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Geron Corporation (GERN) Message Board

tazamatic2002 94 posts  |  Last Activity: Aug 21, 2014 9:49 PM Member since: Jun 1, 2009
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  • tazamatic2002 tazamatic2002 Aug 21, 2014 9:49 PM Flag

    As I have said, I take no sides in this I just pointed out that you forgot to mention the results of the incident you have mentioned. I have served my country in a time of War as my father and grandfather have before me. I wonder have you? My family has seen duty in support of WW1, WW2, and Gulf War1 (Dessert Storm).

  • tazamatic2002 tazamatic2002 Aug 21, 2014 1:24 PM Flag

    I am not pro any side in the Islrael Gaza conflict there is enough complicity on both sides. By the way you fail to mention that he lost his wife and only child in the attack. I would say that Israel hurt him more by that loss than if he had died and they had lived.

  • tazamatic2002 tazamatic2002 Aug 21, 2014 12:02 PM Flag

    Looks like data collection for the hold will be completed in December.

  • Reply to

    Sorafenib Combos with Imetelstat

    by tazamatic2002 Aug 20, 2014 2:02 PM
    tazamatic2002 tazamatic2002 Aug 20, 2014 2:11 PM Flag

    for data behind the Abstract google sorafenib imetelstat and select Doanload Appendix
    7 Cancer types tested p value less than 0001

  • tazamatic2002 by tazamatic2002 Aug 20, 2014 2:02 PM Flag

    Significance

    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.

    Abstract

    Tumor suppressor p53 plays an important role in mediating growth inhibition upon telomere dysfunction. Here, we show that loss of the p53 target gene cyclin-dependent kinase inhibitor 1A (CDKN1A, also known as p21WAF1/CIP1) increases apoptosis induction following telomerase inhibition in a variety of cancer cell lines and mouse xenografts. This effect is highly specific to p21, as loss of other checkpoint proteins and CDK inhibitors did not affect apoptosis. In telomerase, inhibited cell loss of p21 leads to E2F1- and p53-mediated transcriptional activation of p53-upregulated modulator of apoptosis, resulting in increased apoptosis. Combined genetic or pharmacological inhibition of telomerase and p21 synergistically suppresses tumor growth. Furthermore, we demonstrate that simultaneous inhibition of telomerase and p21 also suppresses growth of tumors containing mutant p53 following pharmacological restoration of p53 activity. Collectively, our results establish that inactivation of p21 leads to increased apoptosis upon telomerase inhibition and thus identify a genetic vulnerability that can be exploited to treat many human cancers containing either wild-type or mutant p53.

  • tazamatic2002 tazamatic2002 Aug 20, 2014 1:09 PM Flag

    You left out the extreeme weight loss program where many loose their heads.

  • Reply to

    Amgen has no choice

    by champion_frank Aug 15, 2014 10:58 AM
    tazamatic2002 tazamatic2002 Aug 20, 2014 12:21 PM Flag

    I have said it before nothing will happen until the hold has lifted. AMGEN buying Geron makes a perfect fit and AMGEN currently owns the IP from the company scarlett sold so we wait.

  • Reply to

    Irishtrader

    by tazamatic2002 Aug 19, 2014 11:55 AM
    tazamatic2002 tazamatic2002 Aug 19, 2014 2:11 PM Flag

    ryan I know but I am talking about the ASH comment when the review of Abstracts starts in September, the acceptance notification is in October, and Abstracts post in November

  • tazamatic2002 by tazamatic2002 Aug 19, 2014 11:55 AM Flag

    today you get to see why subman does not trust E2W. I know that some here trade in and out and change their posting tactics with their position but I am a longer term investor. The market gets it wrong most of the time.

  • Reply to

    Tefferi at ASH 2014 still a no show

    by end2war Aug 19, 2014 11:17 AM
    tazamatic2002 tazamatic2002 Aug 19, 2014 11:44 AM Flag

    It would depend on how impressive his data set for RARS MDS is. The guest Speaker list is not the way to track Abstracts and Who is presenting trial data.

  • Reply to

    Tefferi at ASH 2014 still a no show

    by end2war Aug 19, 2014 11:17 AM
    tazamatic2002 tazamatic2002 Aug 19, 2014 11:28 AM Flag

    Yes he has submitted as per CC and the Abstracts do not release until November just like last year. You are a little early to be looking at the listed speaker list for ASH. The way it wors is submission, then selection, and then publication of Absracts.

  • tazamatic2002 tazamatic2002 Aug 18, 2014 10:42 PM Flag

    The cells they are working with come from a long time ago and can be infinitely proliferated so they take no more embryos. They can infinitely proliferate cells to be used for therapy.

