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PubMed1992

[A cellular proliferation study in patients with colorectal cancer, solitary, synchronous and with polyps].

Colonic carcinogenesis is probably related to a disturbance in cell proliferation of the colonic mucosa. The present study was designed to determine whether patients with adenomatous polyps of the colon, which have a tendency to develop synchronous malignancies of the colon, have any disturbance in mucosal cell proliferation. Using flow cytometry the proliferative index, and the S and G2M phases of normal mucosa and tumoral tissue of patients with colorectal cancer (synchronous, alone, or associated with adenomatous polyps) were studied. No differences were found between the there groups of study at the level of proliferation pattern of normal mucosa. Our findings do not support the development of synchronous or metachronous colon cancer in patients with polyps on the basis of different patterns of cell proliferation.

Aged↗

PubMed1992

Distal colonic hyperplastic polyps do not predict proximal adenomas in asymptomatic average-risk subjects.

The significance of distal colonic hyperplastic polyps was investigated in 482 asymptomatic average-risk subjects, aged 50-75 years, in whom fecal occult blood test results were negative and who underwent screening colonoscopy. The incidence of adenomas in the colon proximal to the sigmoid-descending colon junction in subjects with hyperplastic polyps distal to that point was 18% and was similar to the incidence of proximal colonic adenomas in subjects with no distal colonic polyps (15%). The incidence of proximal colonic adenomas in subjects with no distal colonic adenomas was 38% and was significantly greater than the incidence found in individuals with no distal colonic polyps or only hyperplastic polyps. Our data do not support distal colonic hyperplastic polyps as markers for proximal colonic adenomas in asymptomatic average-risk subjects.

Adenoma↗

PubMed1990

Risk and surveillance of individuals with heritable factors for colorectal cancer. WHO Collaborating Centre for the Prevention of Colorectal Cancer.

Heritable and genetic factors pertinent to colon cancer can be divided into three categories: inherited syndromes, genetic epidemiology, and molecular genetics. Familial adenomatous polyposis (FAP) and Gardner syndrome (GS) are rare dominantly inherited syndromes characterized by hundreds to thousands of colonic adenomatous polyps. Colon cancer occurs at a young age in both diseases unless the colon is removed. Peutz-Jeghers syndrome and familial juvenile polyposis are inherited hamartomatous polyposis conditions with a less dramatic, but definite, increased risk for colon cancer. These four polyposis syndromes together account for less than 1% of cases of colon malignancy. Hereditary nonpolyposis colorectal cancer is a dominantly inherited form of colon cancer characterized by an early age of onset and a predilection for proximal colonic tumours. Multiple primary malignancies are frequently observed and one or several adenomatous polyps are often present in affected individuals; 4-6% of colon cancer cases occur in relationship to this syndrome. Genetic epidemiological studies have consistently shown that first-degree relatives of persons with colon cancer have a twofold to threefold increased risk of having colon malignancy. More recent studies have found a similar risk among relatives of those with adenomatous polyps. Studies of colon cancer and adenomatous polyps in pedigrees have further demonstrated that this familial clustering probably occurs on the basis of partially penetrant inherited susceptibilities. These inherited susceptibilities probably interact with environmental factors to give rise to polyp growth and finally colon cancer. Molecular studies have begun to elucidate the genetic mechanisms of colon cancer at the DNA level. The germinal mutation of FAP and GS has been localized to the long arm of chromosome 5. Tissue samples from "random" adenomatous polyps and colon cancers have shown frequent and specific acquired DNA sequence deletions on chromosomes 5, 17, and 18. Mutations and over-expression of the ras oncogene likewise have been observed in such tissues. The chromosome 5 defect in polyp and cancer tissues is probably at the same locus as the germinal mutation of FAP. There is evidence that this locus normally regulates expression of the c-myc oncogene, which in turn probably has a regulatory function in DNA replication. The chromosome 17 deletion is a mutation of the gene for the transformation-associated protein, p53. Appropriate screening starting at a relatively young age is necessary to prevent cancer in the inherited syndromes. Screening is also indicated in close relatives of those with nonsyndromic or common colon cancer in view of the moderately increased risk for colon cancer in this group.(ABSTRACT TRUNCATED AT 400 WORDS)

Colorectal Neoplasms↗

PubMed1995

Distribution of adenomatous polyps in African-Americans.

