His group developed a cell-free system to reconstitute functional model telomeres using synthetic DNA, and studied the mechanism by which telomeres normally stabilize chromosomes and how shortening of the telomeres could cause instability.
Dr. Langmore’s group used new enzymatic assays to determine the structure of telomere DNA in normal and abnormal cells grown in vivo and in vitro, in order to address specific hypotheses about the role of telomeres in aging and cancer.
The telomere hypothesis of aging postulates that as the telomeres naturally shorten during the lifetime of an individual, a signal or set of signals is given to the cells to cause the cells to cease growing.
Dr. Langmore: The telomere hypothesis of cancer is that the function of telomere shortening is to cause cells that have lost normal control over growth to senesce before being able to replicate enough times to become a tumor, thus decreasing the frequency of cancer.
Therefore an individual might have on average long telomeres; but, he might have one chromosome with a very short telomere that could affect cell growth.
“The expression of the enzyme telomerase maintains stable telomere length. Telomerase is not detected in normal cells and telomeres shorten and then the cells stop dividing and enter a phase called cellular senescence.”
“Essentially, we combined the tumor cells containing experimentally elongated telomeres with normal cells and extended the life span of those cell hybrids compared to similar hybrids using cells without experimentally elongated telomeres.”