For a person who’s several months into his second encounter with cancer, Scott Nelson sure seems to have a lot of energy.

While we are meeting over coffee, Nelson’s stimulated state was not induced by caffeine, but instead by a side effect of the pills that he’s been taking to help reduce the size of his prostate cancer. Nelson was prescribed these drugs, known as PARP inhibitors, as part of a clinical trial designed to transform his cancer from inoperable to curable.

Success isn’t guaranteed, but three things give Nelson faith: the support of his family, the ingenuity of his care team, and the knowledge that, nearly 20 years ago, he survived a Stage III pancreatic cancer diagnosis, which is almost always fatal, thanks to another clinical trial.

Survival rate: 2%

On a perfectly normal summer Friday in 2004, just after the Fourth of July, Nelson visited his general practitioner in Hudson, Wisconsin, for a routine check-in on some bothersome digestive issues. The visit was smooth sailing, until an ultrasound technician failed to hide his panicked reaction to Nelson’s results.

“He looks up, he looks me in the eyes, and he runs out of the room,” says Nelson, still visibly shaken by the memory. “[I thought], ‘This is not good.’”

“Not good” was a severe understatement: The scan revealed a large, cancerous tumor on Nelson’s pancreas.

A worry-wracked weekend ensued. “Saturday morning, I went to pull up [pancreatic cancer] on my computer,” Nelson says. “Two percent survival rate. I shut the computer off.”

Nelson soon learned that while his cancer hadn’t yet spread outside his pancreas, he had an advanced and aggressive form of the disease. And unless his tumor shrank, surgery would be impossible. 

Through a series of referrals, Nelson found his way to M Health Fairview hematologist and oncologist Edward Greeno, M.D., now the medical director of the Masonic Cancer Clinic. Greeno was spearheading a pancreatic cancer clinical trial at the Masonic Cancer Center, University of Minnesota for patients just like Nelson.

The clinical trial involved an intensive chemotherapy regimen to shrink Nelson’s tumor to the point where the cancer could be surgically removed. For the first time since his diagnosis, Nelson had a seed of hope that he could build his resolve around.

“If you don’t have a plan, you’re lost. But if you have a plan, at least you can say, ‘I’m making progress. I’m fighting back,’” he says.

Nelson powered through the presurgery routine without knowing if his tumor was shrinking. This necessitated a day-by-day outlook that Nelson now recommends when he speaks with other cancer patients.

“When you get diagnosed, your focus goes from here to here to here,” Nelson says, miming a shrinking motion with his hands. “And your focus is, I want to get through today, and then I’ll plan for tomorrow.”

By November, the chemo regimen was over—and Nelson’s tumor had a near-perfect response.

A few weeks later, surgeons removed the cancerous head of Nelson’s pancreas, the first part of his small intestine, and his gallbladder before reattaching his remaining organs in a process that Nelson now humorously calls “replumbing.”

His large family, a constant source of support during his experience, circled the wagons. “They always were with me,” Nelson says.

The surgery was a success. Nelson was declared cancer-free, just in time for the new year.

Family inheritance

“If you think back to that era, the chance of being cured of pancreas cancer for all comers was low,” says Greeno, who is also a professor in the University of Minnesota Medical School. “The odds were stacked greatly against him.”

In hindsight, Greeno says, the cause of Nelson’s cancer and the reason for his remarkable response to treatment stem from the same culprit: a genetic mutation known as BRCA2, which is associated with an increased risk of hereditary breast, ovarian, prostate, and pancreatic cancers.

Nelson first became aware of BRCA2 when his mother, MaryAnn Nelson, previously a breast cancer survivor, was diagnosed with ovarian cancer in 2002.

Realizing that her diagnosis was consistent with a pattern of disease that had also affected her own mother and grandmother, MaryAnn decided to undergo testing, which revealed the gene mutation.

“She knew that there was something going on in the family—and acted on it,” Scott Nelson says.

He describes his mother’s decision to undergo genetic testing and the subsequent BRCA2 discovery as an incredible gift to his family, arming them with the knowledge that they would need to confront cancer within their ranks.

When Scott Nelson was diagnosed with pancreatic cancer and enrolled in Greeno’s clinical trial, he benefited from a then-unknown link between BRCA2 cancers and a particular chemotherapy drug that happened to be part of the trial regimen.

His diagnosis also prompted Scott’s seven siblings (five of whom are confirmed to have the BRCA2 mutation) and their children to embrace genetic testing and early cancer screening. There have been eight cancer diagnoses among family members with the mutation, and all have survived due to early detection through genetic testing and regular screenings.

Two years after Scott Nelson’s first battle, his eldest brother, Steve, was diagnosed with prostate cancer early enough to be cured with surgery. In 2017, Steve’s regular pattern of screenings detected the early stages of his own pancreatic cancer. The elder Nelson once again opted to pursue surgery, beating cancer for a second time.

The road ahead

It would be easy to describe BRCA2 as a curse for the Nelson clan. But the reality of hereditary cancer is much more complicated.

While the strategy of targeting the BRCA2 mutation with genetic therapy was a “happy accident” for Nelson and Greeno back in 2004, it’s serving as the linchpin of his prostate cancer care plan today.

Guided by M Health Fairview oncologist Emmanuel Antonarakis, M.D., the Clark Endowed Professor of Medicine and associate director of translational research at the Masonic Cancer Center, Nelson is participating in a new clinical trial to test the presurgical effectiveness of PARP inhibitors to shrink prostate cancer.

“We have very good evidence from other clinical trials that PARP inhibitors work extremely well in patients that have BRCA2 mutations,” Antonarakis explains. “Had Scott not had the BRCA2 mutation, there literally would have been no other [presurgery] options for him. 

“So in a paradoxical way, the BRCA2 mutation, which on the one hand may have caused his prostate cancer, was also his saving grace.”

In March, Nelson learned that the PARP inhibitor treatment had indeed been successful: The tumor on his prostate had shrunk to the point that it was able to be surgically removed. 

While he’s excited about putting cancer in his rearview mirror once more, Nelson admits the disease is no easy foe. But with the support of his family, and the firsthand knowledge that life isn’t over even after a diagnosis, he’s ready for whatever comes next.

“[Cancer] is just too big, it’s just overwhelming, both emotionally and physically,” says Nelson. “It’s like you’re on a superhighway, with lots of lanes and vehicles, you’re flying along, and all of a sudden a black curtain drops just in your lane. You have to stop and deal with it.

“Then you get through it, the curtain raises, and you get back on the superhighway of life, knowing that there is always hope, regardless of the severity of the diagnosis.”