Save on your Christmas Gifts and Help Leukemia Patients!

The Gap, Inc. is offering their Give and Get special again this month between Nov 12th and 15th.  You get 30% off your purchase at the Gap, Banana Republic, or Old Navy AND they will give 5% of your purchase to the Leukemia and Lymphoma Society.  That's a win/win in my book!

Go to the website below for the coupon to use in store:
http://www.gapinc.com/giveandget/lls/
Please help us maximize this gift by passing this message along to everyone you know!

Another Great Athlete affected by Leukemia

Today, Kareen Abdul-Jabbar announced that he has been diagnosed with CML.  As I read the article on CNN, I was very pleased to see that he is working with Novartis (manufacturer of Gleevec and Tasigna) to launch an educational program focused on getting treatment and following your treatment plan.  We had also learned that many cancer patients do not take their medication as prescribed, which leads to lower success in treating the disease.

While I'm sad for Mr. Abdul-Jabbar to have to face this diagnosis, I'm pleased to see that he has chosed to get out there educating others about Leukemia and I look forward to seeing the good works he is able to accomplish.

The Birth of a Miracle

If you have ever wondered how a wonder drug like Gleevec gets developed, here is more ifnormation from one of the oncologists behind that drug.  This article made me think about the trial that Hans is entering for Ariad and the impact it may have on the future of CML treatment.

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November 3, 2009
A Conversation With Brian J. Druker, M.D.
Researcher Behind the Drug Gleevec
By CLAUDIA DREIFUS

Dr. Brian J. Druker, 54, an oncologist at Oregon Health and Sciences University and a Howard Hughes Medical Investigator, is one of three winners this year of the Lasker-DeBakey Clinical Medical Research Award, often called the “American Nobel Prize.” Dr. Druker shared the honor with Nicholas B. Lydon, a former researcher for Novartis, and Charles L. Sawyers of Memorial Sloan-Kettering Cancer Center, “for the development of molecularly targeted treatments for chronic myeloid leukemia, converting a fatal cancer into a manageable chronic condition.” Here is an edited version of a conversation that took place last month in New York:

Q. WHAT WAS LIFE LIKE FOR PEOPLE WITH CHRONIC MYELOID LEUKEMIA, OR C.M.L., PRIOR TO YOUR RESEARCH?
A. Life was pretty miserable. If you were over 40, the main therapy was interferon, which prolonged life for maybe a year in perhaps 20 to 30 percent of patients. Interferon made the patients feel awful — like the worst flu. The only other hope was a bone-marrow transplant for younger patients. The problem there was that the death rate in the first year was 25 to 50 percent.
C.M.L. patients were always difficult to see because both of us knew that the clock was ticking and there was virtually nothing that we could do about it.



Q. It must have been depressing to be an oncologist under those circumstances.
A. When I started my training in the 1980s, you rarely cured people. You felt, “if I can give my patient extra time, I’ve been successful.” But I could see there was a transformation of cancer treatment on the horizon thanks to breakthroughs in biochemistry and genomics. I wanted to be part of that, which is why I was a physician-researcher.
The way I’d been trained, cancer was seen as something like a light switch that was stuck in an “on” position. You were given a baseball bat, which was chemotherapy, and told to knock the light out with the bat. I thought, “Why don’t we just try to figure out why the light is stuck on, then we can fix it without breaking everything.”
So I started my laboratory career studying the regulation of cell growth — what turns the switch on, what helps it shut down. And that’s how Gleevec is different from earlier chemotherapies, which basically poisoned every cell in the body in an attempt to kill the cancer. Gleevec turned off the light switch and only killed the cancer cells.



Q. How did the idea behind Gleevec first come up?
A. By the late 1980s, C.M.L., though rare, was a cancer that scientists knew a lot about. We knew, for instance that a chromosomal abnormality existed in every C.M.L. patient. We knew that this abnormality created an enzyme that caused the uncontrolled growth of cancer cells. If you put this enzyme into animals, they got leukemia.
So in 1988, Nick Lydon, who led a drug discovery group at a pharmaceutical company that eventually became Novartis, came to talk to me. He was interested in developing drugs to block a family of cellular enzymes implicated in several cancers. I said to him: “If you want to develop targeted chemotherapies, C.M.L. is the disease to study. We know the most about it — and, if we can figure out a way to block this enzyme, we can turn off the cancer switch.”
So in Nick’s lab at the pharmaceutical company, he began screening for agents that worked on C.M.L. He’d send me his best compounds. I found one, STI571, that was better than the others; it would kill every C.M.L. cell in a petri dish. By 1995, STI571 was a lead compound set for clinical development.



