Time for a "Plan B" in Peritoneal Metastatic Disease.

Abstract

Peritoneal involvement in cancer is the harbinger of a particularly unfavorable prognosis. The peritoneal cavity microenvironment is skewed toward immunoregulatory conditions promoted by macrophage populations and innate-like B-1 B cells, which provide immune privilege to malignant cell foci. In this issue of <i>Cancer Research</i>, Haro and colleagues demonstrate that triggering innate IgM-mediated B-1a immune responses via pathogen- or danger-associated molecular pattern recognition exerts antitumor effects on peritoneal metastases by inducing classical complement cascade activation. Exploitation of innate B-1 humoral responses and noncellular immunity is a promising strategy to counter the "castling" of metastatic tumor cells in the peritoneal immunoprivileged site.<i>See related article by Haro et al., p. 159</i>.