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PubMed1990

Gastrointestinal regulatory peptides in familial adenomatous polyposis.

The etiology of adenomas in the stomach and duodenum in patients with familial adenomatous polyposis (FAP) is unknown. In this study the plasma concentration of epidermal growth factor (EGF), and other gastrointestinal polypeptides with a possible trophic effect on the gastrointestinal mucosa, was unchanged before and after meal stimulation. In 3 of 7 patients an increased EGF immunoreactivity was found in duodenal adenomas. This study has not indicated that regulatory peptides are involved in development of duodenal polyps in FAP, but suggests further studies to determine the role of EGF in FAP.

Adenoma↗
PubMed1999

Analysis of nucleotides and aromatic amino acids in normal and neoplastic colon mucosa by ultraviolet resonance raman spectroscopy.

The objective of this study was to explore the potential of using ultraviolet resonance Raman (UVRR) spectroscopy to analyze normal and neoplastic colon tissue. Ultraviolet light at 251 nm, generated from the third harmonic of a Titanium:Sapphire laser, was used to irradiate the surfaces of surgically resected human colon specimens from six patients, five clinically diagnosed with adenocarcinoma, and one with familial adenomatous polyposis. All grossly neoplastic samples found to contain mucosal dysplasia or invasive adenocarcinoma upon histologic evaluation, were analyzed in parallel with normal tissue obtained from the same specimen and located at least 1 cm away from grossly neoplastic tissue. The colon spectra were modeled as a linear combination of nucleotide, aromatic amino acid, and lipid lineshapes, using chemical standards as a reference. Nucleotide and amino acid contributions to the UVRR spectra were quantified by a least squares minimization method. The least squares minimization spectral model was verified in aqueous solutions, where relative concentrations of free nucleotides and DNA were quantified with < 10% error. Of the 11 neoplastic samples studied from the 6 specimens, 10 showed either a lower amino acid/nucleotide ratio, a lower level of adenyl (A) signal, or both when compared with their normal counterpart. Lower amino acid/nucleotide ratio was present in five of six samples containing only dysplasia, and three of the five samples containing invasive adenocarcinoma. Lower A was present in all five samples containing invasive cancer, and in three of the six samples containing only dysplasia. This lower level of A corroborates previously published biochemistry work showing a lower level of total adenylates in tumor homogenates compared with normal tissue. Our data indicate that surface UVRR may provide unique information about site-to-site changes in cellular metabolites during colon carcinogenesis.

Adenocarcinoma↗
PubMedDate not supplied

[Ileal invaginations caused by Peutz-Jeghers polyposis].

The Peutz-Jeghers syndrome is considered a familial polyposis syndrome. The polyps are of hamartomatous type. The symptomatology is due to the more voluminous polyps which can necrotize, ulcerate, bleed and cause intussusception and intestinal obstruction. A case of ileum-ileal intussusception due to Peutz-Jeghers syndrome is reported. The utility of a genealogic research is underlined and the recent results of the genetic research are evaluated. The surgical therapy of Peutz-Jeghers syndrome can have many aims: 1) to remove all big polyps, 2) to avoid the danger of canceration, 3) to prevent the hemorrhagic or occlusive risks and complications.

Adult↗
PubMed1990

The pelvic ileal reservoir: pathology and pouchitis.

The creation of a pelvic ileal reservoir is associated with inflammatory changes in the reservoir mucosa. Chronic inflammation and villous atrophy are seen in most patients with both ulcerative colitis and familial adenomatous polyposis (FAP), the two prime indications for the operation. The mucosa undergoes a form of colonic metaplasia which is demonstrable by morphological, mucin histochemical, immunohistochemical and proliferation methods. Other pathological features such as mucosal ischaemia, mucosal prolapse, granulomas and pyloric metaplasia are seen in the pouch mucosa and these changes contribute to the confusion over definitions of pouchitis. The term pouchitis denotes a chronic relapsing inflammatory condition of the reservoir which occurs in 10-20% of patients and is one of the more severe long-term complications of reservoir construction. Useful definitions of pouchitis should include clinical, endoscopic and histopathological criteria. There are close associations between pouchitis and an original diagnosis of ulcerative colitis. The cause of pouchitis is currently obscure but there is evidence to suggest it may represent a recurrence of colitis in metaplastic mucosa and may provide a useful human model for colitis. The demonstration of markedly increased proliferative activity in association with colonic metaplasia has worrying connotations. However, dysplasia has not yet been described in colitic reservoirs and very few adenomas have been seen in polyposis reservoirs. Nevertheless the clinical and pathological evidence would indicate that long-term surveillance of the reservoir mucosa by endoscopy and mucosal biopsy is warranted.