OBJECTIVES: Previous research has suggested that polyps and colon cancer occur more commonly in the right colon in African-Americans compared with the general population. The purpose of this study is to determine the pattern of distribution of colonic polyps in African-Americans. METHODS: We retrospectively evaluated 141 colonoscopies in which 179 polypectomies were done. The polyps were described on the basis of anatomical distribution, gross description, size, and histology. Sixty-nine males and 72 females had colonoscopic polypectomies. The mean age was 67 yr (range, 43-91 yr). RESULTS: Seventy-seven (43%) were classified as left sided, and 102 (57%) were right sided. Left-sided polyps were more likely to be pedunculated than right-sided polyps (p < 0.01). Larger polyps were more common on the left side than the right side (p < 0.01), but villous histology was almost as high on the right side as on the left side. Polyps that had the highest malignant potential were found almost as commonly on the right side as on the left side. CONCLUSIONS: This study supports previous work that suggests that there is a significant shift to the right in the anatomical distribution of polyps in African-Americans. It also shows that the malignant potential is as high for right-sided polyps as it is for those on the left. Current screening recommendations may not be effective enough for preventing colon cancer in this population.

Adult↗

PubMed1996

Inward growth of colonic adenomatous polyps.

BACKGROUND & AIMS: Most colon cancers arise from polypoid adenomas, but how these benign lesions develop into malignant neoplasms is not understood. This study examined the migration of epithelial cells within human adenomatous polyps by determining the distribution of proliferating and apoptotic cells and immunoreactivity to transforming growth factor beta (TGF-beta). METHODS: Sections of surgically resected normal (n = 10) and adenomatous (n = 22) formalin-fixed tissue were examined for proliferating cells and TGF-beta isoenzymes 1-3 by immunohistochemistry and apoptotic cells by terminal deoxyuridine nick end-labeling. RESULTS: The distribution of proliferating, apoptotic, and TGF-beta immunoreactive cells was strikingly reversed in adenomatous polyps compared with normal mucosa. Proliferating cells were located in the base of normal colonic crypts and TGF-beta immunoreactive and apoptotic cells near or at the luminal surface, corresponding to the normal migration of colonocytes. In adenomas, increased numbers of proliferating cells were mainly located at the luminal surface and TGF-beta immunoreactive and apoptotic cells were located principally at the crypt base. CONCLUSIONS: This distribution suggests that cell migration in adenomas is not toward the lumen but instead inward toward the polyp base.

Adenomatous Polyposis Coli↗

PubMed1990

[Colonic neoplasms and skin fibromas: common determinants and their significance].

To find common factors for colonic-neoplasias and skin-tags, 157 inpatients, who consecutively had a coloscopy because of intestinal complaints, were intensively examined dermatologically. Regression-analyses showed that the number of colonic polyps were age- (p = 3 x 10(-8)) and sex-dependent (1.9 x 10(-2)) and skin-tags had no influence on the number of colonic polyps. The size of colonic polyps also showed a clear age dependency (p = 3 x 10(-8)). The number of skin-tags were dependent on weight (p = 9 x 10(-3)) and age (p = 1.3 x 10(-2)), its size on the interaction of sex and triglyceride-levels (p = 3 x 10(-8)). Discriminant-analyses identified the following factors as important: age and triglyceride-concentration to recognize a patient with colonic polyps; age, positive Haemoccult-test and number of skin-tags to recognize a patient with tubulovillous adenomas or colonic carcinomas. The essential common factor of colonic polyps and skin-tags was the age. For the recognition of a patient with colonic polyps the age was the most essential factor, skin-tags, on the contrary, were unimportant. The association between colonic polyps and skin-tags therefore was merely an effect of age.

Age Factors↗

PubMed1997

Group II phospholipase A2 is not a major modifier of colonic adenomatous polyps in humans.

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Adenomatous Polyposis Coli↗

PubMed2004

Nonfamilial juvenile polyposis coli in a child: report of a case.

Juvenile polyposis coli (JPC) is an uncommon condition, manifesting as hamartomatous gastrointestinal polyposis with potential malignancy. This report describes a 15-month-old girl who was diagnosed to have nonfamilial JPC accompanied by macrocephaly, clubbed fingers, and mental retardation. Radiography of the colon by a barium enema and total colonoscopy demonstrated numerous colonic polyps. A barium meal study did not show any abnormality in the stomach, duodenum, or small intestine. She died at 6 years of age from hemorrhagic shock due to massive lower gastrointestinal bleeding associated with a rectal prolapse. The related literature is reviewed, and the treatments and complications of JPC in children are also discussed. We emphasize that family members of patients diagnosed with juvenile polyposis should be questioned and undergo appropriate examinations of the entire intestine from the stomach to the rectum.

Adenomatous Polyps↗

PubMed1984

Prospective evaluation of hospitalized patients with nonactive lower intestinal bleeding--timing and role of barium enema and colonoscopy.

