Subject:  (Fist) The ATM gene, BBC leukemia report (fwd)
Date:     Sun, 3 Jan 1999 052722 -0600 (CST)
From:     "Roy L. Beavers" <rbeavers@llion.org>
To:       emfguru <rbeavers@llion.org>
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---------- Forwarded message ----------
Date: Sun, 03 Jan 1999 15:32:53 +1100
From: Stewart Fist 
To: Roy Beavers 
Subject: BBC leukemia report

Roy, this is of interest mainly because of the information that the ATM gene
appears to be associated with special sensitivity of some people to
radiation, and is also closely involved in apoptosis.

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Saturday, January 2, 1999 Published at 10:31 GMT 

BBC News -- Health

Leukaemia could run in families 

 A faulty gene may cause a common form of the disease leukaemia, scientists
have discovered. Previously it was thought that cases of this blood cancer
were "one-offs" but scientists from the Cancer Research Campaign now think
the disease has an hereditary link and could run in families.

 Research, published in the medical journal The Lancet, shows that almost
20% of sufferers of chronic lymphocytic leukaemia (CLL) could have a mutated
version of the gene known as ATM. Of these one in three may have inherited
the fault.

 Lead researcher Malcolm Taylor said: "We have suspected for some time that
a number of patients with this type of leukaemia could be carriers of a
faulty gene. "But the fact that we have been able to isolate the specific
gene and show that it could run in families is certainly a major scientific
step forward."

 Professor Taylor said the discovery should help scientists develop new ways
to repair the defective gene and to stop the onset of CLL.

 CLL is the most common type of leukaemia with 90% of cases affecting people
over the age of 50. The disease can weaken the immune system and leave
sufferers susceptible to other serious infections. But in most cases CLL is
not immediately life-threatening and its progression can be effectively
controlled by drugs for many years.

 Professor Taylor's team believe, however, that problems with the ATM gene
could be responsible for a more aggressive form of the disease.

 Genes - which contain the blueprint of life - come in pairs and if people
are born with one copy damaged, they are more likely to develop cancer if
exposed to other cancer-causing agents. The body has an in-built
"safety-device" which tells damaged cells to "commit suicide" before they
have a chance to grow into a potentially fatal tumour. The ATM gene is
believed to be involved in this process.

 If the gene is "switched off" it cannot instruct cells to die and,
therefore, cancerous cells are able to continue to multiply out of control.

 The new research showed that in 40% of cases the function of ATM was
reduced, and in 15% of cases it was not working at all. This meant that the
suicide response could not be triggered in rogue cells.

 Professor Taylor's team also found that some patients carried the ATM
mutation in all their body cells, not just those in the tumour. This
indicates that the mutation has been passed down genetically from their
parents.

 Professor Taylor said not only would the discovery pave the way for
research into repairing the rogue gene, it would also have implications for
the way in which some leukaemia sufferers are treated with current
chemotherapy and radiotherapy techniques. It is already known that sufferers
of the rare genetic disorder Ataxia Telegiectasia - in which both copies of
the ATM gene are inactive - are unusually sensitive to radiation.

 This sensitivity could be exploited to treat leukaemia sufferers, or it
might mean that standard doses of radiation could be dangerous.

 Professor Gordon McVie, director general of the Cancer Research Campaign,
said: "These findings are extremely exciting because they are taking us yet
another step closer to finding out what causes cancer. "The research is also
particularly significant because we already know the ATM gene is implicated
in some patients with breast cancer and is related to abnormal reactions to
radiation."

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               Stewart Fist - Independent writer and columnist
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                    Ph: +612 9416 7458  Fax: +612 9416 4582
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Reprinted with permission of Roy Beavers, http://www.feb.se/EMF-L/EMF-L.html