Details on how disrupting a pathway used by cancerous cells to
proliferate could be the key to inhibiting the growth and survival of
tumors.
"Identification of genetic markers that predict cancer
cell vulnerabilities and new drugs to exploit such vulnerabilities is a
focal point of cancer research today," says senior author Lee Zou,
associate scientific director of the Massachusetts General Hospital
(MGH) Cancer Center.
Cancer cells survive by avoiding the natural processes of aging and death that normal cells undergo.
In normal cells, repetitive DNA sequences called telomeres regulate
these processes. Telomeres are found at the end of chromosomes,
protecting them and ensuring that cells do not lose genetic information
when dividing.
Over time, telomeres erode and shorten. Once telomeres have been eroded
down to a critically short length, a signal is sent which tells the cell
to stop dividing, protecting the genetic information while
simultaneously cutting short the cell's lifespan.
The other pathway is referred to as the alternative lengthening of
telomeres (ALT) pathway. In this pathway, telomeres are lengthened via
recombination with DNA sequences from other chromosomes.
This new study represents the first time that a therapy has been identified specifically for treating the ALT pathway.
"Cancer cells must rely on either the telomerase enzyme or the ALT
pathway to bypass the normal processes of cell aging and death,"
explains Zou. "Our findings may provide a new direction for the
treatment of ALT-positive cancers, which include osteosarcoma,
glioblastoma and certain pancreatic tumors."
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