[mage lang=”en|es|fr|en” source=”flickr”]telomerase structure function[/mage]
What are scientists still unsure about in regards to telomerase?
I’ve heard that there has been a lot of development in terms of producing drugs that can decrease the amount of telomerase in cancer cells but what are they still unsure about?
Before a cell can divide, the DNA of the chromosomes must duplicate itself. DNA is built up of molecular units called nucleotides, which come in four types abbreviated as A, C, G, and T. Although most of the DNA consists of long complex nucleotide sequences that hold the genetic code, the telomere sections have much simpler sequences repeated many times. The telomere sections have no known function in the genetic code. Each process of duplication results in the loss of a small section of the DNA. The telomere acts as a sort of sacrificial lamb; by losing part of its length, the essential DNA sequences are retained.
Telomerase is normally active only when it is important for cells to continue multiplying, such as during embryonic development. After birth, telomerase becomes inactive, except for the production of sperm cells in the male. However, telomerase activity has been found in up to 90% of all cancers, and has shown promise as a diagnostic tool. In certain cancers, increased activity levels may identify patients that have either favorable or unfavorable prognostic outcomes; while in other cases can distinguish between benign and malignant tumors.
The medical establishment received the report on the relationship between telomerase and cancer with great enthusiasm. Researchers foresaw the development of telomerase inhibitors as new and unique weapons against cancer. After all, if the telomerase in cancer cells could be disactivated, the cancer cells would stop dividing and die after a period like normal cells. Since then, reality has set in, and some unique problems in the development of telomerase inhibitors as therapeutic agents have become apparent.
It appears that telomerase does not become active until the telomeres reach a certain critical minimum size after around 20-30 cell divisions when the cell is approaching the senescence stage. How does this relate to cancer? It may mean that it would not work on very small tumors, and only with patients with more advanced tumors. In addition, some cancers seem to circumvent the need for telomerase. They are able to protect their chromosomes by other means.
Interestingly, work reported last year by the Harvard Medical School indicated that in mice at least, a lack of telomerase can also lead to cancer. The researchers provided an explanation. If the chromosomes of normal cells are deprived of their protective telomere tips, they might break, fuse, or undergo other changes leading to a loss or gain of genes. This, of course, is a hallmark of cancer.
In spite of these reservations, research activity in the area of telomerase inhibitors remains intense, and clinical trials should begin soon. In order to be useful, it is first necessary to demonstrate that a particular cancer gives rise to telomerase activity. In this instance, not only does telomerase activity represent a good diagnostic tool, but could present a very specific target for an anticancer drug. This specificity should make it less toxic than the usual chemotherapeutic drugs, since it would not effect normal cells. Although telomerase inhibitors may not prove to be magic bullets against cancer, they promise to be valuable additions to cancer treatment
[mage lang=”en|es|fr|en” source=”flickr”]telomerase rejuvenation[/mage]
Dr. Aubrey de Grey on Alex Jones’ Infowars 1/3