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Dr. Steven Gallinger is investigating the link between BRCA mutations and particular chemotherapy drugs.Darren Calabrese/The Globe and Mail

Five years after they're diagnosed, only 8 per cent of pancreatic cancer patients are still alive. Toronto journalist Libby Znaimer is one of them.

Six years after receiving novel treatment that shrank her pancreatic tumour to an operable size, Znaimer remains an exceptional case.

"I've been cancer-free ever since," says Znaimer, vice-president of news and information at Toronto's Classical 96.3FM and AM740. "I'm very, obviously, incredibly lucky."

The story of her remarkable recovery has been shared among oncologists and cancer researchers around the world. Yet they're still trying to understand why some pancreatic cancer patients like Znaimer, who carry a BRCA genetic mutation (the same kind that prompted Angelina Jolie to undergo a preventative double mastectomy) respond well to specific chemotherapy drugs, while others don't.

Earlier this year, the Canadian Cancer Society awarded a five-year research grant worth more than $1.2-million to Dr. Steven Gallinger of the University Health Network's Princess Margaret Cancer Centre to investigate further. The Globe asked Gallinger, who treated Znaimer, to share the latest on his work:

What have you found out about the link between BRCA mutations and pancreatic cancer?

We have known about this relationship and have been interested in this for at least 15 years. It's more important now because as we're moving into this era of personalized medicine, what we're noticing – and what everybody is noticing – is that there are subsets of all the major diseases that are different from each other. And naturally because they are genetically very different, the response to chemotherapy and other treatments is going to be very different, too.

In BRCA, we're finding that people with mutations seem to be more sensitive to some chemotherapy drugs. But we need to do more research, which is what the purpose of that grant is. We need to study this phenomenon in greater detail.

What exactly are you studying?

For one thing, Libby's story is the extreme grand slam. There are other patients with the BRCA mutations who have not responded so well and they died. Some patients develop resistance to the drugs. And we don't think it's a one-to-one relationship, meaning you have the mutation, you get the drug and you're cured. It's more complex than that. So we're studying the question in many other patients, in test tube, and in mice models that mimic the same disease.

What was the treatment that worked for Ms. Znaimer?

It was chemotherapy, but it was a very old drug [cisplatin] that had kind of been discarded as being useful in pancreas cancer because the large studies that were done with that drug showed no benefit. But the problem with those large studies is if you don't separate the patients that actually are benefiting, they get diluted in the big picture of the statistics showing no benefit.

That's kind of the problem now. If we are going to try to divide all these big cancers into little groups, it's very hard for the drug companies to come up with designs that are first of all economically useful because they prefer if their drugs are given to everybody, not just a few people. So it's a bit of a catch-22 for the drug industry. But if you're a cancer patient, and you don't have the mutation, then why would you bother with the drug? That's the problem.

This story is being told every minute now all around the world. Because now that we have the technology to sequence the whole genome very efficiently and quickly, every day there's something that's reported that looks like it's an incremental division of a group of patients into smaller, little groups. And one of the smaller, little groups is very different from the other ones and they seem to respond very differently to drugs.

Should people get genetically tested if they're concerned cancer runs in their family?

It's a tough question because it depends on which side of the fence you want to sit on. It's a big ethical dilemma. First of all, do people want to know? Once you find out you're a carrier of one of these mutations, then there's a 50-per-cent chance that your brother and sister are carriers. One of your parents has to be a carrier because they passed it down to you. And half of your children are going to get it, too. So it has implications beyond the person into their family. But if it has an implication for your treatment in a life-threatening disease, like pancreas cancer, then most people say, 'Well, it's kind of a no-brainer. I want to be tested.'

So we are kind of dancing this fine line between ethics, society, freedom of rights, expense – because it's costly. Everybody kind of has a different view. And then there's ethnic groups, like Ashkenazi Jews, who have a higher frequency of these mutations. So there's some people who have advocated testing every Jewish person for these mutations because the implications are pretty significant for your risk of cancer and what's going to happen to you.

This interview has been condensed and edited.

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