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Articles by C. C. Harris
Total Records ( 4 ) for C. C. Harris
  A. J Schetter , N. H. H Heegaard and C. C. Harris
 

Chronic inflammation and infection are major causes of cancer. There are continued improvements to our understanding of the molecular connections between inflammation and cancer. Key mediators of inflammation-induced cancer include nuclear factor kappa B, reactive oxygen and nitrogen species, inflammatory cytokines, prostaglandins and specific microRNAs. The collective activity of these mediators is largely responsible for either a pro-tumorigenic or anti-tumorigenic inflammatory response through changes in cell proliferation, cell death, cellular senescence, DNA mutation rates, DNA methylation and angiogenesis. As our understanding grows, inflammatory mediators will provide opportunities to develop novel diagnostic and therapeutic strategies. In this review, we provide a general overview of the connection between inflammation, microRNAs and cancer and highlight how our improved understanding of these connections may provide novel preventive, diagnostic and therapeutic strategies to reduce the health burden of cancer.

  S. E Olivo Marston , L. E Mechanic , S Mollerup , E. D Bowman , A. T Remaley , M. R Forman , V Skaug , Y. L Zheng , A Haugen and C. C. Harris
 

The role of tumor estrogen receptors (ERs) and serum estrogen in lung cancer is inconclusive. We investigated the hypothesis that ERs and functional single-nucleotide polymorphisms in the estrogen biosynthesis pathway are associated with poorer lung cancer survival. Lung cancer patients (n = 305) from a National Cancer Institute-Maryland (NCI-MD) case–case cohort in the Baltimore metropolitan area were used as a test cohort. To validate, 227 cases from the NCI-MD case–control cohort and 293 cases from a Norwegian lung cancer cohort were studied. Information on demographics, tobacco and reproductive histories was collected in an interviewer-administered questionnaire. Serum estrogen, progesterone, tumor messenger RNA expression of hormone receptors and germ line DNA polymorphisms were analyzed for associations with lung cancer survival. Patients in the highest tertile of serum estrogen had worse survival in all three cohorts (P combined < 0.001). Furthermore, the variant allele of estrogen receptor alpha (ER-) polymorphism (rs2228480) was significantly associated with increased tumor ER- levels and worse survival in all three cohorts [hazard ratio (HR) = 2.59, 95% confidence interval (CI): 1.20– 4.01; HR = 1.76, 95% CI: 1.08–2.87 and HR = 2.85, 95% CI: 1.31–4.36). Other polymorphisms associated with lower serum estrogen correlated with improved survival. Results were independent of gender and hormone replacement therapy. We report a significant association of increased serum estrogen with poorer survival among lung cancer male and female patients. Understanding the genetic control of estrogen biosynthesis and response in lung cancer could lead to improved prognosis and therapy.

  E Tahara , W Yasui , H Ito and C. C. Harris
 

This symposium presented recent progress of the pathogenesis and treatment of lung cancer. Aberrantly increased expression of miR-21 plays a significant role in lung carcinogenesis and is a potential therapeutic target in both epidermal growth factor receptor-mutant and wild-type cases. miR-34 may be necessary for the radiation-induced DNA damage response. Detailed expression profiling analyses of transcriptome have potential to provide increased understanding of the molecular biology of lung cancer. An embryonic signature is present in lung adenocarcinoma only, associated with a worse clinical outcome. Cytoplasmic expression of caveolin and membranous expression of CD26 are specific to mesothelioma. Nectin-4 is a new candidate for serum and tissue biomarker as well as a therapeutic target for lung cancer. Clinical presentations have provided us a great deal information on epidermal growth factor receptor mutations for personalized therapy, combination therapy with inhibitors of the tyrosine kinase activity of epidermal growth factor receptor and cytotoxic agents, antibody-dependent cellular cytotoxicity activity, and current management of lung cancer depending on both the extent of the disease and the treatment approach.

 
 
 
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