A new research study published in the January issue of Cancer Cell provides exciting new information about how to boost the effectiveness of a promising cancer treatment that targets telomeres in an attempt to interfere with the ability of a cancer cell to continuously divide.
Telomeres are DNA sequences found at the ends of chromosomes that play a key role in controlling the life span of cells. With every cell division, telomeres get a bit shorter until eventually they become so short that the enzymes that copy DNA for cell division no longer work properly and the cell stops dividing. In a sense, telomeres function as a kind of counting mechanism that regulates how many times a cell can divide.
In contrast to normal cells, cancer cells divide continuously and uncontrollably. Scientists know that cancer cells produce an enzyme, called telomerase, which prevents telomeres from getting too short so cells can keep dividing. Telomerase is not used by healthy cells, and has been identified as a logical target for anticancer therapeutics. However, recent studies indicate that for this therapy to be effective, telomeres must be in a critically short state, requiring an extended treatment duration that can lead to drug resistance and other problems.
Heidi Hardman | EurekAlert!
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