The TERT promoter mutation does not generate enough telomerase to immortalize the pre-cancerous cells, but does delay normal cellular aging, Hockemeyer said, allowing more time for additional changes that
turns telomerase up.
Hockemeyer and his UC Berkeley colleagues, in collaboration with dermatopathologist Boris Bastian and his colleagues at UCSF, found that immortalization is a two - step process, driven initially by a mutation that
turns telomerase on, but at a very low level.
Learning how to control these switches could allow researchers to
turn telomerase activity up in aging cells or down in cancer cells.
Not exact matches
Mariela Jaskelioff and her colleagues at the Dana Farber Cancer Institute in Boston, Massachusetts, engineered mice with short telomeres and inactive
telomerase to see what would happen when they
turned the enzyme back on.
An estimated 90 percent of all malignant tumors use
telomerase to achieve immortality, and various proposed cancer therapies focus on
turning down the production of
telomerase in tumors.
According to the new theory, the telomeres are short in precancerous cells because
telomerase is
turned on just enough to maintain but not lengthen the telomeres.
New experiments by UC Berkeley and UCSF researchers suggest that immortalization of skin cells, which is essential to
turning them cancerous, is a two - step process: a mutation in nevus cells slightly raises levels of
telomerase, which keep the cells alive long enough for a second change, still unknown, that up - regulates
telomerase to make the cells immortal and malignant.
If cells fail to
turn up
telomerase, they also fail to immortalize, and eventually die from short telomeres because chromosomes stick together and then shatter when the cell divides.
As with all of our other genes, the DNA that encodes the
telomerase enzyme is present in all of our cells — but because it's needed only after quite a few cell divisions have occurred, it's not needed in most cells for most or all of the time, so it's
turned off.
Sometimes
telomerase is a good guy because it helps produce immune cells and stops telomeres from shortening, but it can also make cells immortal, which prompts them to
turn malignant.
So we did this jujitsu where you
turn the power of
telomerase against the cancer cells, and they committed suicide.
«I think the most effective point of intervention will
turn out to be
telomerase,» says Fossel.
Now two reports show that, with the help of an enzyme called
telomerase, human cells can divide forever in the laboratory without
turning cancerous.
«We now have 35 chemicals sitting in our lab that
turn on the
telomerase gene,» says CEO Bill Andrews.
Telomerase is
turned off in most human cells, but cancer cells often must reactivate it so that they can keep dividing like crazy.
Telomere shortening occurs in human cells because the enzyme
telomerase that adds DNA to the telomere is only active in few cell types, namely stem cells, and is
turned off in most other human cells.