When Harvey learned that his melanoma had spread to his lungs in the winter of 2008, he started planning for his death. Despite a down market, he liquidated his stock-market assets to ensure his wife wasn't doubly burdened.
He moved the investment firm in which he is a partner to a smaller space. He didn't take an office - he figured that with his fatal skin cancer he wouldn't live long enough to use it. He hated waste.
"Everybody goes," Harvey (who asked that his surname not be used) said matter-of-factly in the boardroom of his downtown Toronto office.
More than two years later, Harvey, wearing a navy blue suit and tie, is at work on a sunny spring day. Aged 77, he self-consciously pats his thinning scalp. "I used to have a full head of hair," he explains.
Not that he's complaining. In January, Harvey started taking a drug known as PLX4032 in a clinical trial in Philadelphia. If it weren't for those pills - three, vitamin-sized ones in the morning and another three at night - he would be near death.
He points to his chest, where 2.1- and 1.4-centimetre cancers had been found in his lungs. "My tumours," he says now, "are almost imperceptible."
Researchers have made a remarkable breakthrough in the treatment of one of cancer's deadliest forms - about 5,000 Canadians were diagnosed with malignant melanoma last year.
Harvey's new cancer therapy is tailored to a genetic mutation called B-RAF, which affects roughly 60 per cent of patients with melanoma. And it's shrinking tumours, many by more than a third.
It's a significant shift for a disease that had not seen progress for four decades. And it illustrates the power of what is called personalized medicine.
Instead of developing drugs that destroy fast-growing cells - normal as well as cancerous ones, a method that seldom works with later-stage cancer - scientists are now looking to slow or stop the genetic mutations that fuel cancer's growth. And the approach is tailored to patients depending on individual mutations.
It's all about providing the right therapy to the right patient, improving care and even saving money.
CAN A FUTURE CANCER CRISIS BE AVERTED?
At no time has a breakthrough ever been more needed. Unless progress is made in controlling cancer, an estimated 27 million new cases will be diagnosed worldwide by 2050, creating a huge economic and health-care burden.
As a result, research is happening at a dizzying rate: The International Cancer Genome Consortium announced that it is working to catalogue the genetic changes of the 50 most common cancers - 500 genomes from each cancer type.
That makes it the most ambitious biomedical research effort since the Human Genome Project (the international effort to map human genes that was completed in spring, 2003).
For a wretched disease with an equally wretched prognosis (most patients with Stage-4 melanoma die within a year after the cancer has spread), the PLX4032 treatment is a first. Patients at death's door, some unable to get out of bed or hold down food, are now working, shopping and enjoying life - an average of six months more of it.
"We're more than one and a half years out now from the initial studies," said Keith Flaherty, a medical oncologist who led the first trial of the drug PLX4032 while he was at the University of Pennsylvania.
"One and a half years [of survival] in melanoma, is phenomenal. … This is a massive change, to have it under control."
PUTTING THE BRAKES ON CANCER REPRODUCTION
Developing targeted therapies that cause programmed cell death is "our only road forward," according to Dr. Flaherty, who is now director of developmental therapeutics at the Massachusetts General Hospital.
PLX4032 - so new it is not commercially available - is the only targeted therapy for melanoma that works.
But it is not the only targeted cancer medicine. Gleevec turned a potentially killer disease - chronic myeloid leukemia - into a chronic one. Herceptin transformed one of the most aggressive forms of breast cancer into one of the most curable.
Both drugs focus on genetic mutations acquired later in life - ones that are not inborn and are therefore not passed on to children.
These genetic triggers are at the heart of current cancer research. They provide constant signals to cells to reproduce; they are the automotive equivalent to pressing the accelerator in a car. A new drug such as PLX4032 offers the brake.
"We're sequencing a whole genome here. We're going to sequence thousands of cancer-genome tests," said Tom Hudson, president and scientific director of the Ontario Institute for Cancer Research.
