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Articles by S. M. Lippman
Total Records ( 2 ) for S. M. Lippman
  E. H Blackburn , T. D Tlsty and S. M. Lippman
 

Cancer prevention encompasses a wide range of highly developed science and clinical impact. Enunciating these two aspects in the same breath highlights the crucial link between them. The breadth and excitement of current opportunities in the science of cancer prevention have never been greater. Major avenues of such research include the extent and effect of premalignancy, the molecular underpinnings of carcinogenesis and related prevention targets, in vitro model systems of the progression of normal human epithelial cells to tumorigenesis, molecular risk stratification and pharmacogenomic approaches, and many more. We describe the clinical impacts of cancer prevention (with examples in the areas of molecular targeting, vaccines, epidemiology, and behavioral science) and the stage-setting science that facilitated them. In addition, discussed are new prevention opportunities such as interactions between stromal and microenvironmental factors, the control of premalignant stem cell phenotypes through epigenetic reprogramming, and neoplastic cells and various stress responses including those involving telomere biology. The promise of this science, particularly integrative, interdisciplinary research, is to hasten the ability of clinical prevention to reduce the burden of cancer. Cancer Prev Res; 3(4); 394–402. ©2010 AACR.

  I Shureiqi , D Chen , R. S Day , X Zuo , F. L Hochman , W. A Ross , R. A Cole , O Moy , J. S Morris , L Xiao , R. A Newman , P Yang and S. M. Lippman
 

Lipoxygenases (LOX) are key enzymes for the oxidative metabolism of polyunsaturated fatty acids into biologically active products. Clinical data on comparative levels of various LOX products in tumorigenesis are lacking. Therefore, we examined the profiles of several LOX products (5-LOX, 12-LOX, 15-LOX-1, and 15-LOX-2) by liquid chromatography/tandem mass spectrometry in the major steps of colorectal tumorigenesis (normal, polyp, and cancer) in a clinical study of 125 subjects (49 with normal colon, 36 with colorectal polyps, and 40 with colorectal cancer) who underwent prospective colorectal biopsies to control for various potential confounding factors (e.g., diet, medications). Mean 13-hydroxyoctadecadienoic acid (13-HODE) levels were significantly higher in normal colon [mean, 36.11 ng/mg protein; 95% confidence interval (95% CI), 31.56-40.67] than in paired colorectal cancer mucosa (mean, 27.01 ng/mg protein; 95% CI, 22.00-32.02; P = 0.0002), and in normal colon (mean, 37.15 ng/mg protein; 95% CI, 31.95-42.34) than in paired colorectal polyp mucosa (mean, 28.07 ng/mg protein; 95% CI, 23.66-32.48; P < 0.001). Mean 13-HODE levels, however, were similar between the left (mean, 37.15 ng/mg protein; 95% CI, 31.95-42.35) and the right normal colon (mean, 32.46 ng/mg protein; 95% CI, 27.95-36.98; P = 0.09). No significant differences with regard to 12- or 15-hydroxyeicosatetraenoic acid or leukotriene B4 levels were detected between normal, polyp, and cancer mucosae. 15-LOX-1 inhibited interleukin-1β expression. This study establishes that reduced 13-HODE levels are a specific alteration in the LOX product profile associated with human colorectal tumorigenesis. Cancer Prev Res; 3(7); 829–38. ©2010 AACR.

 
 
 
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