|05-08-2002, 07:49 AM||#1|
Join Date: Jul 2001
Location: New Brunswick, NJ, USA
Leukemia gene therapy may be relevant for stem cell transplant therapy
Although this is an older article, this report of a gene therapy for leukemia has some ramifications for spinal cord injury. Let me explain. The p53 gene apparently plays a major role in preventing cancer, allowing the body's immune system to detect and destroy cells with altered genes. Apparently, there is another gene called the ATM gene that helps this process, perhaps by antigen presentation. An abnormal ATM gene "knocks down" the efficacy of the p53 gene. This gene may be used in the opposite way envisioned for leukemia research, i.e. preventing detection and rejection of transplanted cells.
Wednesday, 27 March, 2002, 13:31 GMT
Gene offers leukaemia hope
A rogue gene has been indentified
The discovery of a genetic mistake associated with the most common form of leukaemia in the western world could significantly advance efforts to combat the disease.
Scientists from the Leukaemia Research Fund have identified the error in cases of chronic lymphocytic leukaemia (CLL).
These findings should prove to be a key weapon in treating this form of leukaemia
Dr David Grant More than 2,500 new cases of the disease are recorded each year in Britain.
It has been known for many years that a gene called p53 plays an important role in the majority of human cancers including CLL.
The gene helps to protect the body from cancer by keeping its genetic material healthy.
It ensures that cells that have damaged or altered genes are destroyed if they cannot be repaired.
Damage to this gene is therefore implicated in a number of cancers.
The LRF scientists have now found for the first time that damage to another gene - dubbed ATM - can have a knock-on effect on the p53 gene.
A healthy ATM gene plays a key role in helping the body to detect unwanted damage to DNA.
this mutant gene can deactivate the 'cell destruct' button
Dr Tanya Stankovic But a defective ATM gene can interfere with p53 thereby allowing potentially cancerous cells to multiply.
Dr Tanya Stankovic, from the University of Birmingham, said: "It is almost as if this mutant gene can deactivate the 'cell destruct' button, allowing the rogue cells to multiply.
"It is well known that p53's protein helps protect us from cancer but this is the first time that scientists have shown that another gene can have a knock on effect on p53 function in tumour cells."
The researchers found that around 20% of CLL tumours had a faulty ATM gene, and another 10-15% had an abnormality in the p53 gene.
Scientists believe that patients with this mutant ATM gene may have a more aggressive form of CLL which is more difficult to treat with conventional drugs.
Dr David Grant, Scientific Director of the Leukaemia Research Fund, said: "These findings should prove to be a key weapon in treating this form of leukaemia.
"It is vital that we pick out patients with a poor prognosis at an early stage so we can give