American Association for Cancer Research

March 15 Cancer Research Highlights

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Selected Articles from the March 15, 2006 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 March 15 issue of Cancer Research.


EP4 Receptor Inhibition Effective at Thwarting Experimental Metastasis

Ma et al.
Page 2923
Cyclooxygenase-2 (COX-2) is frequently overexpressed in malignancies, and targeting of COX-2 with selective inhibitors shows promise. Ma et al. considered whether targeting the COX-2 product prostaglandin E2 (PGE2) might also prove therapeutic. Cells respond to PGE2 by expression of four G-protein–coupled receptors (EP1–4). Murine and human breast tumor cells express EP2, EP3, and EP4. Those cells also weakly express EP1. Two independent EP4 antagonists inhibited experimental metastasis to the same degree as the dual COX inhibitor indomethacin. An EP3 antagonist did not effect metastatic potential. Targeting of the EP4 receptor may have application to the control of metastatic disease.

 


EViTAS Profiles Metastatic Phenotypes of Bladder Cancer

Estrada et al.
Page 3078

Tumors of similar histological appearance often differ in aggressiveness and therapeutic response. Current methods to identify high-risk patients and predict response to therapy are limited. Estrada et al. used an orthotopic organ culture model of bladder cancer together with quantum-dot–based fluorescent imaging approaches to obtain quantitative measurements of tumor cell behavior. With this approach, distinct phenotypes were assigned to two metastatic bladder cancer cell lines based on different patterns of invasiveness into the bladder wall. This assay system, EViTAS (ex vivo tumor assay system), is amenable to behavioral profiling of human cancer.

 


Stat3 Drives Metastatic Gene Expression in Brain Melanoma Metastases

Xie et al.
Page 3188

CAN 03-15-06 Xie 3188Brain metastasis is a major cause of morbidity and mortality in patients with melanoma. The molecular changes that lead to brain metastasis remain poorly understood. Xie et al. developed a model to study human melanoma brain
metastasis and found that Stat3 activity is increased in human brain–metastatic melanoma cells. The expression of activated Stat3 is also increased in human brain metastasis specimens when compared with that in the primary melanoma specimens. Increased Stat3 activation enhances brain metastasis, whereas blockade of Stat3 activation suppresses brain metastasis of human melanoma cells in animal models. Furthermore, the results indicate that Stat3 activation plays an important role in dysregulated expression of bFGF, VEGF, and MMP-2 and, hence, angiogenesis and invasion of melanoma cells. Stat3 activation also contributes to brain metastasis of melanoma, which may make it a new potential target for therapy of human melanoma brain metastases.

 


Transcription Inhibitor Limits Survivin While Prompting Cancer Cell Apoptosis

Radhakrishnan and Gartel

Page 3264

CAN 03-15-06 Radhakrishnan 3264Global inhibition of transcription is an effective approach against certain tumors, which depend on labile antiapoptotic proteins for their survival. Radhakrishnan and Gartel report the identification of a novel transcriptional inhibitor, ARC, and show that it down-regulates the antiapoptotic gene survivin in several tumor cell lines. Remarkably, ARC induces apoptosis in human tumor and transformed cells, but not in normal cells, and possesses strong antiangiogenic activity in vitro. Although ARC promotes accumulation of p53, ARCinduced apoptosis in tumor cells is p53-independent, suggesting that it may be useful for treatment of tumors with functionally inactive p53. All of these properties make ARC an attractive candidate for anticancer drug development.


Gene Methylation as a Biomarker in Sputum

Belinsky et al.

Page 3338

A sensitive screening approach for lung cancer could markedly reduce the mortality for this disease. A nested, casecontrol study of incident lung cancer cases from a high-risk cohort was conducted to evaluate promoter methylation of genes in sputum. Six of 14 genes were associated with a >50% increased lung cancer risk. Importantly, the concomitant methylation of three or more of these genes was associated with a 6.5-fold increased risk and a sensitivity and specificity of 64%. This study shows the promise of promoter hypermethylation of a panel of genes as a molecular marker for identifying people at high risk for cancer incidence.