From google pub health publication of june this year
Over 90% of cancer cells express telomerase, which is required for their survival. However, telomerase inhibitors alone have so far failed to provide any significant clinical benefit. Therefore, identifying and targeting genes that can enhance the effects of telomerase inhibitors will greatly benefit a large population of cancer patients. We find that simultaneous inhibition of p21 and telomerase synergistically suppresses tumor growth. We also show that our approach is useful for treating p53 mutant cancers, when used with therapies that restore the function of mutant p53. We anticipate that simultaneous targeting of p21 and telomerase will overcome the current limitation of single-agent telomerase therapeutics and provide an effective method to treat
cancers that rely on telomerase activity for survival.
I believe Gern is going to be extremely cautious going forward...after all those lawsuits .. came after them .. after the fact they did the secondary at 4 bucks and soon after the hold came... i truly believe that science is on our side.. and management had a major hiccup..but after that they learned their lesson and will be very meticulous about how they proceed so it doesn't occur again.. given us more time to buy at these low prices..
i cant find the link .. of any qs 21 in the vaccine so far.. but the association between gsk and agenus qs21 in vaccines is known... i would imagine Garo would of said something by now..
after approval from the FDA; volunteer testing in UK and Africa from September .. is qs21 in this ?
Ah sorry .. i only saw the snyder presentation ..didnt realize Mesa was the second one... my apologies.. yes... def not as positive..
I thought it was pretty positive on Imetelstat..don't understand why you think it wasnt..
that was dated aug 6 of 2014 Clear input
Acta Neuropathol. 2014 Aug 6. [Epub ahead of print]
Telomerase inhibition abolishes the tumorigenicity of pediatric ependymoma tumor-initiating cells.
found this when doing a search as you said.. " Telomerase inhibition abolishes the tumorigenicity of pediatric ependymoma tumor-initiating cells.
Barszczyk M1, Buczkowicz P, Castelo-Branco P, Mack SC, Ramaswamy V, Mangerel J, Agnihotri S, Remke M, Golbourn B, Pajovic S, Elizabeth C, Yu M, Luu B, Morrison A, Adamski J, Nethery-Brokx K, Li XN, Van Meter T, Dirks PB, Rutka JT, Taylor MD, Tabori U, Hawkins C.
Pediatric ependymomas are highly recurrent tumors resistant to conventional chemotherapy. Telomerase, a ribonucleoprotein critical in permitting limitless replication, has been found to be critically important for the maintenance of tumor-initiating cells (TICs). These TICs are chemoresistant, repopulate the tumor from which they are identified, and are drivers of recurrence in numerous cancers. In this study, telomerase enzymatic activity was directly measured and inhibited to assess the therapeutic potential of targeting telomerase. Telomerase repeat amplification protocol (TRAP) (n = 36) and C-circle assay/telomere FISH/ATRX staining (n = 76) were performed on primary ependymomas to determine the prevalence and prognostic potential of telomerase activity or alternative lengthening of telomeres (ALT) as telomere maintenance mechanisms, respectively. Imetelstat, a phase 2 telomerase inhibitor, was used to elucidate the effect of telomerase inhibition on proliferation and tumorigenicity in established cell lines (BXD-1425EPN, R254), a primary TIC line (E520) and xenograft models of pediatric ependymoma. Over 60 % of pediatric ependymomas were found to rely on telomerase activity to maintain telomeres, while no ependymomas showed evidence of ALT. Children with telomerase-active tumors had reduced 5-year progression-free survival (29 ± 11 vs 64 ± 18 %; p = 0.03) and overall survival (58 ± 12 vs 83 ± 15 %; p = 0.05) rates compared to those with tumors lacking telomerase activity. Imetelstat inhibited proliferation and self-renewal by shortening telomeres and inducing senescence in vitro. In vivo, Imetelstat significantly reduced subcutaneous xenograft growth by 40 % (p = 0.03) and completely abolished the tumorigenicity of pediatric ependymoma TICs in an orthotopic xenograft model. Telomerase inhibition represents a promising therapeutic approach for telomerase-active pediatric ependymomas found to characterize high-risk ependymomas.
dont see any news of this or reaction on asty board.?