Telomeres Rule

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Fishermangents
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Joined: Thu Dec 03, 2015 3:39 pm

Telomeres Rule

Post by Fishermangents » Thu Dec 17, 2015 2:43 pm

Interesting article about telomeres, telomerase, cancer and imetelstat.

Some quotes:
'Telomerase balances the telomere shortening that occurs during cell division by adding telomere repeats onto chromosome ends. While the enzyme exists at very low or undetectable levels in normal somatic cells, it is continuously expressed in 80-95 % of tumors, acting to continuously elongate telomeres and conferring a sort of immortality on the rapidly dividing cells.'

'Because of its pivotal role in aging and cancer, the enzyme telomerase has nonetheless become the focus of drug development efforts for anticancer therapeutics, the goal being inhibition of telomerase, leading to a decrease of telomere length, resulting in cell senescence and apoptosis in telomerase-positive tumors.'

'Geron’s Imetelstat, a lipid-conjugated 13-mer oligonucleotide sequence complementary to the RNA template of the telomerase, directly inhibits the enzyme’s activity. Geron has partnered with Janssen Biotech to develop and commercialize Imetelstat worldwide for all indications in oncology, including hematologic myeloid malignancies, and all other human therapeutic uses. Under the collaboration agreement, Janssen is responsible for the development, manufacturing, and commercialization of Imetelstat worldwide. On September 16, 2015, Geron announced the dosing of the first patient in a Phase II trial to evaluate Imetelstat in patients with myelofibrosis.
In a recently published New England Journal of Medicine paper by Gabriela M. Baerlocher, M.D. and colleagues, it was reported that Imetelstat showed disease-modifying activity in Phase II studies of myelofibrosis and essential thrombocythemia. Among thrombocythemia patients, patients achieved a hematologic response, with the majority achieving a hematologic complete response.
In the second paper authored by Ayalew Tefferi, M.D., et al., the investigators found that Imetelstat was active in patients with myelofibrosis but also had the potential to cause clinically significant myelosuppression.'

Full article:
http://www.genengnews.com/insight-and-i ... /77900583/
Genetic Engineering & Biotechnology News, 16 Dec 2015

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