Adenomatous Polyposis Coli↗
PubMed1995

Somatic mutations of the adenomatous polyposis coli gene in gastroduodenal tumors from patients with familial adenomatous polyposis.

We analyzed somatic mutations of the adenomatous polyposis coli (APC), p53, and K-ras genes in gastroduodenal polyps and normal gastroduodenal mucosa from 21 familial adenomatous polyposis patients, using PCR-single-strand conformation polymorphism and direct sequencing methods. Seventy-five polyps were obtained from these patients endoscopically or surgically, and they were histopathologically diagnosed as mild adenoma, moderate adenoma, severe adenoma, adenocarcinoma, and fundic gland polyp. Examining the APC-coding region where somatic mutations in colorectal tumors are known to be clustered, we detected 47 somatic mutations. The frequency of mutation detected was 6 of 9 (67%) in ampullary adenomas, 1 of 2 (50%) in ampullary adenocarcinoma, 11 of 24 (46%) in non-ampullary adenomas, 26 of 29 (90%) in gastric adenomas, and 3 of 11 (27%) in gastric fundic gland polyps. These mutations frequently occurred at codons 1450, 1462-1465, and 1554-1556, the third being a newly found hot spot. All mutations formed stop codons that resulted in truncated APC proteins. K-ras mutation was detected only in an ampullary adenocarcinoma, and p53 mutation was not detected in any of the tumors analyzed. There was no somatic mutation detected in samples of flat mucosa that were diagnosed as normal mucosa both endoscopically and histopathologically. Frequent APC mutations in mild and small adenomas, similar to the findings in severe and large adenomas, suggested that the genetic change in the APC gene occurs in an early stage of forming gastroduodenal adenomas. Moreover, the presence of somatic APC mutations in fundic gland polyps suggests that inactivation of the APC gene plays a role not only in forming adenomas but also in forming hyperplastic polyps in fundic gland mucosa, and there may be some additional steps to the adenoma-carcinoma sequence.

Adenomatous Polyposis Coli↗
PubMed1995

Inhibition of apoptosis during development of colorectal cancer.

Colorectal tumorigenesis proceeds through an accumulation of specific genetic alterations. Studies of the mechanism by which these genetic changes effect malignant transformation have focused on the deregulation of cell proliferation. However, colorectal epithelial homeostasis is dependent not only on the rate of cell production but also on apoptosis, a genetically programmed process of autonomous cell death. We investigated whether colorectal tumorigenesis involved an altered susceptibility to apoptosis by examining colorectal epithelium from normal mucosa, adenomas from familial adenomatous polyposis, sporadic adenomas, and carcinomas. The transformation of colorectal epithelium to carcinomas was associated with a progressive inhibition of apoptosis. The inhibition of apoptosis in colorectal cancers may contribute to tumor growth, promote neoplastic progression, and confer resistance to cytotoxic anticancer agents.

Adenomatous Polyposis Coli↗
PubMed1995

Epithelial proliferation and differentiation in flat duodenal mucosa of patients with familial adenomatous polyposis.

The colonic mucosa in patients with familial adenomatous polyposis (FAP) exhibits altered epithelial cell proliferation, differentiation, and mucin histochemical properties compared with unaffected controls. However, little is known regarding these parameters in FAP-associated duodenal mucosa, an area in which adenomas also develop at a high rate. The purpose of this study is to evaluate the morphologic, mucin histochemical, and proliferative characteristics of the epithelium in the flat duodenal mucosa from 32 patients with FAP (18 with and 14 without adenomas), and compare the results with those observed in 18 non-FAP age-matched controls. The proliferative properties of the epithelium were analyzed immunohistochemically with the MIB-1 antibody, which recognizes the Ki-67 proliferation-associated nuclear antigen in formalin-fixed tissue. No significant differences were detected with regard to the mucin histochemical properties (sialomucins, sulfomucins, and o-acylated sialomucins) or the proliferative characteristics of the duodenal epithelium in FAP versus non-FAP controls. However, FAP-associated duodenal epithelium showed a significant increase in the number of Paneth cells (P = 0.04) and endocrine cells (P = 0.01) per crypt in comparison with controls. This specialized cell hyperplasia occurred in the flat mucosa of FAP patients regardless of the presence or absence of adenomas and may represent a primary defect in the regulation of stem cell differentiation in the duodenum in FAP.

