Cell proliferation of the duodenal mucosa in patients affected by familial adenomatous polyposis

Santucci, Renato; Volpe, L; Zannoni, Ursula; Paganelli, Gian Maria; Poggi, B.; Calabrese, Carlo; Biasco, Guido

doi:10.1053/gast.1997.v113.pm9322510

Cited by 16 publications

(15 citation statements)

References 2 publications

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“…This result is not surprising because the duodenal mucosa is a field at risk of neoplasia in these patients. 15,16 In the present study, patients showed the most frequent genetic defects in the APC gene characterizing the FAP population. 11,17,18 In particular, the data did not show a correlation between type of germline mutation and severity of duodenal polyposis.…”

Section: Discussionsupporting

confidence: 50%

Impact of Surgery on the Development of Duodenal Cancer in Patients with Familial Adenomatous Polyposis

Biasco¹,

Nobili²,

Calabrese³

et al. 2006

Diseases of the Colon &Amp; Rectum

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Section: Discussionsupporting

confidence: 50%

Impact of Surgery on the Development of Duodenal Cancer in Patients with Familial Adenomatous Polyposis

Biasco¹,

Nobili²,

Calabrese³

et al. 2006

Diseases of the Colon &Amp; Rectum

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“…Other investigators have noted that normal duodenal mucosa from patients with FAP exhibits increased cell proliferation and ultrastructural changes in cell adhesion function compared with non-FAP controls (30,31). In addition, several genes, including COX-2, are up-regulated in the normal-appearing colon mucosa of APC MIN mice and in patients with colorectal cancer (32).…”

Section: Discussionmentioning

confidence: 97%

Increased Cyclooxygenase-2 Expression in Duodenal Compared with Colonic Tissues in Familial Adenomatous Polyposis and Relationship to the −765G → C COX-2 Polymorphism

Brosens

Iacobuzio‐Donahue²,

Keller

et al. 2005

Clinical Cancer Research

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Background: Colorectal cancers arising in patients with familial adenomatous polyposis (FAP) can be largely prevented by polyp surveillance and prophylactic colectomy. As a result, duodenal adenocarcinoma has become a leading cause of death in patients with FAP. Cyclooxygenase 2 (COX-2) inhibition is effective against colorectal polyposis in FAP, but is less effective in treating duodenal polyps. We compared the expression of COX-2 in duodenal and colorectal adenomas from patients with FAP and from patients with sporadic neoplasms and correlated expression to a COX-2 promoter polymorphism (À765G!C) that is reported to influence COX-2 expression. Methods: The study population included 36 FAP patients with colonic adenomas, 22 FAP patients with duodenal adenomas, 22 patients with sporadic duodenal adenomas, and17 patients with sporadic duodenal adenocarcinoma. Neoplastic and corresponding normal tissue COX-2 expressions were determined using immunohistochemistry on tissue microarrays. The prevalence and ethnic distribution of a polymorphism in the COX-2 promoter that influences COX-2 expression (À765G ! C) were determined in DNA from 274 individuals by real-time quantitative PCR.Results: Among patients with FAP, histologically normal duodenal mucosa showed higher COX-2 expression than normal colonic mucosa (P < 0.02), and duodenal adenomas had higher COX-2 expression than colonic adenomas (P V 0.01). In addition, the normal duodenum of patients with FAP showed higher COX-2 expression than the normal duodenal mucosa of patients with sporadic adenomas (P < 0.05). COX-2 expression was significantly higher in the normal-appearing (P < 0.01) mucosa of patients with FAP carrying the À765GG genotype compared with those carrying the À765GC or À765CC genotypes. The À765C genotype was more common in African Americans than in Caucasians (52% versus 33%, P < 0.01).Conclusions: High COX-2 expression in the normal and adenomatous duodenal mucosa of patients with FAP may explain the poorer response of these neoplasms to chemoprevention with COX-2 inhibitors. Familial adenomatous polyposis (FAP) is caused by germ-linemutations in the adenomatous polyposis coli (APC) gene, which leads to the development of innumerable adenomatous polyps throughout the colorectum. Without colectomy, colorectal carcinoma is almost inevitable usually by the fifth decade of life. In recent decades, colorectal cancer screening and prophylactic surgery have significantly improved the survival of patients with FAP. However, the life expectancy of patients with FAP is still below that of the general population, largely due to the risk of developing upper gastrointestinal tract malignancy.The duodenum is the second commonest site of adenoma development in patients with FAP, and f5% of patients with FAP will develop duodenal cancer during their lifetime (1 -3). Currently, the main management options for patients with duodenal adenomatosis are endoscopic surveillance and selective surgical resection. Duodenal surgery, either a pancreaspreserving ...

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“…6 The enhancement of cell proliferation was considered to be one of the early steps in gastrointestinal carcinogenesis. Other abnormalities associated with an increased cancer risk were alterations of maturation and apoptosis.…”

mentioning

confidence: 99%

Cell proliferation and ultrastructural changes of the duodenal mucosa of patients affected by familial adenomatous polyposis

et al. 2004

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Cell proliferation of the duodenal mucosa in patients affected by familial adenomatous polyposis

Cited by 16 publications

References 2 publications

Impact of Surgery on the Development of Duodenal Cancer in Patients with Familial Adenomatous Polyposis

Impact of Surgery on the Development of Duodenal Cancer in Patients with Familial Adenomatous Polyposis

Increased Cyclooxygenase-2 Expression in Duodenal Compared with Colonic Tissues in Familial Adenomatous Polyposis and Relationship to the −765G → C COX-2 Polymorphism

Cell proliferation and ultrastructural changes of the duodenal mucosa of patients affected by familial adenomatous polyposis

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