Baker Brothers bought shares in Geron aft ASH ET data back in 2012 at $1.69 average. They recieved AST shares and BTX warrants from their Geron holdings.
His departure from BOD was put out and he is not leaving until May when a replacement is appointed to the BOD.
he always floats the reliable source statement and rumor has it statment with his false statements ment to scare people he is and aways will be a low life.
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irish good to see that everythin is well google Sergei Gryaznov: The Interview click the lower left corner on the pop up Gryaznov is the one who put the lipid backbone into GRN163 creating GRN163L Imetelstat. The interview is insightful.
To make sure they have early readout markers that are actionable for acceleration tward early approval. They want to insure the tial is designed so they can push for breakthrough designation and fas track.
They are going to start a multi center confirmatory phase 2 trial they have already had an exploratory single center phase 2 a 20% rate of PR or CR in an indicationthat no drug has had any PRs or CRs in. The numers you are quoting on percetages do not factor in 20% PR/CR rte for MF a 97% CR/PR rate for ET. CALR ET that takes 3 years to atain CRs with Interferon Alpha takes just 6 weeks on average to atain CRs. The phae 2 MF multicenter trial will start in June the single center phase 2 trial at Mayo is still running right now.
Cancer stem cells (CSCs) are thought to be responsible for tumor progression, metastasis, and recurrence. HER2 overexpression is associated with increased CSCs, which may explain the aggressive phenotype and increased likelihood of recurrence for HER2+ breast cancers. Telomerase is reactivated in tumor cells, including CSCs, but has limited activity in normal tissues, providing potential for telomerase inhibition in anti-cancer therapy. The purpose of this study was to investigate the effects of a telomerase antagonistic oligonucleotide, imetelstat (GRN163L), on CSC and non-CSC populations of HER2+ breast cancer cell lines. The effects of imetelstat on CSC populations of HER2+ breast cancer cells were measured by ALDH activity and CD44/24 expression by flow cytometry as well as mammosphere assays for functionality. Combination studies in vitro and in vivo were utilized to test for synergism between imetelstat and trastuzumab. Imetelstat inhibited telomerase activity in both subpopulations. Moreover, imetelstat alone and in combination with trastuzumab reduced the CSC fraction and inhibited CSC functional ability, as shown by decreased mammosphere counts and invasive potential. Tumor growth rate was slower in combination-treated mice compared to either drug alone. Additionally, there was a trend toward decreased CSC marker expression in imetelstat-treated xenograft cells compared to vehicle control. Furthermore, the observed decrease in CSC marker expression occurred prior to and after telomere shortening, suggesting that imetelstat acts on the CSC subpopulation in telomere length-dependent and -independent mechanisms. Our study suggests addition of imetelstat to trastuzumab may enhance the effects of HER2 inhibition therapy, especially in the CSC population.
ALT-positive cancers - which include osteosarcoma, glioblastoma and certain pancreatic tumors."
Findings could represent a 'novel and important' treatment strategy
For the study, a team was led by Rachel Flynn, assistant professor of Pharmacology & Experimental Therapeutics and Medicine at Boston University School of Medicine (BUSM).
The team set out to examine how certain key proteins act and are expressed in cancer cells using the ALT pathway. They identified a protein called ATR specializing in the regulation of DNA repair and recombination as being crucial to regulating the ALT pathway.
Known ATR inhibitors, VE-821 and AZ20, were then found by the team to selectively destroy certain tumor cells from the panels of cancer cell lines. Eliminating these tumor cells suppressed their ability to elongate their telomeres via recombination and ultimately led to the death of the cancer cells.
"This study suggests that inhibiting ATR may be a novel and important strategy in treating cancers that rely on the ALT pathway, including up to 60% of osteosarcomas and 40-60% percent of glioblastomas," says Flynn.
Being able to specifically target a single protein with modes of therapy can be extremely beneficial, as Flynn goes on to explain:
"Such targeted treatments would only affect cancer cells and have little effect on the surrounding healthy tissue, potentially minimizing the harsh and debilitating side effects experienced with traditional cancer therapies."
Clinical trials of telomerase inhibitors are underway, but up to 10% of tumors would not respond to this type of drug on account of using the ALT pathway. Flynn explains, however, that testing tumors to identify which pathway they use is not routine practice.
"If VE-821 or other ATR inhibitors are clinically successful, it would support such testing and may lead to more personalized and targeted therapeutic regimens for several cancers refractory to traditional chemotherapeutics."
The authors conclude by writing that their findings offer an unexplored direction for future preclinical and clinical studies.
Last year, Medical News Today reported on a study finding that the genes behind longer telomeres are associated with an increased risk of brain cancer.
Agroup of researchers has identified a new potential treatment method that could prevent several kinds of aggressive tumor from growing.
Telomeres are located at the end of chromosomes and protect the genetic information found within.
The study, published in Science, details how disrupting a pathway used by cancerous cells to proliferate could be the key to inhibiting the growth and survival of tumors.
"Identification of genetic markers that predict cancer cell vulnerabilities and new drugs to exploit such vulnerabilities is a focal point of cancer research today," says senior author Lee Zou, associate scientific director of the Massachusetts General Hospital (MGH) Cancer Center.
Cancer cells survive by avoiding the natural processes of aging and death that normal cells undergo.
In normal cells, repetitive DNA sequences called telomeres regulate these processes. Telomeres are found at the end of chromosomes, protecting them and ensuring that cells do not lose genetic information when dividing.
Over time, telomeres erode and shorten. Once telomeres have been eroded down to a critically short length, a signal is sent which tells the cell to stop dividing, protecting the genetic information while simultaneously cutting short the cell's lifespan.
Cancer cells attempt to promote cellular mortality by lengthening telomeres. There are two major pathways of telomere elongation and in most cases, an enzyme called telomerase extends telomeres.
The other pathway is referred to as the alternative lengthening of telomeres (ALT) pathway. In this pathway, telomeres are lengthened via recombination with DNA sequences from other chromosomes.
This new study represents the first time that a therapy has been identified specifically for treating the ALT pathway.
"Cancer cells must rely on either the telomerase enzyme or the ALT pathway to bypass the normal processes of cell aging and death," explains Zou. "Our findings may provide a new direction for the treatment of
yes he was referingto 2015 but the Geron Jansen data transfer and changes to trial design may push it to June as Scarlett has said.
irish yes I have. I am of the opinion that the MDS data willbe presented at a major scientific meeting and these are the 4 likely meetings. I hope he will present the MDS data by the end of June so there will be no delay to the start of the MDS phase 2 trial tenatively set for the end of 2015. I would also like to see Jansen start the phase 2 MF trial sooner than June.