Hey porkchop, I am not sure why you sent me to yahoo, but it was informative. I must point out one more time that human cells don't have cell walls as you somehow don't seem to grasp. I read the abstract of this paper, which was in the yahoo link you cited. It states that exposure of PS makes tumor cells more immunogenic.
<<We determined whether the presence of phosphatidylserine (PS) in the outer membrane leaflet of human tumor cells correlated with their recognition by activated human monocytes. Three tumorigenic cell lines, A375 melanoma and A431 and Colo-16 carcinomas, and a normal human epidermal keratinocyte line (NHEK) were incubated with monocytes activated to the tumoricidal state by ?-interferon and lipopolysaccharide. Activated human monocytes bound to and lysed all tumorigenic targets, while the nontumorigenic NHEK were neither bound nor killed. Semiquantitative analysis of PS in the outer leaflet of the cells revealed that the tumorigenic cells expressed 3–7-fold more PS than did the nontumorigenic NHEK. To determine whether enhanced PS expression on the tumor cells was responsible for their recognition by activated monocytes, NHEK were supplemented with exogenously supplied analogues of PS and phosphatidylcholine. PS-labeled NHEK but not phosphatidylcholine-labeled nor control NHEK bound to activated human monocytes. These results suggest a role for PS in monocyte recognition of tumor cells.>>
This is the point poorgradstudent was making with respect to apoptotic cells and their immunogenicity. It is also the opposite of the claims made by some PPHM longs on this board, that the exerted PS inhibits the immune responses and is how tumor cell evade the immune system. I did mention that tumor cells evade the immune system by turning down their MHC presentation, didn't I? If the PS is important for monocyte recognition, then one could argue that having an anti-PS antibody might actually inhibit the immune response. It seems a more promising approach would be to use Bavi as a drug conjugate. I assume the NSCLC trills is with the naked monoclonal Ab, right?
The abstract of the 4th paper (http://ajcp.ascpjournals.org/content/132/5/756.abstract) is a correlative study using Annexin V binding as surrogate for PS exposure on the cell surface. There was a negative correlation between high PS and prognosis/survival. While one might infer as the authors do, that PS is somehow promoting tumor cell survival, a different interpretations is that effectors downstream of PS eversion have been disabled, an this allows such PS bearing cells to survive. Granted I didn't read the manuscript, but that is what my view of the abstract is.
In summary, nothing you asked me to read is a slam dunk, and some of it might argue against use of a naked anti-PSA antibody as an effect anti-cancer strategy.
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