"There's going to be a generation of useful tests and drug combinations. In cancer, you don't want to develop a new drug if the target isn't known in advance."
David Hogg is one of Canada's leading melanoma researchers. Like others, he was discouraged with the therapies available to melanoma patients - chemotherapy, the treatment mainstay for the past 40 years, only worked to shrink tumours by 5 to 15 per cent.
"The bottom line here is, by and large, chemotherapy in melanoma is dead," said Dr. Hogg, a medical oncologist and attending physician at Toronto's Princess Margaret Hospital. "We need better drugs. We need to do better for our patients. Doing the same old thing is not an option."
Canadian hospitals are starting to enroll patients in the third phase of the PLX4032 trial, to confirm the drug's effectiveness, monitor side effects, compare it to commonly used treatments and collect information that will allow it to be used safely.
Eligible melanoma patients are those with inoperable Stage 3 tumours or those diagnosed with Stage 4.
The new therapy, Dr. Hogg said, "represents the first glimmer of hope that we might be able to change the course of the disease."
Ravi Amaravadi, a medical oncologist and assistant professor at the University of Pennsylvania, where Harvey was treated, called it a "really, really big deal.
"Yes, there are questions around it. … But this has a 70-to-80-per-cent response rate, which is melting tumours away in front of your eyes."
PRAYING FOR A TRIAL SPOT
Sitting in the boardroom, Harvey can't name a precise cause for his melanoma, though he says he was always covered with moles; he was closely followed by doctors who over two decades did many biopsies.
Most often, malignant melanoma is caused by undue exposure to sunlight, and while it accounts for a small fraction of all skin cancers, it makes up most of the deaths.
His problems began in February, 2008, when a troubling, painful bump on his shoulder - he thought it was a cyst - was found to be melanoma.
A scan that May confirmed the worst-case scenario: The disease had spread to his lungs. He immediately went onto chemotherapy, but by June, 2009, he had become resistant to conventional treatment.
He was offered spots in several clinical trials, but none seemed like a good enough bet. Nearing what he thought was the end, he had accepted his fate: "I'm comfortable. I'm not in pain. I'm mentally calm about my mortality."
But his brother, based in Philadelphia, wasn't ready to let him go and so enrolled him in the PLX4032 trial, turning Harvey's resignation to excitement - until he discovered it was enrolling only seven patients, and he was No. 28 on the list. That was in November, 2009.
"By this time, my friends are familiar that I have this sickness," Harvey said at the time. "And I have 200 people praying for me every day."
Those prayers were answered: The criteria to get into the trial were very tight, and so many patients were cut that Harvey eventually made it to No. 7.
Leslie Fecher, who specializes in melanoma, started him in January this year with four pills twice daily, later reduced to two sets of three due to side effects (fatigue and dizziness).
CLOSING IN, BUT UNLIKELY TO SHUT THE TRAP
"This is still an ongoing study, still a drug under investigation," says Dr. Fecher, a medical oncologist at the University of Pennsylvania's Abramson Cancer Center.
"It's a very exciting development in the field of melanoma, because of the response rate we've seen, which is higher than we've seen with other agents."
But no single path is likely to be definitive, Dr. Fecher adds. Figuring out which mutations fuel a particular cancer's growth is a sneaky game of tag: The disease will find new pathways, spurring more investigations for more drugs to shut or slow them down.
But at least for now, scientists are closing in.
And for patients, it spells a reprieve.
Harvey is making plans again. He has signed a lease for an apartment in Florida for next winter.
He still doesn't have an office at work, but his desk, in an area that looks like an open waiting room, is decorated with photographs of family and friends.
PLX4032 is not a drug without its side effects: Squamous-cell cancer on his ear, neck and chest had to be removed. But that was more of an annoyance than anything.
Still, the future is "every single day," Harvey says.
And he remembers what a physician told him when he first learned his cancer had spread and his time seemed limited: "Don't let any doctor tell you when you are going to die."
Lisa Priest is a reporter who specializes in health issues for The Globe and Mail.