FW: CF NEWS FROM AROUND THE WORLD

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CF NEWS FROM AROUND THE WORLD

CF News From Around the World

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Newsday (New York)

October 28, 2003 Tuesday NASSAU AND SUFFOLK EDITION

HEADLINE: Antibiotic May Control, Not Cure Cystic Fibrosis

BYLINE: By Delthia Ricks. STAFF WRITER

   An old-line antibiotic used for years against common infections may

have the remarkable ability to correct a genetic flaw in cystic

fibrosis, a finding that ultimately may lead to a new way of treating

the intractable genetic disease.

   Gentamicin, long a staple in the fight against bacteria, has the

unusual ability to override a major genetic defect in cystic fibrosis

and tweak DNA transcription involved in the entrance and exit of

chloride in cells.

   Just as a boss' memo must be transcribed for dispersal to workers,

something similar must occur in the transcription of messages from DNA,

the master text of life. Messages contained within DNA must be read and

then transcribed by the cellular stenographer, RNA, before a key protein

involved in proper chloride activity can be made.

   People with cystic fibrosis have specific DNA mutations, garbling

instructions for production of the protein that chaperones chloride

through channels.

   A study by Israeli researchers has shown that gentamicin corrects the

nonsense, allowing chloride to be escorted effortlessly in and out of

cells.

   The new work promises a way of controlling the disease, but probably

not curing it, doctors say. Moreover, the drug likely will be effective

only against the type of mutation predominantly seen among people of

Ashkenazi Jewish descent. Yet developing gentamicin as a therapy remains

years away.

    " The bottom line here is not to think of gentamicin as an

antibiotic, " said Dr. Durie, director of the Cystic Fibrosis

Center at the Hospital for Sick Children in Toronto. " Its role in this

study has nothing to do with [treating] infection. "

   Durie, an expert on cystic fibrosis who was not associated with the

experiments, said the discovery opens a window on research,

demonstrating that a well-known drug may have the power to influence

genes.

    " The idea behind this paper is that this concept can be used in other

genetic diseases, " he said.

   Poor chloride transport is a hallmark of cystic fibrosis. For years,

scientists have known that when chloride cannot pass freely through cell

membranes, the result can devastate physiologic function: the lungs,

digestion and, in males, fertility.

   People with cystic fibrosis have an array of symptoms, the most

serious of which is a viscous mucus in the lungs. Additionally, they are

consumed by persistent infections, coughing, wheezing and shortness of

breath. Mucus accumulation can provide a breeding ground for infections,

which can be deadly.

   The gentamicin discovery comes amid a flurry of developments in which

old antibiotics are being found to play new tricks.

   Researchers last year at Stony Brook University found that an altered

form of tetracycline could prevent the cascade of molecular events

leading to heart attacks. Dr. Lorne Golub of Stony Brook's dental school

began the studies more than two decades ago, stripping away

tetracycline's " side chains " - chemicals that give the drug its

antibacterial punch - and leaving behind a potent anti-inflammatory

medication.

   Golub, who named the stripped-down version Periostat in the 1980s as

a dental treatment, has found in recent studies that it helps prevent

blockage of blood vessels by plaque.

   The antibiotic minocycline is being tested against amyotrophic

lateral sclerosis, Lou Gehrig's disease. And scientists recently

announced that clioquinoline, an antibiotic lastused in the 1970s, is

being resurrected for tests in people with Alzheimer's disease.

   Testing gentamicin against cystic fibrosis, Durie said, is a sharp

departure from the gene therapy approach, which captured scientific

imagination in the 1980s and is still being pursued, though so far

without a cure. The process involves inserting a copy of " a good gene "

with correct chloride transport information into patients' cells.

   But if further study supports the gentamicin findings, the answer to

other, rarer DNA miscodes in cystic fibrosis already may be on pharmacy

shelves.

   The gentamicin discovery came from the work of Dr. Wilchanski

of Shaare Zedek Medical Center in Jerusalem, who studied 19 children

with well-defined miscues in a gene dubbed CFTR. He reported in a recent

issue of The New England Journal of Medicine that administering the

antibiotic as nose drops

- two drops given three times daily for 14 days - corrected the genetic

flaw, but only in cells lining nasal tissue.

   Scientists did not administer enough medication to reach the

children's lungs or to have an impact on symptoms. Their next step is to

test gentamicin's ability to affect pulmonary function.

   About 1,000 different types of CFTR miscues have been identified. The

type defined by Wilchanski, called a " stop mutation, " affects a majority

of people with cystic fibrosis in Israel. In the United States, about 5

percent of people, many of Ashkenazi descent, have the mutation. Another

type, known as delta-508, is more commonly diagnosed in the United

States, Europe and Canada.

   Regardless of the mutation, disease manifestations are the same.

   Israeli scientists counted three " nonsense codes " as culprits in the

" stop mutation. " Nonsense coding is estimated to occur in 60 percent of

cystic fibrosis cases in Ashkenazi Jews.

   Cystic fibrosis occurs mostly in whites and strikes one in every

3,200 live Caucasian births in this country, and 1,000 new cases are

diagnosed annually, according to statistics from the Cystic Fibrosis

Foundation. An estimated 30,000 children and adults in the United States

are afflicted and have an average life expectancy of 33.4 years.

    " This is a very important proof of principle, " Dr. Beall,

president of the foundation in Bethesda, Md., said of Wilchanski's work.

" There is still a long way to go, " he added, to show that gentamicin can

correct the anomaly in the lungs.

   Beall said other disorders, such as Duchenne's muscular dystrophy and

Hurler 's syndrome, also may respond to correction by a member of the

antibiotic family to which gentamicin belongs: aminoglycosides. Other

members include streptomycin, neomycin, kanamycin and clindamycin.

   Despite excitement over gentamicin, Beall said researchers are also

pursuing " a number of small molecules in clinical trials " as well as

gene therapy.

    " Our goal is to try as many different approaches to tackle this

disease as possible, " he said.

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