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Nobody knew it then, but the genetic mutation came to Utah by wagon with the Hinman family. Lyman Hinman found the Mormon faith in 1840. Amid a surge of religious fervor, he persuaded his wife, Aurelia, and five children to abandon their 21-room Massachusetts house in search of Zion. They went first to Nauvoo, Illinois, where the faith’s prophet and founder, Joseph Smith, was holding forth—until Smith was murdered by a mob and his followers were run out of town. They kept going west and west until there were no towns to be run out of. Food was scarce. They boiled elk horns.The children’s mouths erupted in sores from scurvy. Aurelia lost all her teeth. But they survived. And so did the mutation. Earlier this year, I met Gregg Johnson, Lyman and Aurelia’s great-great-great-great grandson. The genetic mutation that had traveled the Mormon Trail was now in Gregg, one of hundreds of the Hinmans’ descendants in the Utah area. Gregg is 61, with blue eyes and a white goatee. He frequently travels for his job as a craftsman for Mormon temples, but Utah is still home. “I’m just a Salt Lake City boy,” he says.

The mutation that came with the Hinmans turns out to be a troublesome one. It lies dormant just long enough for people to have children and pass the mutation along, but not long enough to watch their children start their own lives. Gregg’s mother died of colon cancer at age 47. Her mother also died early of colon cancer, as did her mother. And who knows how many other relatives succumbed, stretching all the way back when the Hinmans came to Utah. Gregg knows the history of this mutation in a gene called APC because he’s spent more than 30 years in a series of studies at the University of Utah—made possible by a vast trove of Mormon genealogy records. Detailed family trees make it easier to trace genes that cause disease. After the Hinmans and other pioneers settled in the state, the Mormon church kept records that over time became an unusually detailed and complete genealogy. In the 1970s, university researchers had the foresight to combine these genealogy records with the state cancer registry to create what ultimately became the Utah Population Database. So when scientists began suspecting a genetic cause for cancer, they went hunting through the Mormon family trees. They found patterns of deadly inheritance: BRCA1, one of the infamous cancer mutations, as well as mutations for cardiac arrhythmia and melanoma. And of course, they found the APC mutation behind the colon cancer in Gregg’s family. Utah became an accidental genetics laboratory. When Lyman hitched his wagon for Utah a century and a half ago, he ended up setting a course for colon cancer research.

The Church of Jesus Christ of Latter-day Saints, or the Mormon church, has one of the largest genealogy databases in the world. Today, it operates a family-history library just steps from the temple in downtown Salt Lake City, where banks of computers await visitors interested in digital genealogy records. The Church has physical records, too. They are stored on microfilm under 700 feet of rock in the climate-controlled Granite Mountain Records Vault, secured with doors so heavy they’re supposed to withstand a nuclear blast. Mormons are, by stereotype, family oriented, and this intense interest in family trees is a matter of theology. Mormons believe in baptism of the dead—including, in some cases, the long-dead. The baptisms are meant to give those who did not find the gospel of Jesus Christ in their mortal lives a chance at salvation, so that entire families stretching back generations might be reunited, forever together in Heaven. (This practice has attracted controversy, especially when the dead have included Holocaust victims.) The actual ceremonies are performed by proxy in temples. Members of the church line up and step forward for baptism as the name of an ancestor appears on a screen. But first, you need names. So the Church sends crews around the world to collect records of the dead. In the 1970s, one such genealogy team looking for old parish records arrived in Parma, Italy, where a young American named Mark Skolnick was working on his Ph.D. thesis.

