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OCZ Technology Group AŞ Message Board

hokiestock 2 posts  |  Last Activity: Nov 21, 2015 10:22 AM Member since: Jul 10, 2012
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  • Celldex has checked in a lot of the current trials on going over the last 2 months. I expect a full 2016 report pretty soon. Noticed the Rindo study in newly diagnosed patients is probably ready for a glance around January. This below is one of the most important.

    I encourage everyone to visit who invests in biotech to check whats going on.

    A Study of Varlilumab (Anti-CD27) and Ipilimumab and CDX-1401 in Patients With Unresectable Stage III or IV Melanoma
    This study is currently recruiting participants. (see Contacts and Locations)
    Verified November 2015 by Celldex Therapeutics
    Celldex Therapeutics
    Information provided by (Responsible Party):
    Celldex Therapeutics Identifier:
    First received: March 25, 2015
    Last updated: November 16, 2015
    Last verified: November 2015
    History of Changes

  • Reply to

    Combination therapy...

    by raysfrom98 Nov 20, 2015 3:35 PM
    hokiestock hokiestock Nov 20, 2015 8:28 PM Flag

    All of cancers have combination therapy but the unique thing is that the mechanism are no longer break you down and hope the body can recover. Actually the data is suggesting that BET Inhibitors are going to be synergistic with EGFRV111. Rintega and GPNMB have not even scratched the surface on their possible combinations. That is why many other companies are also exploring the EGFRV111 not EGFR but specifically the site where Rintega works.

    Epidermal growth factor receptor (EGFR) gene amplification and mutations are the most common oncogenic events in glioblastoma (GBM), but the mechanisms by which they promote aggressive tumor growth are not well understood. Here, through integrated epigenome and transcriptome analyses of cell lines, genotyped clinical samples, and TCGA data, we show that EGFR mutations remodel the activated enhancer landscape of GBM, promoting tumorigenesis through a SOX9 and FOXG1-dependent transcriptional regulatory network in vitro and in vivo. The most common EGFR mutation, EGFRvIII, sensitizes GBM cells to the BET-bromodomain inhibitor JQ1 in a SOX9, FOXG1-dependent manner. These results identify the role of transcriptional/epigenetic remodeling in EGFR-dependent pathogenesis and suggest a mechanistic basis for epigenetic therapy.