Search PubMedSearch

PubMed · 8311790

Hyperplastic polyps.

Abstract

A colonoscopy and colonoscopic polypectomy service was established at Wellington Hospital, New Zealand in April 1975. Between April 1975 and March 1990 1157 polyps were either removed or biopsied and examined histologically. Twenty-five polyps were lost. Patient-age seemed to increase through the spectrum hyperplastic, tubular, tubulovillous, villous, and polypoid carcinoma. Sessile < 6 mm in diameter hyperplastic polyps were more numerous than small adenomatous polyps. Pedunculated tumours were most commonly adenomata in all sizes, whereas sessile tumours in the rectum and sigmoid colon were usually hyperplastic. As polyp size increased the numbers of hyperplastic polyps decreased relative to the numbers of adenomatous polyps. The majority of hyperplastic polyps were found in the distal colo-rectum. Site distribution for hyperplastic polyps corresponded to the site distribution for colorectal carcinomata. One of five patients with hyperplastic index polyps was found to have an adenomatous polyp at follow-up. Strong evidence for a sequential relationship between hyperplastic and adenomatous polyps was not found in this study. It is unlikely that an aggressive attitude to the investigation and removal of hyperplastic polyps will have a significant effect on the later development of colorectal cancer.

Explore related subjects

Keep this discovery

Explore connections, maps & timelines

BibTeXRIS

W H Isbister. 1993. Hyperplastic polyps.. https://doi.org/10.1111/j.1445-2197.1993.tb00513.x

Cite the original work for its findings. Save a collection to share your selection of sources.

KEEP EXPLORING

Related citations

Risk of colorectal cancer in the families of patients with adenomatous polyps. National Polyp Study Workgroup.

BACKGROUND: The adenoma-adenocarcinoma sequence in colorectal cancer suggests an increased risk of colorectal cancer in the families of patients with adenomatous polyps. METHODS: A random sample of participants in the National Polyp Study who had newly diagnosed adenomatous polyps were interviewed for information on the history of colorectal cancer in their parents and siblings. The risk of colorectal cancer in family members was analyzed according to the characteristics of the patients with adenomas and in comparison with a sample of patients' spouses, who served as controls. RESULTS: Among the patients with adenomas, 1199 provided information on whether they had a family history of colorectal cancer. After the exclusion of families for which information was incomplete and of 48 patients who had been referred for colonoscopy solely because they had a family history of colorectal cancer, there were 1031 patients with adenomas, 1865 parents, 2381 siblings, and 1411 spouse controls. The relative risk of colorectal cancer, adjusted for the year of birth and sex, was 1.78 for the parents and siblings of the patients with adenomas as compared with the spouse controls (95 percent confidence interval, 1.18 to 2.67). The relative risk for siblings of patients in whom adenomas were diagnosed before 60 years of age was 2.59 (95 percent confidence interval, 1.46 to 4.58) as compared with the siblings of patients who were 60 or older at the time of diagnosis and after adjustment for the sibling's year of birth and sex and a parental history of colorectal cancer. The risk increased with decreasing age at the time of the diagnosis of adenoma (P for trend < 0.001). The relative risk for the siblings of patients who had a parent with colorectal cancer, as compared with those who had no parent with cancer, was 3.25 (95 percent confidence interval, 1.92 to 5.52), after adjustment for the sibling's year of birth and sex and the patient's age at diagnosis. CONCLUSIONS: Siblings and parents of patients with adenomatous polyps are at increased risk for colorectal cancer, particularly when the adenoma is diagnosed before the age of 60 or--in the case of siblings--when a parent has had colorectal cancer.

Adenomatous Polyps

Telomerase activity associated with acquisition of malignancy in human colorectal cancer.

Shortening of telomeres may contribute to the control of the proliferative capacity of normal cells, and telomerase, the enzyme that elongates telomeric DNA, may be essential for unlimited cell proliferation. We have shown previously that telomerase activity is present in human cells immortalized in vitro and in metastatic ovarian carcinoma cells but is undetectable in normal cultured cells or normal tissues. We have determined the temporal pattern of telomerase activity during colorectal carcinogenesis in man. We report that telomerase activity is associated with acquisition of malignancy as it is detectable in colorectal carcinoma but not in adenomatous polyps. Mutations leading to reactivation or upregulation of the enzyme may represent an additional required event in the multistep development of colorectal cancer.

Adenomatous Polyps

Expression of prostaglandin G/H synthase-1 and -2 protein in human colon cancer.

Prostaglandin G/H synthase (PGHS), a key enzyme leading to the formation of prostaglandins, is the target of nonsteroidal antiinflammatory drugs. Two forms of the enzyme have been identified, PGHS-1 and PGHS-2. Epidemiological evidence has suggested that aspirin and other nonsteroidal antiinflammatory drugs may reduce the risk of colorectal cancer. We examined by immunoblot analyses the expression of human PGHS-1 and PGHS-2 protein in 25 matched colon cancer and nontumor tissues, 4 premalignant polyps, 5 control colon tissues from noncancer patients, and 3 matched normal and cancerous breast tissue samples. PGHS-1 was detected in all normal and tumor tissue. In contrast, PGHS-2 was not detected in 23 of 25 normal colon tissues but was detected in 19 of 25 colon tumors. PGHS-2 protein was not observed in four human premalignant polyp samples, control colon from noncancer patients, or matched normal or cancerous breast tissues. These results suggest that the beneficial effects of nonsteroidal antiinflammatory drugs in colon cancer may be mediated by inhibition of PGHS-2.

Adenomatous Polyps