As luck would have it, Skolnick was using parish records to construct a genealogy database of his own. His thesis looked at how genes spread as people from different Italian villages moved and intermarried. The study was a nice “theoretical exercise,” he says, but nothing practical really came of it. Meanwhile, because he spoke Italian, Skolnick helped translate for the Mormon team that came to microfilm parish records. “I was a lowly gofer,” he says. A great many things, however, would come out of this. When Lyman hitched his wagon for Utah a century and a half ago, he ended up setting a course for colon cancer research. The Mormon church, Skolnick realized, was sitting on a vast trove of population genetics data. After finishing his thesis, he got a job at the University of Utah, where he set out to combine Mormon church records and cancer registry data into what would become the Utah Population Database. The genealogies and cancer records were a daunting amount of data, especially in an era when money was tight and computers were still the size of refrigerators. “It was like going from one year to the next to try to get the funding,” recalls Lisa Cannon-Albright, one of Skolnick’s graduate students at the time. They worked out of an old VA hospital building, infested with bats and painted an awful pale green. Getting all that data into the computer was a low-tech slog. Skolnick convinced the church to let him copy 186,000 pages of family records covering all the pioneers who came on the Mormon trail. The records went back eight generations and comprised about 1.6 million people in total. A team of typists, many of them genealogy enthusiasts, turned the handwritten records into a digital database. The data entry took the equivalent of 15 person-years.

As Skolnick was casting around for projects that could use the database, he met a young gastroenterologist named Randall Burt. Having grown up in Salt Lake City, Burt had recently returned to take up a fellowship at the University of Utah. He’s a gregarious guy, with a knack for putting patients facing colonoscopies at ease. “I just think of him as a big teddy bear,” one of his former patients told me. Gregg’s mother was one of Burt’s patients. By the time of her diagnosis, it was already too late to cure her colon cancer. She died a year later. Burt and his colleagues were seeing other families like Gregg’s, where colon cancer had cut down whole branches of the family tree. What’s more, when you looked at the young, still-healthy members of these families, their colons were also strange—covered in dozens of mushroom-like growths called polyps that can turn cancerous. The doctors called it attenuated familial adenomatous polyposis. They didn’t yet know what caused the profusion of polyps, but they reasoned if they could trace it through the family trees, they could identify who had the mutation and eventually the mutation itself. “I can’t tell you how many reunions where I’ve been to eating corn and potato salad and talking polyps.” In retrospect, finding a mutation whose effects are so stark does not sound difficult. And indeed, today it isn’t especially difficult. But in the early 1980s, still two decades away from the first draft of a human genome, finding a gene was hard—especially if you weren’t so sure the gene even existed. Perhaps, as many thought at the time, cancer is simply a product of lifestyle or other environmental factors. Tracing a genetic mutation back to a common ancestor is no easy task either. Family trees get exponentially bigger as you go back in time: You have two parents, four grandparents, eight great grandparents, and so on. Eight generations back, you have hundreds of ancestors. A family tree for the Mormon pioneers is more like a tangled bush.

To prove that the polyps were hereditary—rather than just the unfortunate result of say, a family living in the same house drinking the same toxic water—the researchers needed to find more families elsewhere that looked like Gregg’s. So they went looking through the Utah Population Database. With the family trees and cancer registry data, they could identify clusters of colon cancer. Then Burt and his team hit the road with his colon screening scopes—driving through Utah but also Idaho and Wyoming, where descendants of Mormon pioneers had settled. They set up in local hospitals and spent a day looking for colon polyps in the local population. “These dairymen would come in between milking the cows, and the next day cowboys would come in,” he says. And they went to family reunions. “I can’t tell you how many reunions where I’ve been to eating corn and potato salad and talking polyps,” says Burt. They took blood for genetic tests and invited patients to schedule future colon screenings.

It helped that the Mormons they were studying lived up to their reputation for friendliness. “I don’t know if people told you how receptive they are to research,” says Cannon-Albright, who herself comes from a Mormon background. “People recognize what you're doing. ‘It won’t help me but it’ll help my kids and kids’ kids,’ and they were in just like that.” Participating in the study required an invasive colon screening and a blood draw. Still, she says, “Nobody ever said no.”

