Tuesday, August 07, 2012 10:10:29 AM
The microenvironment of the tumor is created by cytokines/chemokines that are released by the tumor
or in response to the tumor, like TGF-beta which is immunosuppressive. Feedback loops are
set up between the tumor and immune cells which switch the immune cells to a pro-tumor state.
See the figure in my post # 77572. Bavi binds to the beta2-GPI which is bound to the PS displayed
on the tumor vasculature, apoptotic tumor cells and maybe exosomes. It also will bind directly to the M2
macrophages switching them to M1. When a new tumor appears elsewhere in the body the local
tumor microenvironment is still in a pro-tumor state until treated. We do know that Bavi can lead
to immunity, as was seen in the rat study of glioblastoma when 13% of the surviving rats developed
immunity to rechallenge by the tumor cells. That study used radiation + bavi.
Antiphosphatidylserine antibody combined with irradiation damages tumor blood vessels
and induces tumor immunity in a rat model of glioblastoma.
He J, Yin Y, Luster TA, Watkins L, Thorpe PE.
Clin Cancer Res. 2009 Nov 15;15(22):6871-80.
FREE: http://www.ncbi.nlm.nih.gov/pubmed/19887482
There is the possibility that some of the patients still alive in the second-line NSCLC trial have
developed immunity, but the only way to tell is to see if they stay alive and don't have recurrent disease.
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