August 16, 2004 –
Ben Swann-KFOX Morning News Anchor/Reporter
It’s been 5-years since the cancer drug Gleevec was introduced in clinical trials to treat a Chronic Leukemia. Gleevec was so successful, that it received one of the fastest approvals ever for a cancer therapy. Now researchers are studying it’s application in other cancers.
You’d never know looking at him now that 4-years ago, Ken Geihsler was fighting for his life. He was diagnosed with chronic myelogenous leukemia, or CML. After six months on interferon, his disease was progressing and he was suffering side effects. All that changed when he entered a clinical trial at M. D. Anderson Cancer Center studying Gleevec.
Ken Geihsler-Patient: “I’ve been on the study four years. The results have been fantastic, as far as I’m concerned. I don’t even feel like I’m sick. In fact, people keep saying that there’s no way that you can absolutely have cancer or have leukemia the way you look, the way you act, the energy you have and all the activities you are involved in.”
Gleevec is what is known as a targeted therapy; in this case, a drug specifically designed to inhibit certain proteins involved in the development of CML.
Dr. Hagop Kantarjian-M. D. Anderson Cancer Center: “It’s like a magic bullet that removes the protein that causes the cancer cells to become cancer and to progress, and so by removing the feeding system or the protein, those cancer cells die, and the normal cells come back. So, in the past, we talked about an average survival in CML of 3 to 5 years. Now, we estimate that the average survival is going to be 15 years and that perhaps half of the patients will have complete elimination of the disease.”
The success of Gleevec in treating CML, demonstrated to researchers how effective targeted therapies can be in cancer treatment. The concept of targeted therapy is being studied in a wide range of cancers. Meanwhile, Ken whose 66-years-old, continues on Gleevec, with minimal side effects.
Ken Geihsler-Patient: “I certainly will not object to taking the Gleevec for the rest of my life.”
If you would like more medical news, visit our health partners websites:
M.D. Anderson Cancer Center:http://www.mdanderson.org/
The Mayo Clinic:http://www.medicaledge.org
Baylor College of Medicine:http://public.bcm.tmc.edu/
August 16, 2004 –
SAN JOSE, Calif. — Cancer researchers at Stanford University have identified a small population of cells in leukemia that seed the growth of the deadly cancer.
The discovery of the cells, called cancer stem cells, explains past failures in leukemia treatments and holds the promise of refocused therapies.
“We were missing the boat because we were targeting the wrong cell,” said researcher Catriona Jamieson, who wrote the study published in Thursday’s New England Journal of Medicine.
This finding adds to the growing understanding of cancer stem cells, thought to be pivotal to the disease.
Like embryonic stem cells, cancer stem cells have the ability to perpetuate themselves. But unlike embryonic stem cells, they produce only cancer — not healthy tissues.
The new Stanford study found the cancer stem cell behind a slow-growing form of leukemia called chronic myelogenous leukemia.
One of the strategies of current cancer treatment is to kill as many cells as possible. This new research suggests that the existing strategy may not work because it targets many cells — not just the cells that are driving the disease. Most treatments don’t cure this chronic form of leukemia although they do slow its progress.
The cancer stem cells work this way:
When a person is healthy, signals in the body tell it to produce new blood cells. These signals reach stem cells, which mature into various types of blood cells. When a person has leukemia, the genetic makeup of their stem cells is flawed. The signal to make new cells stays on constantly, so someone with leukemia produces more and more abnormal cells.
The cancer cells crowd out normal cells in the bone marrow, making people sick.
The institute’s next goal is to find out why there is a flaw in the genetic makeup of the cell, said Irving Weissman, director Stanford Institute for Cancer/Stem Cell Biology and Medicine. “Why does a normal cell mutate and gain the ability to self-renew?” he asked.
Additionally, the institute plans to broaden its research to include the study of other types of cancer stem cells. “We will spend the next few years looking at one cancer at a time,” he said.
A member of the National Ballet of Cuba practices before a rehearsal of ‘Cinderella,’ on the top floor of a century-old mansion housing Alicia Alonso’s company dance studio, in Havana