American Association for Cancer Research

June 15 Cancer Research Highlights

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Selected Articles from the June 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 June 15 issue of Cancer Research.


Twin Study Shows High Mutagen Heritability

Wu et al.
Page 5993
Numerous studies suggested that mutagen sensitivity is a promising cancer susceptibility marker; however, the heritability of mutagen sensitivity has not been established. Wu et al. used a classical twin study design to examine the role of genetic and environmental factors on mutagen sensitivity. The intraclass correlation coefficients were significantly higher in monozygotic twins than in dizygotes for sensitivity to four different mutagen challenges. Applying biometric genetic modeling, they calculated a genetic heritability of 40.7%, 48.0%, 62.5% and 58.8% for bleomycin, BPDE, γ-radiation and 4NQO sensitivity, respectively. This study provides the strongest and most direct evidence that mutagen sensitivity is highly heritable.

 


Hypermethylated Pro-Apoptotic Gene Marks Late Stage Lung Cancer

Machida et al.
Page 6210

CAN 06-15-06 Machida 6210Hypermethylated gene promoter sequences are promising cancer markers. Such hypermethylation often marks early, pre-invasive, tumor stages. However, as shown through immunohistochemistry and in situ and liquid PCR methylation assays, hypermethylation and silencing of the pro-apoptotic gene, ASC/TMS1, is a late-stage lung cancer marker. In sputum, ASC/TMS1 hypermethylation mimics the high incidence of this change in stage III lung adenocarcinomas is seldom present in high-risk, cancer-free smokers, but is positive in 24% of clinically cancer-free individuals previously resected for stage I non-small cell lung cancer and who have very high risk for persistent or recurrent disease. Hypermethylation of ASC/TMS1 in sputum merits further study as a prognostic marker in patients resected for
early-stage lung cancer.


Prolonged Antibiotics Increases HER-2/neu Tumor Risk in Mouse Model

Rossini et al.
Page 6219

CAN 06-15-06 Rossini 6219Some epidemiological studies have suggested a positive association between antibiotic use and risk of breast cancer. Rossini et al. evaluated the role of prolonged antibiotic treatments on tumor development in HER-2/neu proto-oncogene transgenic female mice, which spontaneously develop mammary carcinoma. The results indicated that a prolonged exposure to antibiotic determined a significantly higher risk of tumor development and an increase in ductal branching and terminal buds in comparison to controls. Further studies are critical to understand the mechanism by which antibiotic treatments influence mammary gland differentiation.


 

Targeting Notch3 Amplification May Suppress Ovarian Cancer

Park et al.

Page 6312

To explore DNA copy number alterations in high-grade serous carcinomas, Park et al. applied SNP array analysis and identified a frequently amplified region on chromosome 19p13.12. Comprehensive mRNA expression analysis of all the genes within the minimal amplicon leads to the identification of Notch3 as the candidate amplified oncogene. Furthermore, inactivation of Notch3 by both g-secretase inhibitor and Notch3-specific siRNA suppressed cell proliferation and induced apoptosis in the cell lines that overexpressed Notch3. The results suggest inactivation of Notch3 can be a potential therapeutic approach in ovarian carcinomas.


Methylation Inhibitors Reverse Aberrantly Silenced Genes

Gore et al.

Page 6361

Optimal re-expression of most genes silenced through promoter methylation requires the sequential application of DNA methyltransferase inhibitors followed by histone deacetylase inhibitors in tumor cell cultures. Gore et al. treated patients with myelodysplastic syndrome or acute myeloid leukemia with the methyltransferase inhibitor 5-azacitidine followed by the histone deacetylase inhibitor sodium phenylbutyrate. Major responses associated with cytogenetic complete response developed in patients receiving prolonged dosing schedules of 5-azacitidine. Demethylation of p15 or CDH-1 was demonstrated only in clinical responders. This study provides the first demonstration that molecular mechanisms responsible for clinical responses to DNMT/HDAC inhibitor combinations may include reversal of aberrant epigenetic gene silencing.