A prospective evaluation of 176 hospitalized patients with nonactive lower intestinal bleeding demonstrated that a barium enema is not a necessary prerequisite for a sensitive and safe total colonoscopic examination. Colonoscopy was better in detecting colonic polyps and colon cancers than barium enema. It was concluded that colonoscopy without prior barium enema provides a sensitive diagnostic approach to hospitalized patients with nonactive lower intestinal bleeding. This approach does not interfere with the early use of angiography and may shorten hospitalization.

Adult↗

PubMed1999

Laparoscopic-assisted colonoscopic polypectomy: technique and preliminary experience.

BACKGROUND: The majority of colonic polyps found at endoscopy are suitable for diathermy snare excision via colonoscope. Due to location or size, some are deemed unsafe to treat in this manner and therefore require colectomy. This study describes the technique and early results of a laparoscopic-assisted colonoscopic polypectomy technique that can be used to manage such polyps and thereby avoid laparotomy and colectomy. METHODS: Colonoscopy with simultaneous laparoscopy was utilized to locate the site of the polyp. The colon was mobilized, if required, and the polyp resected by electrosurgical snare via the colonoscope while the serosal aspect of the colon was monitored laparoscopically. RESULTS: The technique has been tried successfully in six patients. Three polyps were in the cecum and three were within the left colon. The size of the polyps ranged from 3 to 7 cm. All polyps were benign on histological examination. The patients were discharged on the day following the procedure. There were no complications. CONCLUSIONS: The combination of laparoscopy with colonoscopic resection of a select group of large polyps represents a safe alternative to colonic resection.

Adult↗

PubMed1981

Colonic adenomatous polyp with focal squamous metaplasia.

A case of adenomatous polyp of the colon with focal squamous metaplasia is reported. Squamous metaplasia has been described in both neoplastic and non-neoplastic conditions of the colon. However, it has not previously been documented to occur in adenomatous polyp. The histogenesis, possible predisposing factors, and clinical significance of the lesion are discussed.

Adenoma↗

PubMed1995

Serum retinoic acid levels in patients with resected benign and malignant colonic neoplasias on beta-carotene supplementation.

To determine whether patients with colon cancer metabolize beta-carotene differently from benign colon polyp patients, a normal control group (n = 13) and groups of resected colon polyp patients (n = 29) or resected colon cancer patients (Dukes A and B1, n = 21) were supplemented with placebo or beta-carotene (30 mg/day) taken with their morning meals for three months. Serum samples at zero and three months of the study were analyzed blindly for retinoic acid and beta-carotene. The results showed that beta-carotene levels in the serum of colon polyp and colon cancer groups were 8- to 12-fold higher than in the untreated control or the placebo-treated groups. The benign polyp subjects (n = 17) receiving beta-carotene showed a significant rise in serum trans-retinoic acid at three months compared with Time 0. The trans-retinoic acid values from the colon cancer group receiving beta-carotene (n = 11) or placebo (n = 10) were significantly lower than the values from the beta-carotene-supplemented colon polyp group. It appears that trans-retinoic acid levels in response to beta-carotene supplementation are different between treated cancer and benign patients because of different body demands for retinoic acid.

Adult↗

PubMed1994

Knowledge of the adenomatous polyposis coli gene and its clinical application.

Familial adenomatous polyposis (FAP) is one of the most clearly defined and well understood of the inherited colorectal cancer syndromes. It is an autosomal dominant condition with high (> 90%) penetrance. Clinically, it is characterized by multiple (> 100) adenomatous polyps in the colon and rectum; variant features in addition to the colonic polyps may include polyps in the upper gastrointestinal tract and other extracolonic manifestations. Since the risk of colorectal cancer in untreated FAP is virtually 100%, screening and intervention for at-risk persons has consisted of annual colon examinations by endoscopy beginning around puberty. The objective of this regimen is early detection of colonic polyps in those who have FAP, followed by preventive colectomy. Because of recent findings that most cases of FAP are due to mutations of the adenomatous polyposis coli gene at chromosome 5q21, genetic testing will probably be incorporated as the first step in the management of individuals at risk for this condition, and screening regimens can be modified. Genetic counselling about the consequences of presymptomatic gene testing is an important component of this process.

Adenomatous Polyposis Coli↗

PubMed2006

Ligand activation of peroxisome proliferator-activated receptor beta inhibits colon carcinogenesis.

