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Macrophages, cancer and rejection

Posted Feb 17 2011 10:23am

Development of the vasculature of solid cancers (tumour angiogenesis) is a promising target for therapy, leading to interest in proteins such as angiostatin , endostatin and tumstatin . These generally act to inhibit tumor angiogenesis, but there’s also been a fair amount of recent interest in renormalizing the somewhat strange vasculature of cancers to increase the supply of oxygen and improve delivery of therapeutic agents.

A recent paper in Cancer Cell 1 explores this concept a little, apparently finding that histidine-rich glycoprotein (HRG), which is secreted by the liver, has anti-tumour effects through the re-polarization of macrophages. This paper was evaluated by Guido Serini and Giulio Gabbiani , who study the cell-extracellular matrix interactions that occur during blood vessel formation.

I say ‘apparently’ because Tobias Vogt has raised an interesting question . He wonders if the effects the authors see is a result of host rejection, as it’s human HRG used, in a mouse host. With less than 70% identity between the two sequences, this does seem like a valid concern.

But I don’t know much about this—immunology is generally stuff that happens to other people in my book, unless you’re talking big angry macrophages or, actually, “Smoldering inflammation” (from Serini & Gabbiani’s evaluation). Any immunologists/cancer biologists out there care to chime in?

Rolny, C., Mazzone, M., Tugues, S., Laoui, D., Johansson, I., Coulon, C., Squadrito, M., Segura, I., Li, X., & Knevels, E. (2011). HRG Inhibits Tumor Growth and Metastasis by Inducing Macrophage Polarization and Vessel Normalization through Downregulation of PlGF Cancer Cell, 19 (1), 31-44 DOI: 10.1016/j.ccr.2010.11.009

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