PDF Version for Printing
The articles referenced in this Highlights section will be available online in HTML and PDF formats to all interested users at no charge until the next issue of Cancer Research is published. Click on the article title to view the complete article.
View the Table of Contents for the May 1 issue of Cancer Research.
Page 3178
Page 3323
Page 3421
Page 3467
Host-tumor immunosurveillance can be undermined by a tumor counter-immunosurveillance mechanism involving tumor-stimulated natural killer T cells that produce interleukin-13 (IL-13), a cytokine that inhibits tumor cell–targeting cytotoxic CD8+ T cells by inducing the production of transforming growth factor-β1 (TGF-β1). In this study, the key receptor used by IL-13 to induce TGF-β1 in this mechanism, IL-13Rα2, was identified and its expression was shown to be blocked in vivo by TNF-αR-Fc (etanercept). The latter, a well-known agent for the treatment of autoimmunity, was then shown to inhibit the development of two types of experimental tumors and to thus emerge as a possible antitumor therapy.
Sutherland et al. Page 3495 Using genetically engineered mice, Sutherland and colleagues show that specific conditional deletion of IGF-IR in the epithelial compartment of the prostate caused cell-autonomous proliferation with hyperplasia and that apoptosis and cellular senescence programs were ultimately induced concomitant with increased steady-state levels of p53. The authors also show that abrogation of IGF-IR in a spontaneous cancer model dependent, in part, on p53-depletion could promote the emergence of aggressive disease. Therefore this study indicates that IGF-IR signaling plays a critical role in tissue homeostasis and differentiation and that initiatives to therapeutically target IGF-I in prostate cancer should proceed cautiously as abrogation of IGF-IR facilitated the growth of tumors with compromised p53 activity.
Page 3495