There is considerable debate whether peroxisome proliferator-activated receptor beta/delta (PPARbeta/delta) ligands potentiate or suppress colon carcinogenesis. Whereas administration of a PPARbeta ligand causes increased small intestinal tumorigenesis in Apc(min/+) mice, PPARbeta-null (Pparb-/-) mice exhibit increased colon polyp multiplicity in colon cancer bioassays, suggesting that ligand activation of this receptor will inhibit colon carcinogenesis. This hypothesis was examined by treating wild-type (Pparb+/+) and Pparb-/- with azoxymethane, coupled with a highly specific PPARbeta ligand, GW0742. Ligand activation of PPARbeta in Pparb+/+ mice caused an increase in the expression of mRNA encoding adipocyte differentiation-related protein, fatty acid-binding protein, and cathepsin E. These findings are indicative of colonocyte differentiation, which was confirmed by immunohistochemical analysis. No PPARbeta-dependent differences in replicative DNA synthesis or expression of phosphatase and tensin homologue, phosphoinositide-dependent kinase, integrin-linked kinase, or phospho-Akt were detected in ligand-treated mouse colonic epithelial cells although increased apoptosis was found in GW0742-treated Pparb+/+ mice. Consistent with increased colonocyte differentiation and apoptosis, inhibition of colon polyp multiplicity was also found in ligand-treated Pparb+/+ mice, and all of these effects were not found in Pparb-/- mice. In contrast to previous reports suggesting that activation of PPARbeta potentiates intestinal tumorigenesis, here we show that ligand activation of PPARbeta attenuates chemically induced colon carcinogenesis and that PPARbeta-dependent induction of cathepsin E could explain the reported disparity in the literature about the effect of ligand activation of PPARbeta in the intestine.

Animals↗

PubMed2004

Colonic neoplastic polyps: biopsy is not efficient to exclude malignancy. The Trafford experience.

The biological behaviour of the polyp depends entirely on its histological subtype. Adenomas are the classic precursors to carcinoma. Polyp biopsy can differentiate neoplastic (adenoma and carcinoma) from non-neoplastic polyps (hyperplastic, inflammatory, hamartomatous). Due to potential sampling error, biopsy does not always differentiate between adenoma and carcinoma. Our aim was to investigate the degree of this potential sampling error. We carried out a study to compare the results of biopsies vs. total tissue examinations in a cohort of 433 neoplastic polyps. In this study 18.5% of carcinomatous polyps show definitive malignant elements only when the entire polyp is presented to the pathologist. We have therefore adopted a special reporting template if the polypoidal tumour is either biopsied or incompletely excised. The study also showed that within adenomas there could be variance of architectural patterns between the biopsy and the whole specimen. In this series, biopsying malignant colonic polyps gives rise to 18.5% false negative results and therefore it is significantly less efficient in the diagnosis of malignancy compared to total polyp examination.

Adenoma↗

PubMedDate not supplied

[Report of a case of Gardner's syndrome: clinical and epidemiologic considerations and review of the literature].

Familial adenomatous polyposis is a hereditary clinical syndrome characterised by the presence of numerous adenomatous polyps of the colon and rectum and by lesions in other organs. The disease affects various different tissues and characteristically presents a variable biological and clinical behaviour. Colon polyps are precancerous lesions and the certainty of their malignant evolution within the 3rd-4th decades of life is now practically an established, extensively documented fact. Recently, new methods of genetic screening, prevention and early diagnosis and, as a result, more advanced treatment protocols have been introduced in clinical practice, thus offering young patients diagnosed as suffering from familial adenomatous polyposis better prospects and a better quality of life. The patient in our case came in for medical observation for abdominal pain experienced close to the scar of a previous appendectomy and for the presence of an abdominal tumefaction on the same side. Initially the patient underwent surgical resection of the growth that proved to be a desmoid tumour of the abdominal wall. The results of the pathology examination and the patients' long-term disease and family history led to a presumptive diagnosis of familial adenomatous polyposis, which was then confirmed by the appropriate instrumental examinations. Genetic tests on the patient's relatives yielded the same diagnosis in some of them. On the basis of our personal experience and a thorough review of the literature we can safely state that no medical treatment currently available is capable of reducing, let alone definitively eliminating colon polyps. To date, then, the therapeutic options most commonly adopted are colectomy with ileo-rectal anastomosis and total conservative proctocolectomy with an ano-ileal pouch anastomosis. These two types of surgical procedures yield different results in terms of functional capability and oncological radicality with their respective repercussions on the patient's quality of life. The choice of the most appropriate surgical procedure is made on the basis of a series of parameters such as age, site of the polyps, number of polyps, degree of cell atypia of the polyps, and patient willingness to undergo regular check-ups. The current tendency advocated by the various authors is to perform a total colectomy as soon as possible.

