BBR3610

12/01/2010 - "Interestingly, upon attenuation of autophagy by RNAi-mediated knockdown of ATG5 or ATG6/BECN1, no change in cell viability was observed, suggesting that the autophagy is neither an effective protection against BBR3610 nor an important part of the mechanism by which BBR3610 reduces glioma cell viability. "
12/01/2010 - "Here, we report that BBR3610 induces early autophagy in glioma cells. "
07/01/2006 - "Together, these findings support continued development of BBR3610 for clinical use against glioma and provide a framework for future investigation of mechanism of action."
07/01/2006 - "In subcutaneous xenografts of U87MG glioma cells, BBR3610 approximately doubled the time it took for a tumor to reach a predetermined size and significantly extended survival when these cells were implanted intracranially. "
02/15/2011 - "Combining BBR3610 and PX-866 resulted in synergistic killing of cultured glioma cells and an extension of survival in an orthotopic xenograft animal model. "

07/01/2006 - "In subcutaneous xenografts of U87MG glioma cells, BBR3610 approximately doubled the time it took for a tumor to reach a predetermined size and significantly extended survival when these cells were implanted intracranially. "
12/01/2010 - "BBR3610 is a polynuclear platinum compound, in which two platinums are linked by a spermine-like linker, and studies in a variety of cancers, including glioma, have shown that it is more potent than conventional platinums and works by different means. "

02/15/2011 - "Here, we tested the hypothesis that combining BBR3610, the most potent polynuclear platinum, with a phosphoinositide-3-kinase (PI3K) inhibitor would promote apoptosis and enhance the impact on glioblastoma cells. "
02/15/2011 - "Combined action of the dinuclear platinum compound BBR3610 with the PI3-K inhibitor PX-866 in glioblastoma."

09/01/2007 - "We have examined the mechanisms by which the multinuclear platinum chemotherapeutic BBR3610 kills human colon cancer cells. "
09/01/2007 - "Low-dose BBR3610 toxicity in colon cancer cells is p53-independent and enhanced by inhibition of epidermal growth factor receptor (ERBB1)-phosphatidyl inositol 3 kinase signaling."