Adenomatous Polyposis Coli↗
PubMedDate not supplied

[The surgical treatment of diffuse polyposis coli in children].

Results of surgical treatment of patients with diffuse polyposis of the colon (a juvenile form) are analyzed. During 1979-1990 20 ileoanal and 8 ileorectal anastomoses were performed with demucosation of the rectum. The operative intervention is performed by an original method without temporary creation of ileostoma. Long-term results of treatment allow recommendations of these operations for use in pediatric practice.

Adenomatous Polyposis Coli↗
PubMed2000

Polyethylene glycol 8000 and colon carcinogenesis: inhibition in the F344 rat, promotion in the Min mouse.

It has recently been reported that 5% polyethylene glycol 8000 (PEG 8000; Mr 8000) in the diet markedly inhibits the development of colonic tumors in carcinogen-treated rats. To assess the possible use of this agent as a preventive or treatment agent for patients with familial adenomatous polyposis, we determined the effect of PEG 8000 on spontaneous carcinogenesis in the Min mouse. PEG at a 5% concentration in the diet of Min mice did not affect the number of small intestinal or cecal tumors but did increase the number of colon tumors and the number of animals with colonic tumors (2 of 18 versus 12 of 22 animals; P < 0.001). Although the chemopreventive effect of PEG 8000 in rats is remarkable, we suggest a cautious approach in long-term testing of PEG as a chemopreventive agent for subjects at risk for colonic neoplasia.

Adenomatous Polyposis Coli↗
PubMedDate not supplied

[Potential use of current X-ray contrast studies in the detection of small intestinal polyps in the Peutz-Jeghers syndrome].

The paper presents the results of studies of the small bowel in 9 patients with the Peutz-Jeghers syndrome. The indications for the study were the clinical picture of gastrointestinal bleeding and the symptoms of ileus. The author's intubation enterographic procedure using the better composition of barium suspension and an infusion system for administering contract substances into the small bowel, an improved fractional contrasting procedure, and a procedure employing the agent Entero-view was applied for contrasting the small bowel. All the procedures revealed an obvious picture of polyposis of the small bowel. The minimum size of detected tumors was 0.3-0.4 cm in diameter. Emphasis is laid on the quantitative image of neoplasms with Entero-view and the therapeutic effect of intubation enterography in evolving small-small intestinal intussusception.

Adolescent↗
PubMed1993

Neoplastic transformation arising in Peutz-Jeghers polyposis.

PURPOSE AND METHODS: To clarify the potential for malignancy of Peutz-Jeghers polyposis, we investigated 75 gastrointestinal polyps resected surgically or endoscopically from seven patients with this syndrome. RESULTS: There were 19 polyps in the stomach, 18 in the duodenum, 22 in the small intestine, and 16 in the large intestine, and these were histologically composed of 1 pyogenic granuloma, 1 cancer in adenoma, 2 adenomas, and 71 Peutz-Jeghers polyps. Nine of these Peutz-Jeghers polyps were accompanied by an adenomatous component, and, in addition, two of these showed a cancerous transformation with stalk invasion. A total of 12 neoplastic polyps (16 percent) were found in three relatively young patients (aged 20, 25, and 43 years), all of which were pedunculated and located either in the duodenum or in the jejunum. There was no statistical significance in size between the neoplastic polyps (mean +/- SD, 20.1 +/- 10.8 mm) and the completely hamartomatous polyps (mean +/- SD, 15.8 +/- 9.0 mm). Moreover, the configuration of these types of polyps seemed similar. CONCLUSION: Neoplastic transformation is not a rare event, and our results may indicate evidence of a hamartoma-adenoma-carcinoma sequence in Peutz-Jeghers polyposis.

