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Journal of Histochemistry and Cytochemistry, Vol. 51, 303-309, March 2003, Copyright © 2003, The Histochemical Society, Inc.

ARTICLE

DNA Ploidy and Markovian Analysis of Neoplastic Progression in Experimental Pancreatic Cancer

Russell G. Postiera, Megan R. Lernera,d, Stan A. Lightfootb,d, Rick Vannarathb, Mary M. Lanea,d, Jay S. Hanasc, and Daniel J. Bracketta,d
a Departments of Surgery, Oklahoma City, Oklahoma
b Pathology, Oklahoma City, Oklahoma
c Biochemistry & Molecular Biology, Oklahoma City, Oklahoma
d University of Oklahoma Health Sciences Center, and Veterans Administration Medical Center, Oklahoma City, Oklahoma

Correspondence to: Russell G. Postier, PO Box 26901, Dept. of Surgery, U. of Oklahoma Health Sciences Center, Oklahoma City, OK 73190. E-mail: Russell-Postier@ouhsc.edu

Computer-assisted analysis of DNA ploidy and nuclear morphology were used to elucidate changes in the cell nucleus that occur during the development of experimental pancreatic cancer. Ductal pancreatic adenocarcinoma was induced in 49 Syrian hamsters by SC injection of N-nitrosobis (2-oxopropyl) amine; twenty hamsters served as controls. Groups of animals were sacrificed every 4 weeks for 20 weeks and adjacent sections of pancreatic tissue were H&E and Feulgen-stained for light microscopy and computer assisted cytometry. Pancreatic ductal cells were classified as normal, atypical, or malignant; tissue inflammation (pancreatitis) was also noted when present. DNA ploidy and nuclear morphology evaluation (Markovian analysis) identified an atypical cell stage clearly distinguishable from either normal or malignant cells; pancreatitis preceded this atypia. The DNA ploidy histogram of these atypical cells revealed a major diploid peak and a minor aneuploid peak. The receiver operator characteristic curve areas for a logistic regression model of normal vs atypical cells was 0.94 and for atypical vs malignant was 0.98, numbers indicative of near-perfect discrimination among these three cell types. The ability to identify an atypical cell population should be useful in establishing the role of these cells in the progression of human pancreatic adenocarcinoma. (J Histochem Cytochem 51:303–309, 2003)

Key Words: pancreatic cancer, DNA ploidy, Markovian analysis, premalignant neoplastic lesion, pancreatitis, atypia, adenocarcinoma


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