modified messenger RNA I believe this wording has been used in some of herons patents
Messenger RNA hangs around long enough to add about a thousand nucleotides and then dissipates
Stanford Medicine News Center,
very interesting article sounds like gern IP
I always appreciate your knowledgable insights thanks
ITS GOING TO BE EXTREMELY IMPORTANT what other cancer drug do you know of that attacks cancer cells on so many different levels
The big question in my mind, could targeting homologous recombination and telomerase also be effective in other Adenocarcinomas such as nsclc lung cancer, prostate cancer ,Pancreatic cancer, Esophageal cancer and Colorectal cancer. Remember ( MASSIVE TELOMERE ATTRITION)
BAC cells. Telomerase inhibitor prevents telomere elongation but induces RAD51/HR, which contributes to telomere maintenance/stabilization and prevention of apoptosis, reducing the efficacy of treatment. Combining HR inhibition with telomerase renders telomeres more vulnerable to degradation and significantly increases/expedites their attrition, leading to apoptosis. We therefore demonstrate that a therapy targeting HR and telomerase has the potential to prevent both tumor growth and genomic evolution in BAC.
Targeting homologous recombination and telomerase in Barrett's adenocarcinoma: impact on telomere maintenance, genomic instability and tumor growth.
Oncogene 2014 Mar 22;33(12):1495-505. Epub 2013 Apr 22.
R Lu, J Pal, L Buon, P Nanjappa, J Shi, M Fulciniti, Y-T Tai, L Guo, M Yu, S Gryaznov, N C Munshi, M A Shammas
Homologous recombination (HR), a mechanism to accurately repair DNA in normal cells, is deregulated in cancer. Elevated/deregulated HR is implicated in genomic instability and telomere maintenance, which are critical lifelines of cancer cells. We have previously shown that HR activity is elevated and significantly contributes to genomic instability in Barrett's esophageal adenocarcinoma (BAC). The purpose of this study was to evaluate therapeutic potential of HR inhibition, alone and in combination with telomerase inhibition, in BAC. We demonstrate that telomerase inhibition in BAC cells increases HR activity, RAD51 expression, and association of RAD51 to telomeres. Suppression of HR leads to shorter telomeres as well as markedly reduced genomic instability in BAC cells over time. Combination of HR suppression (whether transgenic or chemical) with telomerase inhibition, causes a significant increase in telomere attrition and apoptotic death in all BAC cell lines tested, relative to either treatment alone. A subset of treated cells also stain positive for β-galactosidase, indicating senescence. The combined treatment is also associated with decline in S-phase and a strong G2/M arrest, indicating massive telomere attrition. In a subcutaneous tumor model, the combined treatment resulted in the smallest tumors, which were even smaller (P=0.001) than those that resulted from either treatment alone. Even the tumors removed from these mice had significantly reduced telomeres and evidence of apoptosis. We therefore conclude that although telomeres are elongated by telomerase, elevated RAD51/HR assist in their maintenance/stabilization in
Telomerase contributes to fludarabine resistance in primary human leukemic lymphocytes( abstract)
We report that Imetelstat, a telomerase inhibitor that binds to the RNA component of telomerase (hTR), can sensitize primary CLL lymphocytes to fludarabine in vitro. This effect was observed in lymphocytes from clinically resistant cases and with cytogenetic abnormalities associated with bad prognosis. Imetelstat mediated-sensitization to fludarabine was not associated with telomerase activity, but with the basal expression of Ku80. Since both Imetelstat and Ku80 bind hTR, we assessed 1) if Ku80 and Imetelstat alter each other's binding to hTR in vitro and 2) the effect of an oligonucleotide complementary to the Ku binding site in hTR (Ku oligo) on the survival of primary CLL lymphocytes exposed to fludarabine. We show that Imetelstat interferes with the binding of Ku70/80 (Ku) to hTR and that the Ku oligo can sensitize CLL lymphocytes to FLU. Our results suggest that Ku binding to hTR may contribute to fludarabine resistance in CLL lmphocytes. This is the first report highlighting the potentially broad effectiveness of Imetelstat in CLL, and the potential biological and clinical implications of a functional interaction between Ku and hTR in primary human cancer cells.
Not sure but the article I was reading indicated it was issued but the time period was very short so I think there is a very good possibility that it is just an application
issued March 26,2015
The problem(as i see it) is that many cells especially the bodies own non cancerous stem cells also are telomerase positive at times. I believe that this approach would have a tendency to destroy a large portion of these cells and other cells that are telomerase positive in the body. I think these researchers know that this is not a viable approach but that is only an opinion