Adolescent↗
PubMed1999

The genetic background modifies the spontaneous and X-ray-induced tumor spectrum in the Apc1638N mouse model.

The effect of the genetic background on the tumor spectrum of Apc1638N, a mouse model for attenuated familial adenomatous polyposis (FAP), has been investigated in X-irradiated and untreated F1 hybrids between C57BL/6JIco-Apc1638N (B6) and A/JCrIBR (A/J), BALB/cByJIco (C) or C3H/HeOuJIco (C3). Similar to the ApcMin model, the Apc1638N intestinal tumor multiplicity seems to be modulated by Mom1. Moreover, several additional (X-ray-responsive) modifier loci appear also to affect the Apc1638N intestinal tumor number. The genetic background did not significantly influence the number of spontaneous desmoids and cutaneous cysts in Apc1638N. In general, X-irradiation increased the desmoid multiplicity in Apc1638N females but had no effect in males. The opposite was noted for the cyst multiplicity after X-rays. Surprisingly, X-irradiated CB6F1-Apc1638N females were highly susceptible to the development of ovarian tumors, which displayed clear loss of the wild-type Apc allele.

Adenomatous Polyposis Coli↗
PubMed1994

Glutathione S-transferase Mu phenotype in patients with familial adenomatous polyposis and in unaffected controls.

Patients with familial adenomatous polyposis (FAP) are at high risk for duodenal tumors, the distribution of which suggests that bile is important in their development. Studies of the bile of FAP patients suggest that it contains an excess of active carcinogens. Defective hepatic metabolism of carcinogens might account for these findings. The isozyme glutathione S-transferase mu (GST-mu) plays a major role in the hepatic metabolism of carcinogens. Peripheral blood GST-mu status reflects hepatic GST-mu status. The concentration of GST-mu was therefore measured by enzyme-linked immunosorbent assay of heparinized peripheral blood samples taken from 31 unrelated patients with FAP and from 38 unrelated control patients. FAP and control patients were matched for age, sex, diet, and smoking status. The median GST-mu concentration (micrograms per milliliter) was 0.5 (interquartile range, 0 to 11.6) in the FAP group and 8.85 (0.9 to 29.4, p = 0.0013) in the control group. Of the 31 FAP patients, ten had no detectable GST-mu activity compared with only one of the 38 controls (p = 0.002), while 71% of FAP patients had GST-mu concentrations less than a supplied positive control, compared with 50% of control patients (p = 0.064). Abnormal hepatic metabolism of carcinogens by GST-mu might contribute to the development of intestinal tumors in patients with FAP.

Adenomatous Polyposis Coli↗
PubMed1990

[Intestinal polyps in childhood].

From 1965 to 1987, 230 polypectomies were performed in patients between 8 month to 16 years old, 147 boys and 83 girls. The most frequent symptom was rectal bleeding and the most frequent location was the rectosigmoid (96%). The polyps measured from 0.8 to 2 cm., in only one case the polyp measured more than 5 cm. causing duodenal obstruction and it was associated with a gastric polyp. Solitary polyps represented 93.9% of all cases, Peutz-Jeghers syndrome 1.73 and juvenile polyposis 0.87%. In that period 3 cases of colonic carcinoma in children over 9 years old were diagnosed. The histology of 200 polyps were reviewed. In 21 cases the diagnosis was modified (10.5%). The juvenile polyp (J.P.) was the most frequent type (93%). The usual histopathological pattern was observed in 71.5% of the J.P., early lesions (26.3%) and hyperplastic changes (2.1%). Six cases were tubular adenoma and one tubulovillous. The multiple juvenile polyposis was found in girls (13 and 14 years old). None of the patients with Peutz-Jeghers syndrome had gonadal tumor. Endoscopic polypectomy in children is a safe and effective treatment for colorectal polyps. This study provides information on the clinicopathologic findings in argentinian children with intestinal polyps treated by polypectomy over a 22 year period. It emphasizes that juvenile polyps is the most frequent pattern however other lesions can be present in gastrointestinal tract and also associated with others tumors. Patients with polyps should be followed at regular intervals which can be modified according to the histologic type and family history.

Adenoma↗