  • Reply to

    ASTY pipeline

    by tazamatic2002 Aug 18, 2014 12:31 PM
    tazamatic2002 tazamatic2002 Aug 18, 2014 4:39 PM Flag

    AST-VAC1 –
    Autologous Monocyte
    – Derived Dendritic
    Cells (infused cells
    derived from the
    treated patient) Cancer Prostate: 240,000 new cases per year in U.S. Phase I study in metastatic prostate cancer completed (Journal of Immunology, 2005, 174: 3798-3807).
    Acute myelogenous leukemia: more than 12,000 new cases per year in U.S. Phase I/II study in acute myelogenous leukemia completed. Manuscript in preparation.

    CHND1 –
    Chondrocytes Osteoarthritis 25 million total patients in U.S. Cells derived and partly characterized.

    Early non-clinical studies have been performed in animal models of osteoarthritis.

    Degenerative Disk Disease 400,000 new spinal fusion cases per year in U.S. Pre-clinical research.

    CM1 –
    Cardiomyocytes Heart Failure 6 million total patients in U.S. Cells derived and characterization studies performed (parameters analyzed showed normal cell functions in vitro).
    Myocardial Infarction 900,000 new cases per year in U.S. Proof of concept in three animal models of disease.
    Scalable manufacturing established.
    First in man clinical trial designed.

  • tazamatic2002 by tazamatic2002 Aug 18, 2014 12:31 PM Flag

    AST-OPC1 – Glial
    Cells Current development focus:
    Spinal Cord Injury 12,000 new cases per year in U.S. Phase I Trial completed in U.S. 5 Patients treated – no serious adverse events related to the OPC1 drug product to date.
    Additional potential markets:
    Multiple Sclerosis (“MS”) 180,000 new cases per year in U.S. Proof of principle achieved in animal models.

    Canavan's Disease(2) Rare Proof of principle achieved in animal models.

    Stroke 800,000 new cases per year in U.S. Pre-clinical research.

    AST-VAC2 –
    Dendritic Cells Current development focus:
    Non-small Cell Lung Cancer 166,000 new cases per year in U.S. Cells derived and characterization studies performed (parameters analyzed showed normal cell functions in vitro(3)).
    Proof of concept established in multiple human in vitro(3) systems. Scalable manufacturing methods under development.

  • Reply to

    Amgen has no choice

    by champion_frank Aug 15, 2014 10:58 AM
    tazamatic2002 tazamatic2002 Aug 18, 2014 12:20 PM Flag

    Geron Management will not sell it now they will wait for the hold to lift and price to go higher.

  • tazamatic2002 tazamatic2002 Aug 14, 2014 9:16 PM Flag

    Nexavar does not work as well as Imetelstat at supressing tumors the big thing is Imetelstat and Nexavar combined is a huge winner according to the Yale study.

  • tazamatic2002 tazamatic2002 Aug 14, 2014 5:50 PM Flag

    biopearl found this first

  • tazamatic2002 tazamatic2002 Aug 14, 2014 3:57 PM Flag

    37 pages long lol need to use my reading glasses. The abstract

    Significance

    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.

    Abstract

    Tumor suppressor p53 plays an important role in mediating growth inhibition upon telomere dysfunction. Here, we show that loss of the p53 target gene cyclin-dependent kinase inhibitor 1A (CDKN1A, also known as p21WAF1/CIP1) increases apoptosis induction following telomerase inhibition in a variety of cancer cell lines and mouse xenografts. This effect is highly specific to p21, as loss of other checkpoint proteins and CDK inhibitors did not affect apoptosis. In telomerase, inhibited cell loss of p21 leads to E2F1- and p53-mediated transcriptional activation of p53-upregulated modulator of apoptosis, resulting in increased apoptosis. Combined genetic or pharmacological inhibition of telomerase and p21 synergistically suppresses tumor growth. Furthermore, we demonstrate that simultaneous inhibition of telomerase and p21 also suppresses growth of tumors containing mutant p53 following pharmacological restoration of p53 activity. Collectively, our results establish that inactivation of p21 leads to increased apoptosis upon telomerase inhibition and thus identify a genetic vulnerability that can be exploited to treat many human cancers containing either wild-type or mutant p53.

  • tazamatic2002 tazamatic2002 Aug 14, 2014 3:53 PM Flag

    Ryan the back ground info is in the pdf you find when you google CDKN1A Imetelstat. The PDF is the apendix of the Yale Abstract pubished By the National Accademy of Scince. The PF is 32 pages long. table on page 10 shows cancer types and drug combos tested.
    page 13 to top of page 19 discusses various p valuss from the various combinations in the tables.
    Graphs on page 35 show the combo of Imetelstat with Sorafenib in 5 Cancer types.

  • Reply to

    Imetelstat Cost

    by blackmarango Aug 13, 2014 5:24 PM
    tazamatic2002 tazamatic2002 Aug 13, 2014 6:47 PM Flag

    More people on trial means increased costs this includes the other IND that is currently running.

    The fact they know the mechanism of action in MPNs and it will be presented at ASH by Accademic collaberators.

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