January 15 Cancer Research Highlights

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Selected Articles from the January 15, 2008 Issue

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 January 15 issue of Cancer Research.

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Gene Module Maps Guide Targeted Therapy for Human Cancer

Wong et al.

Page 369

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MicroRNA-214 Targets PTEN

Yang et al.

Page 425

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COX-2 Expression Decreases in Breast Cancer Progression

Zhao et al.

Page 467

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VEGF Modulates sVEGFR-2

Ebos et al.

Page 521

Vascular endothelial growth factor (VEGF) is a potent proangiogenic protein that activates VEGF receptor (VEGFR) tyrosine kinases expressed by vascular endothelial cells. Using spontaneously growing tumors and both localized and metastatic human tumor xenografts, Ebos and colleagues evaluated the relationship between sVEGFR-2 and tumor burden as well as underlying factors governing protein level modulation in vivo. Their results indicate that increasing tumor burden leads to decreased circulating sVEGFR-2 in a manner largely mediated by VEGF-induced VEGFR-2 down-regulation. This may help explain recurring clinical findings of inverse plasma level changes between VEGF and sVEGFR-2, as well as be pertinent to clinical exploitation of plasma sVEGFR-2 levels as a surrogate biomarker of VEGF-dependent tumor growth. 

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Lapatinib Inhibits Erb Mutants

Page 571

The clinical efficacy of targeted tyrosine kinase inhibitors is variable and difficult to predict with high accuracy. Gilmer and colleagues set out to characterize the effects of NSCLC-associated mutations in epidermal growth factor receptor (EGFR; ErbB1) and HER2 (ErbB2) on interactions with the dual tyrosine kinase inhibitor lapatinib. EGFR deletion mutants were relatively resistant to lapatinib-mediated inhibition of receptor autophosphorylation in recombinant cells expressing the variants, whereas EGFR point mutations had a modest or no effect. Two HER2 insertional variants found in NSCLC were less sensitive to lapatinib inhibition than two HER2 point mutants. These results suggest that cell line genetic heterogeneity and/or multiple determinants modulate the role played by EGFR/HER2 in regulating cell proliferation. 

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