There is a flower in my garden that spreads so rapidly it has become a pest, and it has resisted all efforts to kill it.
Now it turns out that the flower — a common bachelor button — and it's more famous relative, feverfew, may have the power to kill cancer.
That's far from certain at this point, but clinical trials are set to begin soon in England to determine whether a modified derivative from this plant is safe to administer to terminal leukemia patients. If it does no harm to the patients, clinical trials will start in this country, possibly within six months, to determine whether the flower does indeed kill cancerous cells in the blood while leaving healthy cells alone.
A successful outcome would be an astonishing breakthrough in the fight against cancer because this type of treatment approaches the disease from a new direction, but because most new drugs fail during the rigorous trials this could turn into just another false hope. However, laboratory tests on cancer cells at the University of Rochester Medical Center have been encouraging enough to at least lead to a next step — testing the drug for safety.
"We don't want to raise false hopes here," said lead researcher Craig T. Jordan of the University of Rochester. "If something bad happens at the phase one trial, we won't go beyond that."
It has taken years to get this far because the road to cancer cures is littered with failed promises, but there were hints many years ago that there was something special about feverfew. The journey from the garden to the cancer ward involved many researchers, helped by some critical breakthroughs in our understanding of cancer. It's not the same battle today that it was just a decade or so ago.
This story begins a couple of centuries ago when people depended upon herbs for medical treatment. Certain plants were known to help alleviate pain and feverfew, which looks a lot like a daisy, was used to ease headaches and inflammation. An extract from the plant, parthenolide, was eventually isolated and packaged in pills, and it is sold today in health food stores as a treatment for migraine, arthritis and other ailments.
There were hints years ago that the chemical might also be useful in the fight against leukemia, but an early trial ended in failure because it was not absorbed into the blood and thus could not attack cancerous blood cells even if it had the power to do so.
Meanwhile, cancer research had turned up a surprising development. In 1977, John Dick of the University of Toronto made a remarkable discovery. He found that some of the cancerous cells in leukemia were stem cells, those magical cells that morph into different kinds of adult cells, like blood cells. Could it be, a few scientists wondered, that aberrant stem cells actually cause cancer?
If true, to have any hope of ever eradicating cancer scientists would need to figure out how to get to the stem cells and stop the disease at its roots. Scientists around the world began searching for stem cells in all sorts of cancers, and found them nearly everywhere they looked — in breast cancer, and later in the brain and bone. Those findings have led some scientists to conclude that many, and possibly all, tumors begin at the stem cell level.
The news electrified the University of Rochester's Jordan and his then-graduate student Monica L. Guzman. About 10 years ago, Guzman began studying the molecular structure of stem cells.
"We were trying to find differences between the normal stem cells and the leukemia stem cells," Guzman said. She found one key difference. The cancer cells had what the researchers call a "survival factor," a mechanism for staying alive.
"The normal stem cells don't have it," she added.
Bingo. If Jordan and Guzman could figure out how to inhibit the survival factor, the cancerous cells would die and the normal cells would be left alone.
Guzman's earlier work on the molecular structure of stem cells suggested a possible course. The researchers now knew enough about stem cells to try and match the cancerous cells with a chemical that could inhibit the survival factor. When they gave the cancerous cells a dose of parthenolide, they hit pay dirt.
"It was very effective on the leukemia stem cells without harming the normal stem cells," Guzman said.
Very encouraging findings, but there was still the problem of absorption. If the drug just passed through the body without remaining in the blood, it couldn't do its work. So Jordan and Guzman turned to colleague Peter Crooks, an internationally known biochemist at the University of Kentucky. Crooks has discovered scores of drugs and holds more than 100 patents. He combined parthenolide with dimethylamino, producing a water-soluble chemical that the scientists believe will attack leukemia at its roots.
A successful outcome will set it apart from other drugs because it would eliminate the source of the cancerous cells, thus there should be no relapses. But of course what works in a laboratory frequently doesn't work in the real world.
"This is a molecule that has never been introduced in a patient before," said Jordan, painfully aware that even discussing his research could lead to heartbreak for thousands of leukemia patients and their families.
So the first step is to ensure that the treatment does no harm. The patients that are awaiting the phase one trial have already been treated with virtually every cancer drug that's available, and all of them failed. They are hanging on mostly to hope. Phase one will begin by the end of this year, and could be completed in about six months.
"But if you say six months to one of these patients they think it's an eternity," Jordan said.
The initial trial will take place in England under the direction of a British colleague of Jordan's who has already been approved to test the drug for safety. If the drug's successful there, Jordan expects numerous trials to begin almost immediately in the United States.
Because the drug is designed to attack cancerous stem cells, it's possible it will be useful in the treatment of various cancers, including breast and prostate, but at this point that's very uncertain.
But if it works on any of those, it will signal a turning point in the fight against one of the most dreaded diseases on the planet. Unfortunately, that's a very big if.
Lee Dye is a former science writer for the Los Angeles Times. He now lives in Juneau, Alaska.