Adolescent↗

PubMed2005

[The association of obesity and left colonic adenomatous polyps in Korean adult men].

OBJECTIVES: We wanted to evaluate the relationship between obesity and left colonic adenomatous polyps in Korean adult men. METHODS: This study was conducted among 575 adults men (aged between 40 and 69), who had colonoscopy done from January to December 2002 during a routine health examination at Health Promotion Center, Ulsan University Hospital. The patients' colons were examined up to splenic flexure by using fiberoptic colonoscopy. A questionnaire survey on behavioral factors and physical measurements were also done. The body mass index (BMI) and waist-hip ratio (WHR) were used as the indices of obesity. The BMI was categorized into three levels: normal (BMI < or = 22.9), overweight (23 < or = BMI < or = 24.9), and obese (BMI > or = 25.0). The WHR was categorized into four levels with cut-off points at the 30th, 60th, and 90th percentile of the control group. Age, education, smoking, alcohol use and exercise were controlled for by performing multiple logistic regression analysis. RESULTS: There were 99 cases of colonic adenomatous polyps. Four hundred seventy six subjects with normal colonoscopy findings served as the control. The BMI and WHR were associated with the adenomatous polyps (odds ratio, 1.81 [95% CI=1.02-3.19] for a BMI > or = 25.0 as compared with a BMI < or = 22.9, odds ratio, 3.94 [95% CI = 1.77-8.77] for a WHR > or = 0.95 as compared with a WHR < or = 0.86). The BMI was not associated with the risk of adenomatous polyps after additional adjustment was made for the WHR, but the association between the WHR and adenomatous polyps was still positive and independent of the BMI (odds ratio, 4.15 [95% CI=1.63-10.59]). CONCLUSIONS: The results support that obesity, and particularly abdominal obesity, can be associated with an increased risk of incurring colonic adenomatous polyps.

Adenomatous Polyps↗

PubMed1995

Effect of beta-carotene supplementation on indices of colonic cell proliferation.

BACKGROUND: Epidemiologic studies have shown that consuming foods containing beta-carotene is associated with a decreased incidence of colon cancer. The validity of this association has recently been questioned. It is not known if the rate of colonic cell proliferation differs among individuals with or without a history of colonic polyps or cancer and if proliferation changes in response to beta-carotene. PURPOSE: This study was intended to (a) determine whether differences exist in colonic cell proliferation in individuals with and without prior colonic polyps or tumors, (b) demonstrate that beta-carotene accumulates in colonic mucosa following dietary supplementation, and (c) determine whether mucosal beta-carotene accumulation influences colonic cell proliferation. METHODS: Subjects were enrolled in the phase I study from June 1991 until February 1994. The participants included 20 individuals (11 males and nine females, aged 62.3 +/- 8.9 years [means +/- SD]) with normal colons (as judged by recent colonoscopy), 40 (24 males and 16 females, aged 59.6 +/- 10.1 years) with a history of colonic polyp(s), and 41 (30 males and 11 females, aged 67.2 +/- 9.7 years) with prior colon cancer. The subjects in the last two groups consumed either 30 mg of beta-carotene or placebo each morning for 3 months. This dose of beta-carotene has no known toxic effects, but it can increase the serum level by approximately 10-fold. beta-carotene concentration in serum and colonic tissue was quantitated by high-pressure liquid chromatography in samples collected before and after supplementation with beta-carotene or placebo. Cellular proliferation was assessed on the basis of tissue ornithine decarboxylase activity, urinary polyamine excretion, and proliferating cell nuclear antigen expression. The differences in colonic cell proliferation parameters due to beta-carotene supplementation, within and among different groups, were evaluated by the Wilcoxon matched-pairs signed ranked test and the Mann-Whitney test, respectively. All statistical tests were two-sided. RESULTS: Colonic cell proliferation did not differ in samples obtained from individuals with and without prior colonic polyp(s) or cancer. beta-carotene concentrations in serum and colonic tissue were significantly increased in groups receiving beta-carotene (P < .001). However, cell proliferation did not differ, as judged by any of the three measures, among samples from all experimental groups collected before and after supplementation with beta-carotene. CONCLUSIONS: Dietary supplementation with beta-carotene for a period of 3 months does not alter colonic cell proliferation in individuals with a history of colonic polyps or cancer. IMPLICATIONS: The mechanism by which beta-carotene might reduce colon cancer incidence does not appear to involve or result in a change in cell proliferation in the normal colonic mucosa as studied in individuals with a history of colonic polyps or cancer.

Adult↗