Slowly, after hundreds of colon screenings and blood draws, a picture began to emerge. All of the families with this profusion of polyps seemed to have the exact same mutation, which pointed to a common ancestor. Those common ancestors, we now know, are Lyman and Aurelia. It’s not clear which one of the couple had the gene, but they passed it along to at least two of their five children. In 1991, research groups in Utah and at Johns Hopkins simultaneously discovered the gene, which became known as APC. In the decades since, this colon cancer research has kept going at University of Utah. Deborah Neklason, who took over Burt’s research after he retired, keeps a large white roll of paper in her office. She took it out when I visited and motioned me over to the big wood conference table, where she unfurled it and kept unfurling it, until half of it ran off the edge. It was the Hinmans’ pedigree on paper. Actually it was only part of it. The family had five branches: A, B, C, D, E, corresponding to each of Hinmans’ children, and this pedigree covered just branch E. Neklason found that she wanted to show me: a square with a black dot in the middle. It was Gregg—square for male, a dot to mark him as a carrier. Neklason’s office is in the university’s Huntsman Cancer Institute, a hospital and research center founded by businessman Jon Huntsman Sr. The Huntsmans wield unusual influence even for wealthy donors—hence a recent and ugly power struggle with university administrators—and this influence is apparent even in campus geography. The university’s building climbs up the foothills on Salt Lake City’s eastern edge, and the Huntsman Cancer Institute, wrapped in green glass, sits at the campus’s highest elevation. It’s more alpine ski resort than hospital. Huntsman jokes that when cancer is cured, he’s turning it into a Ritz-Carlton. The Utah Population Database, which began in the bat-infested old VA hospital, is set to move into the Huntsman’s new wing later this year.

Last February, then Vice President Joe Biden spoke at the Huntsman to promote his cancer moonshot. The event took place in the institute’s cafeteria, though calling it a hospital cafeteria is a bit of a disservice. Bon Appetit named it one of the world’s “coolest workplace cafeterias,” thanks to the floor-to-ceiling glass that overlook the mountains around Salt Lake City. On that day though, the windows were blacked out, per the request of the Secret Service. Gregg spoke at the event, too, and he was starstruck. (“Joe is Joe. He’s cool. I would have voted for him in a heartbeat.”) He swallowed his nervousness and began telling his family’s story, starting with his mother’s diagnosis. After his mother’s death, Gregg began seeing Burt for regular colonoscopies. Polyps, if removed early enough, never become cancerous. Each time Gregg had a colonoscopy, he got hundreds of polyps snipped off. He’s been doing this long enough that he can hold forth about how it used to be. “It used be,” he says, “you had to drink an Imperial gallon, five quarts of saline solution, within an hour and keep it down.” He paused to grimace. “Just thinking about it now makes my skin crawl.” The prep for colonoscopies requires much less liquid now, and it tastes a lot better. Stop putting off your colonoscopy, he added, slipping into the role he often plays for his family and friends, encouraging people to get tested.

Gregg has two sons, Dan and Patrick. The mutation has a 50-50 chance of being passed on, and the laws of chance were followed perfectly in this case: Dan, the older son, has the mutation, and Patrick does not. Dan is 32 now, at the point where he’s thinking about having kids. Having watched his father live a pretty much normal life despite this ticking time bomb of a mutation has given him an equanimous outlook. “That doesn’t affect my decision at all,” he says. In the future, Dan might not need such regular colonoscopies either. Gregg participated in a recent clinical trial using two drugs called sulindac and erlotinib to prevent polyps in the duodenum, a section of the small intestine that is difficult to reach with a scope. It worked beautifully for shrinking polyps, though it did have some side effects that are being ironed out in a follow-up trial. Gregg’s digestive tract was the “poster child” for the initial study. “The advancements are amazing,” says Dan, “It's so cool, even in the time that Dad's started with this.” In this era of hype about precision medicine, Gregg’s family shows its power—as it’s already being applied. The particular mutation in Gregg’s family only accounts for a tiny sliver of colon cancers in the U.S., but the research on his family may have a much larger impact. The APC gene is known as a tumor suppressor gene. Gregg’s family members are born with a mutation in APC, but it is also possible and common to acquire a mutation in the APC gene over one’s lifetime, through random chance or environmental exposure. Eighty percent of all colon cancers have such a mutation. “It’s such an early step in colon cancer, it’s perfect target for prevention,” says Neklason. If something can prevent colon cancer in this high-risk family, then perhaps it could prevent it in the rest of us too. That’s in part why the clinical trial results were so exciting.