Q. So Gleevec was on its way?
A. Not quite. Gleevec was a completely different class of drugs than what was used against cancer. Most researchers thought it wouldn’t work. Then, in 1996, before we were about to go to trials, Nick’s company merged with another, and he left. Gleevec was now caught in the changeover. I lobbied with the new executives. After some ambivalence, they agreed to go forward with Phase 1 trials. I think they felt it wouldn’t work and they could get rid of us afterwards.
But during clinical trials we saw this miracle: Once the patients were up to effective doses, we got a 100 percent response rate.



Q. Had that ever happened before in a clinical trial?
A. No. Never. You’d see patients where interferon wasn’t working, and they’d been issued a death sentence. Suddenly, all their hopes for the future were restored, and, with minimal side effects! This was around 1999, and the Internet chat rooms were just beginning. Patients in the trials began talking to each other like they’d never done before. I’d see a patient, and I’d read about it on the Internet that night: “few side effects,” “100 percent response.” Patients would come to me and say, “My doctor has never heard of this drug.” I’d never written it up. I hadn’t presented the data. Their doctors thought I was a charlatan. For a lot of people, Gleevec was simply too good to be true. But these once-dying patients were getting out of bed, dancing, going hiking, doing yoga. The drug was amazing.
Now the drug company had to make another decision. They hadn’t made enough drugs for a large-scale Phase 2 trial. But patients knew about Gleevec, and many more wanted to be included in the trials. Through the Internet, they generated a petition that landed on the C.E.O.’s desk, asking for greater access. That’s how Phase 2 was rapidly expanded.



Q. YOUR FRIEND AVICE MEEHAN OF THE HOWARD HUGHES MEDICAL INSTITUTE SAYS THAT YOU HAVE THE MOST AMAZING PERSEVERANCE. IS THAT WHAT IT TOOK TO MAKE GLEEVEC HAPPEN?
A. I think I’m more perseverance than smarts. There’s a basketball player who says, “Hard work beats talent when talent doesn’t work hard.” Well, I work hard. I understood that this project was too good to give up on. My patients needed me to do something to help them. I did everything I could by getting them a drug I thought would work.
When the drug looked like it was finally going to be approved, I was interviewed by a reporter from People magazine, Alexandra Hardy. She asked, “Who are your good friends?” I said: “I don’t have any. I work, eat, sleep, go to the gym.” She said: “You’re pathetic. You’ve got no balance in your life.”
Well, there is now. Alexandra and I got married, and we have three wonderful children.


Q. Gleevec was ultimately proved effective against two cancers, right?
A. Ten. It’s now F.D.A.-approved for 10. Gleevec went to market for a small disease, 50,000 patients, and it later got tested for other things. It’s now used by 200,000 patients worldwide.


Q. Do you see any of that?
A. I don’t see a penny, though that never was an issue for me. When I obtained the compound, it was already patented. I wasn’t going to get to test it if I tried to put my mark on it. I wanted to work on it because I thought it was going to be the way to treat C.M.L.



You know, my patients were people who’d been told “to get their affairs in order” because they were going die soon. And now some of them play with grandchildren they’d thought they’d never live to see. That’s worth more than money.

Hans update

For those of you who are also following the story of our friend Hans, he is beginning a clinical trial for a new drug created by Ariad.  I believe this is a Phase 1 trial, meaning it is at the very early stages of testing the drug, but it has shown a very good response for CML patients who are resistant to Gleevec and Sprycel.  Even more importantly, it is one of the first drugs to have an impact on the T315I mutation of leukemia.  Hans's most recent mutation testing showed that he has that mututation, so continuing with Gleevec or Sprycel doesn't really make sense.

He will have to travel to Portland for some of his treatment, but thankfully it is not further away.

Tyler and I would ask that our friends join us in praying for Hans to receive successful treatment.  The trial certainly looks like a promising option, but a little extra help is always worthwhile!

Old Guys Rule

Tyler celebrated his 43rd birthday yesterday, although he insists it is the first of many.  He's actually planning to celebrate his Dad's birthday (in honor of his donated marrow) and his transplant date as birthdays as well.  I'm thinking that I might go broke with that many birthdays, but Tyler certainly deserves some fun this year.

Actually, he decided to spend his day golfing with his brother (a round of golf is an outstanding gift idea for Tyler!) and then we had a movie night. Tyler had chosen some classic movies to watch for his birthday, so we enjoyed The Way We Were (although a week early because it arrived before his birthday and he didn't want to wait), Fast Times at Ridgemont High, and Monty Python's Search for the Holy Grail.

Although we had to interrupt the movies for trick or treaters, we really enjoyed a chance to get back to one of our favorite things.  One of our very first dates was a movie night, so we always enjoy a chance to relive that!

Happy Halloween!