Size-dependent increase in the levels of prota-glandin metabolites in adenomas of patients with familial adenomatous polyposis (FAP)

Yang, VW; Shields, J. J.; Hamilton, SR; Ew, Spannhake; Wc, Hubbard; Hylind, LM; Robinson, CR; Giardiello, F. M.

doi:10.1016/s0016-5085(98)82903-x

Cited by 56 publications

(75 citation statements)

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“…13,39,40 Also, the concentration of prostanoids in adenomas increases with the size of the adenomas. 13 The elevation in our 4-year study of mucosal prostanoid levels above baseline in the placebo group of FAP patients who were initially phenotypically negative further supports the role of prostanoids in progression of colorectal neoplasia. This is the first observation, to our knowledge, of the natural history of these compounds in human colorectal mucosa during the development of neoplasia.…”

Section: Discussionsupporting

confidence: 59%

“…13,17 Briefly, specimens were thawed on ice and manually homogenized in a glass microhomogenizer (Kontes Scientific Glassware, Vineland, NJ) in 50 μL HBSS (138 mmol/ L NaCl, 5 mmol/L KCl, 4 mmol/L HaHCO 3 , 5.6 mmol/L D-glucose, 0.3 mmol/L Na 2 HP 4 , and 0.3 mmol/L KH 2 PO 4 ) containing 1 mmol/L CaCl 2 and transferred to a microcentrifuge tube. An additional 60 μL of the same solution was used to rinse the homogenizer and then added to the initial homogenate.…”

Section: Measurement Of Prostanoids Levelsmentioning

confidence: 99%

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Prostanoids, ornithine decarboxylase, and polyamines in primary chemoprevention of familial adenomatous polyposis

et al. 2004

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Section: Discussionsupporting

confidence: 59%

Section: Measurement Of Prostanoids Levelsmentioning

confidence: 99%

Prostanoids, ornithine decarboxylase, and polyamines in primary chemoprevention of familial adenomatous polyposis

et al. 2004

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“…This is unlikely for the following reasons. First, the reduction of alkaline SMAse was seen also in the normal appearing mucosa of FAP patients and histological features of randomly taken colonoscopic biopsies from normal appearing mucosa of FAP patients rarely show any adenomatous epithelial proliferation (Yang et al, 1998). Secondly, the similar values per mg protein of another brush border enzyme, alkaline phosphatase support that the reduction of alkaline SMase is specific.…”

Section: mentioning

confidence: 68%

Familial adenomatous polyposis is associated with a marked decrease in alkaline sphingomyelinase activity: A key factor to the unrestrained cell proliferation?

et al. 1999

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SummaryThe hydrolysis of sphingomyelin generates key molecules regulating cell growth and inducing apoptosis. Data from animal cancer models support an inhibitory role for this pathway in the malignant transformation of the colonic mucosa. In the intestinal tract, a sphingomyelinase with an optimum alkaline pH has been identified. We recently found that the activity of alkaline sphingomyelinase is significantly decreased in colorectal adenocarcinomas, indicating a potential anticarcinogenic role of this enzyme. To further examine whether the reduction of sphingomyelinase is present already in the premalignant state of neoplastic transformation, we measured sphingomyelinase activities in patients with familial adenomatous polyposis (FAP) and in sporadic colorectal tubulovillous adenomas. Tissue samples were taken from adenomas and surrounding macroscopically normal mucosa from 11 FAP patients operated with ileorectal anastomosis, from three FAP patients with intact colon, from 13 patients with sporadic colorectal adenomas and from 12 controls. Activities of acid, neutral and alkaline sphingomyelinase were measured together with alkaline phosphatase. In FAP adenoma tissue, alkaline sphingomyelinase activity was reduced by 90% compared to controls (P < 0.0001), acid sphingomyelinase by 66% (P < 0.01) and neutral sphingomyelinase by 54% (P < 0.05). Similar reductions were found in the surrounding mucosa. In sporadic adenoma tissue, only alkaline sphingomyelinase was reduced significantly, by 57% (P < 0.05). Alkaline phosphatase was not changed in FAP adenomas, but decreased in the sporadic adenomas. We conclude that the markedly reduced levels of alkaline sphingomyelinase activities in FAP adenomas and in the surrounding mucosa may be a pathogenic factor that can lead to unrestrained cell proliferation and neoplastic transformation.

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“…There is no ready explanation for these conflicting results. Yang et al 47 found that with familial adenomatous polyposis, elevation of tumoral prostaglandins was not seen until the lesion reached 6 -7 mm in diameter. It is conceivable that the innately slow pace of pituitary tumor growth and metastasis underlies the noted discrepancies between COX-2 expression and the growth rate of pituitary tumors.…”

Section: Discussionmentioning

confidence: 99%

Cyclooxygenase‐2 expression in human pituitary tumors

Vidal

Kovács

Bell

et al. 2003

Cancer

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BACKGROUNDCyclooxygenase‐2 (COX‐2) plays a role in progression of colon, breast, pancreas, and lung carcinomas. The authors investigated COX‐2 expression in pituitary tumors.METHODSExpression of COX‐2 was evaluated in 164 surgically removed human pituitary tumors. Correlation of COX‐2 with MIB‐1, a cell proliferation marker, as well as angiogenesis, patient age, gender, tumor type, size, invasiveness, and metastatic potential was investigated.RESULTSCyclooxygenase‐2 immunoreactivity was confined to the cytoplasm of tumor cells, whereas the nuclei were unlabeled. Few normal peritumoral adenohypophysial cells showed slight COX‐2 cytoplasmic immunoreactivity. The staining intensity and the percentage of immunopositive cells were higher in tumors. Most pituitary tumors (96%) were COX‐2–immunopositive. Expression was strong in 60 (44%), moderate in 39 (28%), and weak in 32 (24%). Male gonadotroph adenomas and null cell adenomas showed a high level of COX‐2 expression. Growth hormone‐producing adenomas, prolactin‐producing adenomas, thyrotropic hormone‐producing adenomas, female gonadotroph adenomas, silent adrenocorticotropic hormone‐producing adenomas, and silent subtype 3 adenomas had a low level of COX‐2 expression. Significant correlation was demonstrated with patient age, but not with tumor size, invasiveness, and MIB‐1 labeling indices. Expression was medium to high in 76% of macroadenomas and in only 45% of microadenomas. Strong correlations were noted with angiogenesis markers, such as microvessel density and surface density.CONCLUSIONSCorrelation with angiogenesis suggests that COX‐2 may be involved in the regulation of angiogenesis in pituitary tumors. Phamacologic inhibition of COX‐2 activity might suppress angiogenesis in pituitary tumors and may provide a novel approach for medical therapy. Cancer 2003;97:2814–21. © 2003 American Cancer Society.DOI 10.1002/cncr.11387

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Size-dependent increase in the levels of prota-glandin metabolites in adenomas of patients with familial adenomatous polyposis (FAP)

Cited by 56 publications

References 0 publications

Prostanoids, ornithine decarboxylase, and polyamines in primary chemoprevention of familial adenomatous polyposis

Prostanoids, ornithine decarboxylase, and polyamines in primary chemoprevention of familial adenomatous polyposis

Familial adenomatous polyposis is associated with a marked decrease in alkaline sphingomyelinase activity: A key factor to the unrestrained cell proliferation?

Cyclooxygenase‐2 expression in human pituitary tumors

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