A study at Washington University School of Medicine in St. Louis may aid efforts to tailor smoking-cessation treatments to cigarette smokers, based on their DNA. The researchers are recruiting 720 smokers from the St. Louis area who want to kick the habit. Study participants will provide DNA samples, from saliva, that will be analyzed to identify genetic variations that influence smoking behavior, lung cancer risk and the effectiveness of smoking-cessation treatments.
SMOKING IS LINKED TO CANCER AND TO CHRONIC OBSTRUCTIVE PULMONARY DISEASE. RESEARCH HAS SHOWN THAT IT SHORTENS A PERSONS LIFESPAN BY ABOUT 12 YEARS. BUT STILL, MANY PEOPLE SMOKE, AND ITS VERY DIFFICULT TO QUIT. SO RESEARCHERS AT WASHINGTON UNIVERSITY SCHOOL OF MEDICINE IN ST. LOUIS ARE AIMING TO MATCH UP TREATMENTS WITH THE DNA OF INDIVIDUAL SMOKERS. THEYRE RECRUITING SMOKERS WHO WANT TO QUIT, AND THEY HOPE TO LEARN WHETHER ITS POSSIBLE TO MATCH SMOKERS WITH THERAPIES, BASED ON GENETIC INFORMATION. JIM DRYDEN REPORTS
MOST SMOKERS KNOW THE HABIT IS BAD FOR THEM AND WANT TO QUIT, BUT THAT DOESNT MEAN THEY CAN. WASHINGTON UNIVERSITY NICOTINE RESEARCHER LI-SHIUN CHEN SAYS MOST PEOPLE WHO TRY TO QUIT FAIL, AND SO HER RESEARCH GROUP HAS BEEN STUDYING DNA TO FIND WAYS TO IMPROVE THE ODDS FOR THOSE WHO WANT TO STOP SMOKING.
(act) :21 o/c evidence-based treatments
Quitting smoking is very hard. Most people who smoke have tried to
quit smoking multiple times throughout their life, and only about
5 percent succeed without the help of treatments. And even with
treatments, research shows that a persons genes effect how they
respond to medications. So our goal is to help people quit smoking
with evidence-based treatments.
CHEN SAYS PREVIOUS RESEARCH HAS SHOWN THAT SMOKERS WITH HIGH-RISK GENE VARIANTS ARE LIKELY TO SMOKE LONGER AND DEVELOP CANCER SOONER THAN THOSE WHO SMOKE BUT DONT HAVE THOSE DNA VARIATIONS.
(act) :16 o/c low-risk genotypes
People with the high-risk genetic markers, they are less likely
to quit on their own. They would have a delayed quitting by four
years, and they will have lung cancer, actually, four years earlier,
compared to those with the low-risk genotypes.
THE GOOD NEWS, SHE SAYS, IS PEOPLE WITH THE HIGH-RISK GENETIC MARKERS ALSO SEEM MORE LIKELY TO BENEFIT FROM NICOTINE-REPLACEMENT THERAPY.
(act) :17 o/c only counseling
The same group of people, with the high-risk genetic markers, is
more likely to respond to medication, and medications dont help
everyone equally. It is possible that different smokers would need
different medications, or even some smokers require only counseling.
SO THE WASHINGTON UNIVERSITY RESEARCHERS ARE DIVIDING UP SMOKERS TRYING TO QUIT INTO 3 GROUPS: ONE GROUP WILL GET COUNSELING AND NICOTINE REPLACEMENT PATCHES AND LOZENGES; A SECOND WILL RECEIVE THE DRUG VARENICLINE, ALSO CALLED CHANTIX, PLUS COUNSELING; AND THE REST WILL GET 7 WEEKS OF COUNSELING BUT WONT GET ANY DRUGS. CHEN SAYS BY COMPARING OUTCOMES AND LOOKING AT DNA, THIS STUDY COULD MAKE IT POSSIBLE TO TAILOR THERAPIES TO SMOKERS.
(act) :11 o/c genetic markers
Our goal is to match people up with the medication that is most
likely to help them and least likely to give them any side effects,
so we are going to look at multiple genetic markers.
STUDY PARTICIPANTS WILL PROVIDE A SALIVA SAMPLE PRIOR TO THE START OF THE STUDY. THEN CHEN AND HER COLLEAGUES WILL LOOK AT HOW SUCCESSFUL STUDY SUBJECTS ARE AT QUITTING AND LOOK FURTHER AT HOW THEIR GENETIC MARKERS WORK TOGETHER WITH THE TREATMENTS. SHE SAYS HER GROUP IS RECRUITING MORE THAN 700 PEOPLE AGES 21 AND OLDER, AND SHE SAYS THAT ALTHOUGH SOME OLDER SMOKERS THINK IT MAY BE TOO LATE FOR THEM TO HELP THEMSELVES BY QUITTING, CHEN SAYS ITS NEVER TOO LATE, AND EVEN OLDER SMOKERS CAN ADD BACK YEARS TO THEIR LIVES IF THEY KICK THE HABIT NOW.
(act) :13 o/c quit smoking
It can delay, or eliminate lung cancer. Research has shown that
it can also delay COPD, the chronic obstructive pulmonary disease
(or emphysema). Its never too late to quit smoking.
CHEN SAYS EVERY SMOKER CAN BENEFIT SOMEHOW FROM QUITTING, AND SHE WANTS TO MAKE IT EASIER FOR THEM TO DO THAT. IM JIM DRYDEN