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Articles by L Mao
Total Records ( 4 ) for L Mao
  A. S Tsao , D Liu , J Martin , X. m Tang , J. J Lee , A. K El Naggar , I Wistuba , K. S Culotta , L Mao , A Gillenwater , Y. M Sagesaka , W. K Hong and V. Papadimitrakopoulou

Epidemiologic and preclinical data support the oral cancer prevention potential of green tea extract (GTE). We randomly assigned patients with high-risk oral premalignant lesions (OPL) to receive GTE at 500, 750, or 1,000 mg/m2 or placebo thrice daily for 12 weeks, evaluating biomarkers in baseline and 12-week biopsies. The OPL clinical response rate was higher in all GTE arms (n = 28; 50%) versus placebo (n = 11; 18.2%; P = 0.09) but did not reach statistical significance. However, the two higher-dose GTE arms [58.8% (750 and 1,000 mg/m2), 36.4% (500 mg/m2), and 18.2% (placebo); P = 0.03] had higher responses, suggesting a dose-response effect. GTE treatment also improved histology (21.4% versus 9.1%; P = 0.65), although not statistically significant. GTE was well tolerated, although higher doses increased insomnia/nervousness but produced no grade 4 toxicity. Higher mean baseline stromal vascular endothelial growth factor (VEGF) correlated with a clinical (P = 0.04) but not histologic response. Baseline scores of other biomarkers (epithelial VEGF, p53, Ki-67, cyclin D1, and p16 promoter methylation) were not associated with a response or survival. Baseline p16 promoter methylation (n = 5) was associated with a shorter cancer-free survival. Stromal VEGF and cyclin D1 expression were downregulated in clinically responsive GTE patients and upregulated in nonresponsive patients at 12 weeks (versus at baseline). An extended (median, 27.5 months) follow-up showed a median time to oral cancer of 46.4 months. GTE may suppress OPLs, in part through reducing angiogenic stimulus (stromal VEGF). Higher doses of GTE may improve short-term (12-week) OPL outcome. The present results support longer-term clinical testing of GTE for oral cancer prevention.

  E. S Kim , W. K Hong , J. J Lee , L Mao , R. C Morice , D. D Liu , C. A Jimenez , G. A Eapen , R Lotan , X Tang , R. A Newman , I. I Wistuba and J. M. Kurie

Non–small cell lung cancer is the primary cause of cancer-related death in Western countries. One important approach taken to address this problem is the development of effective chemoprevention strategies. In this study, we examined whether the cyclooxygenase-2 inhibitor celecoxib, as evidenced by decreased cell proliferation, is biologically active in the bronchial epithelium of current and former smokers. Current or former smokers with at least a 20 pack-year (pack-year = number of packs of cigarettes per day times number of years smoked) smoking history were randomized into one of four treatment arms (3-month intervals of celecoxib then placebo, celecoxib then celecoxib, placebo then celecoxib, or placebo then placebo) and underwent bronchoscopies with biopsies at baseline, 3 months, and 6 months. The 204 patients were primarily (79.4%) current smokers: 81 received either low-dose celecoxib or placebo and 123 received either high-dose celecoxib or placebo. Celecoxib was originally administered orally at 200 mg twice daily and the protocol subsequently increased the dose to 400 mg twice daily. The primary end point was change in Ki-67 labeling (from baseline to 3 months) in bronchial epithelium. No cardiac toxicities were observed in the participants. Although the effect of low-dose treatment was not significant, high-dose celecoxib decreased Ki-67 labeling by 3.85% in former smokers and by 1.10% in current smokers—a significantly greater reduction (P = 0.02) than that seen with placebo after adjusting for metaplasia and smoking status. A 3- to 6-month celecoxib regimen proved safe to administer. Celecoxib (400 mg twice daily) was biologically active in the bronchial epithelium of current and former smokers; additional studies on the efficacy of celecoxib in non–small cell lung cancer chemoprevention may be warranted. Cancer Prev Res; 3(2); 148–59

  M Seth , Z. S Zhang , L Mao , V Graham , J Burch , J Stiber , L Tsiokas , M Winn , J Abramowitz , H. A Rockman , L Birnbaumer and P. Rosenberg

Rationale: Cardiac muscle adapts to increase workload by altering cardiomyocyte size and function resulting in cardiac hypertrophy. G protein–coupled receptor signaling is known to govern the hypertrophic response through the regulation of ion channel activity and downstream signaling in failing cardiomyocytes.

Objective: Transient receptor potential canonical (TRPC) channels are G protein–coupled receptor operated channels previously implicated in cardiac hypertrophy. Our objective of this study is to better understand how TRPC channels influence cardiomyocyte calcium signaling.

Methods and Results: Here, we used whole cell patch clamp of adult cardiomyocytes to show upregulation of a nonselective cation current reminiscent of TRPC channels subjected to pressure overload. This TRPC current corresponds to the increased TRPC channel expression noted in hearts of mice subjected to pressure overload. Importantly, we show that mice lacking TRPC1 channels are missing this putative TRPC current. Moreover, Trpc1/ mice fail to manifest evidence of maladaptive cardiac hypertrophy and maintain preserved cardiac function when subjected to hemodynamic stress and neurohormonal excess. In addition, we provide a mechanistic basis for the protection conferred to Trpc1/ mice as mechanosensitive signaling through calcineurin/NFAT, mTOR and Akt is altered in Trpc1/ mice.

Conclusions: From these studies, we suggest that TRPC1 channels are critical for the adaptation to biomechanical stress and TRPC dysregulation leads to maladaptive cardiac hypertrophy and failure.

  C Liang , L Mao , D Ware and L. Stein

Automated evidence-based gene building is a rapid and cost-effective way to provide reliable gene annotations on newly sequenced genomes. One of the limitations of evidence-based gene builders, however, is their requirement for transcriptional evidence—known proteins, full-length cDNAs, or expressed sequence tags (ESTs)—in the species of interest. This limitation is of particular concern for plant genomes, where the rate of genome sequencing is greatly outpacing the rate of EST- and cDNA-sequencing projects. To overcome this limitation, we have developed an evidence-based gene build system (the Gramene pipeline) that can use transcriptional evidence across related species. The Gramene pipeline uses the Ensembl computing infrastructure with a novel data processing scheme. Using the previously annotated plant genomes, the dicot Arabidopsis thaliana and the monocot Oryza sativa, we show that the cross-species ESTs from within monocot or dicot class are a valuable source of evidence for gene predictions. We also find that, using only EST and cross-species evidence, the Gramene pipeline can generate a plant gene set that is comparable in quality to the human genes based on known proteins and full-length cDNAs. We compare the Gramene pipeline to several widely used ab initio gene prediction programs in rice; this comparison shows the pipeline performs favorably at both the gene and exon levels with cross-species gene products only. We discuss the results of testing the pipeline on a 22-Mb region of the newly sequenced maize genome and discuss potential application of the pipeline to other genomes.

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