Immunohistochemical characteristics of duodenal adenomas in familial adenomatous polyposis with special reference to cell kinetics.
The duodenum is the second most frequent site of cancer in patients with familial adenomatous polyposis (FAP). The main objective of this study was to evaluate the cell kinetics in duodenal and ampullary adenomas in FAP. The endoscopic and biopsy findings of duodenal adenomas in 22 FAP subjects and 18 non-FAP subjects were compared. Adenomas in FAP included 15 ampullary adenomas and 17 nonampullary adenomas. The cell kinetics was evaluated by immunohistochemistry for Ki-67, p53, bcl-2, and cyclooxygenase 2 (COX2), and the apoptotic index (AI) as determined by terminal deoxynucleotidyl transferase-mediated dUTP-biotin nick-end labeling (TUNEL) method. Any correlations between the indices for cell kinetics and the endoscopic findings were identified. All 50 adenomas were histologically verified to be tubular adenoma with low-grade dysplasia. Neither the expression of Ki-67, p53, bcl-2, and COX2 nor the AI differed substantially between FAP and non-FAP subjects. In patients with FAP, duodenal adenoma tended to have a higher Ki-67-labeling index than the ampullary adenoma (54.3 +/- 11.3 versus 46.8 +/- 12.7; .05 < P < .1). In addition, the Ki-67-labeling index in endoscopically normal or slightly enlarged ampullary adenoma was significantly higher than that in markedly enlarged ampullary adenoma (51.8 +/- 11.4 versus 39.4 +/- 11.3; P < .05). Duodenal adenoma in FAP subjects was not found to have a higher proliferative activity or a smaller degree of apoptosis compared with those in non-FAP subjects. The smaller proliferative activity in larger ampullary adenoma may thus be related to the static nature of ampullary adenoma in FAP.
Esaki
Motohiro
M
Department of Medicine and Clinical Science, Graduate School of Medical Sciences, Kyushu University, Fukuoka, Japan. mesaki@intmed2.kyushu-u.ac.jp
Matsumoto
Takayuki
T
Yao
Satoshi
S
Nakamura
Shotaro
S
Hirahashi
Minako
M
Yao
Takashi
T
Iida
Mitsuo
M
D000236:Adenoma / Q000209:etiology / Q000378:metabolism* / Q000473:pathology*; D011125:Adenomatous Polyposis Coli / Q000150:complications*; D000328:Adult; D000368:Aged; D014670:Ampulla of Vater / Q000378:metabolism / Q000473:pathology; D017209:Apoptosis / Q000502:physiology*; D049109:Cell Proliferation; D003138:Common Bile Duct Neoplasms / Q000378:metabolism / Q000473:pathology; D051546:Cyclooxygenase 2; D004379:Duodenal Neoplasms / Q000209:etiology / Q000378:metabolism* / Q000473:pathology*; D005260:Female; D017491:Genes, APC; D006801:Humans; D007150:Immunohistochemistry; D020287:In Situ Nick-End Labeling; D019394:Ki-67 Antigen / Q000378:metabolism; D008297:Male; D008565:Membrane Proteins; D008875:Middle Aged; D009154:Mutation; D018807:Polymorphism, Single-Stranded Conformational; D011451:Prostaglandin-Endoperoxide Synthases / Q000378:metabolism; D019253:Proto-Oncogene Proteins c-bcl-2 / Q000378:metabolism; D016159:Tumor Suppressor Protein p53 / Q000378:metabolism
D019394:Ki-67 Antigen; D008565:Membrane Proteins; D019253:Proto-Oncogene Proteins c-bcl-2; D016159:Tumor Suppressor Protein p53; D051546:Cyclooxygenase 2; C496540:PTGS2 protein, human; D011451:Prostaglandin-Endoperoxide Synthases