fraumeni syndrome, or LFS, have a hereditary genetic condition with just one working p53 gene in all the cells in their body. They also have more than a 90 percent lifetime risk of cancer—along with their affected family members. Over half the time, LFS cancers occur at a very young age, including childhood. The lack of a working p53 gene in patients with LFS is responsible for their extremely high rate of cancer.

But p53 is also very important in people without LFS. In fact, the p53 gene is broken in at least half of all human tumors, leading to initial tumor development. There is also evidence that p53 stops working as we age, an observation that correlates with increased cancer risk in the aging population. Without our p53 superhero, it is difficult to prevent the development of cancer.

CONTINUUM: Was there an “aha” moment when you first realized the potential of elephant genes for the future of cancer research?

SCHIFFMAN: Yes. A few years ago, I attended a medical conference to learn why we develop cancer. Carlo Maley, a biologist and associate professor at the Biodesign Institute in the School of Life Sciences at Arizona State University, gave a presentation, and it changed my life forever. He talked about something called Peto’s Paradox, the observation that cancer occurrence does not correlate with the number of cells or lifespan of an organism.

For instance, the rate of cancer in elephants is much lower than cancer in humans despite the fact that an elephant has 100 times more cells than a human, and elephant cells continue to divide over and over again throughout the 60- to 70-year lifespan of an elephant. Half of all men and a third of all women will develop cancer in their lifetime, but less than 5 percent of elephants appear to develop cancer. And that’s the paradox. With elephants having so many dividing cells for so long, but so little cancer, it’s clear that they must have developed a genetic mechanism for cancer resistance.

CONTINUUM: How did you connect the dots between elephant and human cancer resistance and the number of copies of p53?

SCHIFFMAN: At the conference, Dr. Maley reported that when he looked at the genome of African elephants, his team discovered that elephants have 40 copies of p53. I nearly fell out of my seat when I heard that. Dr. Maley said they couldn’t find any other animals with that many copies of p53, and although he didn’t know for certain, this might be the reason why elephants are so resistant to cancer.

After his presentation, I introduced myself to Dr. Maley and told him about my lab at Huntsman Cancer Institute at the University of Utah and about Primary Children’s Hospital, where we’re taking care of children with LFS, collecting their cells, trying to understand why their cells are more susceptible to cancer. “You just said that elephants have 40 copies of p53 and almost never get cancer. Our patients only have one copy of p53 and always get cancer,” I said. “What if somehow we could get elephant blood and test it next to the blood from our patients with Li-Fraumeni syndrome to try to determine for sure why elephants don’t get cancer?” Dr. Maley was very excited by this idea and asked me how I was ever going to get elephant blood, and I said, “I have no idea.” He said, “Well, give me a call if you find out.”

CONTINUUM: How did you get the elephant blood, and how do you go about studying it?

SCHIFFMAN: A few weeks later, my kids and I were visiting Utah’s Hogle Zoo. We arrived just as the daily elephant show was starting and sat down on the steps to watch. Out stepped Eric Peterson, the elephant keeper. “These are our African elephants,” Eric explained. “You can tell they are African elephants because of their big ears. They have big veins on the back of their ears to circulate the blood. That’s how they stay cool.” And then, and I swear it’s true, he said, “Did you know that once a week here at the Hogle Zoo we draw blood from the elephants to make sure they’re healthy?” That was it! A light bulb went off.

Schiffman watches as veterinarian Ashley Settles takes a blood sample from one of the herd at the Ringling Bros. Center for Elephant Conservation. (Photo courtesy Ringling Bros.)

The show ended, and Eric thanked everyone for coming and then invited anyone with questions to find him upfront. I immediately headed to Eric to ask my question. After introducing myself, I simply asked, “How can I get some elephant blood?” Eric explained the process of submitting an application to the zoo’s scientific review committee. After months of paperwork, we received permission for Eric and his team to collect extra blood for our research while doing their weekly blood draw. Since that day, the fantastic people in my lab take a weekly trip to the Hogle Zoo to pick up the elephant blood— still warm—to bring back to the lab to study.

From there, our team sorts the elephant white blood cells and intentionally treats the cells to cause DNA damage, which you can think of as pre-cancer. We were excited to learn that many of the elephant cells self-destructed with their extra copies of p53, whereas half as many human cells died despite their DNA damage, and hardly any cells from LFS patients died. Based on this and other laboratory experiments, we believe that these extra p53 copies in elephants may help to protect them from cancer.

CONTINUUM: We understand you’ve now partnered with Ringling Bros. to study other species of elephants as well. Could you tell us about that?

SCHIFFMAN: In addition to the African elephants at Utah’s Hogle Zoo, we have been working with the Asian elephants from Ringling Bros. and Barnum & Bailey Circus. It turns out that Ringling Bros. has a Center for Elephant Conservation and owns the largest herd of elephants in the Western Hemisphere. Similar to what we do with the zoo, we study blood that is already being collected for regular care of the elephants.

We have learned that Asian elephants also have multiple copies of the p53 gene that help to promote a very robust cell death when DNA damage is present. This entire project has been an absolutely amazing partnership between Ringling Bros. Center for Elephant Conservation, Utah’s Hogle Zoo, Primary Children’s Hospital, and our lab at Huntsman Cancer Institute.

CONTINUUM: What are your studies showing? Any surprises? And what’s next?

SCHIFFMAN: Science is great because it takes you places you don’t expect to go. Our hypothesis was that elephant cells would repair the DNA-damaged cells extremely quickly. But the elephant cells were not repairing faster; they were repairing at the same rate as human cells. Then we looked closer and found that in the elephant blood, there was much more cell death—more than twice as many elephant cells were dying than in humans.

So although the p53 in elephants wasn’t repairing cells quickly, it was killing the cell quickly so it could no longer divide—much more efficient. We thought to ourselves, evolution has done it again! Taking a step back, this makes perfect sense. If you want to prevent cancer, this is the way to do it, kill the cell before it can ever go on to become cancer. We are now working to insert p53 from elephants into human cancer cells to see if there is any effect and to find out if there is a way we can translate these laboratory findings into clinical medicine. With enough research, support, and effort, we hope that the first clinical trials could begin within the next three to five years.

THE RESULTS OF THE RESEARCH by Schiffman and his team were published in the October 2015 issue of the Journal of the American Medical Association (JAMA) and were met with phenomenal interest. The article was ranked as the No.2 most popular story in JAMA for 2015 and was named one of the top 100 science articles around the world for 2015. It also made the cover of Newsweek and has generated more than 20,000 individual news stories to date.

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