Local researchers yesterday revealed that they have discovered a gene that could lead to the development of alternative drugs to treat leukemia.
Most types of leukemia are characterized by an abnormal proliferation of immature blood cells in the bone marrow, many of which then spill into the bloodstream throughout the body, the National Science Council (NSC) told a press conference.
Though effective treatments already exist for some types of leukemia, such as Gleevec, which can help chronic myelogenous leukemia (CML) patients live as long as 15 years, their high price tags — costing at least NT$75,000 a month — become a financial burden for sufferers who have to take it throughout their lifetime.
Studies also show that about 20 percent of CML patients develop resistance to Gleevec.
To understand how the abnormal cells can be annihilated so that symptoms of leukemia can be alleviated, a council-sponsored research team looked into the chemical mechanism of Gleevec and discovered a gene that could lead to the development of alternative drugs.
“CML cells, like many other types of cancer cells, are anti-apoptosis [resistant to decay]. However, apoptosis is a natural stage of cell life cycle and should not be sidestepped,” said project leader Chang Zee-fen (張智芬), a professor at the National Taiwan University’s Institute of Biochemistry and Molecular Biology.
“We chose to study CML because although most types of leukemia are characterized by the growth and spillage of immature blood cells, the condition is especially severe in CML patients,” Chang said.
“If we can find a drug that produces the same effect as Gleevec, we may be able to find an alternative treatment,” she said.
CML is caused by a chromosomal translocation, where parts of the BCR gene on chromosome 22 become fused to the ABL gene on chromosome 9, forming a BCR-ABL gene product that is called a “Philadelphia chromosome,” which produces tyrosine kinase proteins, she said.
“What we found was when Gleevec suppresses the BCR-ABL kinase, a gene called Gfi-1B on chromosome 13 increases, which in turn suppresses Bcl-xL expression,” Chang said.
Since Bcl-xL is a protein responsible for a CML cell’s anti- apoptosis property, increasing Gfi-1B activity allows CML cells to die when they are supposed to, she said.
“In short, as long as we have a chemical that can raise Gfi-1B activity — not necessary by administering Gleevec — we can design synthetic lethality for the CML cells,” Chang said.
“It is very possible that a cheaper, existing drug can already perform such a function; this finding not only opens up possibilities for alternative treatments for CML patients, but can also be applied to treatment of all leukemia sufferers,” Chang said.
Further research should be conducted to find such drugs, she said.
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