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PubMed1983

Peanut lectin-binding sites in polyps of the colon and rectum. Adenomas, hyperplastic polyps, and adenomas with in situ carcinoma.

Peanut lectin (PNA) has a specificity for the disaccharide beta-D-Gal-(1 leads to 3)-D-GalNac which is the purported antigenic determinant for the T blood group antigen (TAg). This TAg is considered the immediate precursor of the MN blood group substance. In normal colonic epithelium, PNA binds to the supranuclear (stalk) portion of epithelial cells. This corresponds to the detection of beta-DGal-(1 leads to 3)-D-GalNac in nascent oligosaccharide chains in the Golgi cisternae prior to addition of terminal sialic acid. Colonic carcinomas bind PNA in the "region" of the glycocalyx or in the apical portion of the cell, which represents incomplete glycoprotein synthesis. Eighty-two percent of tubular adenomas, 80% of villous adenomas, and 91% of adenomas with in situ cancer expressed PNA in a supranuclear distribution, reminiscent of normal colonic epithelium. This stalk distribution was seen in goblet cells. Twenty-five percent of tubular adenomas, 43% of villous adenomas and 60% of adenomas with in situ cancer (adenoma portion) expressed PNA in an apical cytoplasmic and/or glycocalyx pattern among nonmucinous columnar cells. In 80% of the cases, the in situ cancer itself expressed PNA in an apical cytoplasmic and/or glycocalyx pattern. Fetal and most colon cancer cells fail to produce mucin goblets and make incomplete glycoproteins. The cytologic localization of TAg by PNA corresponds to the cells' ability to produce mucin goblets. Most adenomas consist of goblet cells, localize TAg to the stalk, and probably make complete MN glycoprotein as does normal colonic epithelium. However, in adenomas, nonmucinous columnar cells localize TAg to the apical cytoplasm and/or glycocalyx region and represent incomplete blood group glycoprotein synthesis.

Adenoma↗
PubMed1995

A pilot study of DNA aneuploidy in colorectal adenomas and risk of adenoma recurrence.

This case-control study examined whether DNA aneuploidy in colorectal adenomas is a risk factor for subsequent adenoma recurrence. Cases (recurrent polyp formers) were defined as persons with diagnoses of new adenomas at 2 colonoscopies following the index (first) adenoma diagnosis; controls were persons with no new adenomas at a follow-up at least 1 year after the index diagnosis. Cases (n = 22) and up to 3 controls (n = 29) were matched for factors known to be associated with polyp recurrence or aneuploidy: (a) age; (b) histology; (c) number of index polyps; and (d) size of largest index polyp. The largest adenoma from the index colonoscopy was removed from the paraffin block and analyzed for DNA content abnormalities by flow cytometry. On the basis of the observed distribution of aneuploidy in case-control sets, the point estimate for the relative odds of recurrence given aneuploidy in the index polyp was infinity (P < 0.035), and the lower bound for the 95% confidence interval was 2.02. We conclude that in this convenience sample, DNA aneuploidy increased the risk of recurrent colorectal adenomas. Larger, preferably prospective studies are needed before DNA content flow cytometric analysis of colorectal adenomas can be recommended as a routine clinical practice, but these results do suggest that polyp ploidy should be assessed in research studies using adenomas as end points or intermediate end point markers.

Adenoma↗
PubMed1997

Nuclear area measurements of parathyroid adenoma, parathyroid hyperplasia and thyroid follicular adenoma. A comparison.

OBJECTIVE: To determine whether nuclear area (NA) measurement could help to differentiate parathyroid adenoma, parathyroid hyperplasia and thyroid follicular adenoma in aspirated smears. STUDY DESIGN: Aspirated smears of 15 patients with parathyroid adenoma, 11 patients with parathyroid hyperplasia and 11 patients with thyroid follicular adenoma were included. NA of 100 cells in each case were measured by image analysis; then the mean and coefficient of variation were calculated. RESULTS: There was no statistically significant difference in the mean of NA between parathyroid adenoma and parathyroid hyperplasia, but the former displayed greater NA variation. Thyroid follicular adenoma revealed a significant elevation in the mean of NA when compared with parathyroid lesions and also shared the feature of greater NA variation when compared with parathyroid hyperplasia, as noted in parathyroid adenoma. CONCLUSION: Quantitative assessments on NA and calculation of their coefficient of variation are helpful in differentiating between parathyroid adenoma, parathyroid hyperplasia and thyroid follicular adenoma.

Adenoma↗
PubMed1995

A randomized surveillance study of patients with pedunculated and small sessile tubular and tubulovillous adenomas. The Funen Adenoma Follow-up Study.

BACKGROUND: We wanted to assess the influence of various surveillance intervals on the risk of new neoplasia after removal of pedunculated and small sessile tubular and tubulovillous adenomas. METHODS: After initial colonoscopic polypectomy patients were randomized to surveillance with either 2 years (group A) or 4 years (group B) between colorectal examinations. RESULTS: The cumulated risk of a patient having new adenomas was 35.0% (28.7-41.4%) in group A and 35.5% (28.4-42.7%) in group B after 48 months. The risk increased to 44.9% (36.0-53.9%) and 60.1% (48.5-71.7%), respectively, after 96 months. The risk of significant neoplasia (carcinoma or adenoma with villous structure, severe dysplasia, or diameter > 10 mm) was 5.2% (2.3-8.1%) and 8.6% (3.8-13.3%) after 48 months and 8.6% (4.2-13.0%) and 17.4% (7.6-27.2%) after 96 months. More than one adenoma at first examination was associated with higher risk of new adenomas. Furthermore, we found a tendency for age above 60 years and male gender to be associated with higher risk of new adenomas. More than two adenomas at first examination was the only factor found to be associated with a higher risk of new significant neoplasia. One patient in group A and two patients in group B developed cancer, which is not significantly different from the number expected (3.43) in the average Danish population (RR = 0.9, 0.2-2.6). CONCLUSION: After colonoscopy with removal of all polyps, colorectal examination at 4 years resulted in a similar risk of new adenomas compared with examinations at 2 and 4 years. However, new significant neoplasia tended to be more frequent when first surveillance was at 4 years. Extending the surveillance to 8 years also tended to increase the risk more in the group being examined every 4 years, but reduction of the number of surveillance examinations by more than 50% and a probable reduction of complications from surveillance examinations themselves may justify a recommendation for the longest interval.

Adenoma↗
PubMed1994

Clonal karyotypic abnormalities in colorectal adenomas: clues to the early genetic events in the adenoma-carcinoma sequence.

Cytogenetic analysis of short-term cultures from colorectal adenomas revealed acquired clonal chromosome aberrations in 14 of 17 tumors. In 4 adenomas, only numerical changes were found, whereas 10 had structural rearrangements. Trisomy 7 was found as the sole change in one of the tumors and together with other numerical changes in another. A +7 was also present in one case with structural aberrations. Other recurrent numerical aberrations were -14 and -18, both found in 2 adenomas with structural karyotypic changes; in addition, one chromosome 14 was lost in one of the tumors with only numerical changes. The chromosome most often involved in structural aberrations was chromosome 1. In 6 cases, the rearrangements led to changes in 1p, always with loss of material. The breakpoints were at 1p32-36. One adenoma had deletion of 1p as the only change. Other chromosomes that were involved in changes in more than 2 cases were chromosomes 8, 13, and 17. These rearrangements typically led to gain of 8q and 13q and loss of 17p. The adenomas with structural abnormalities were generally larger and had a higher degree of dysplasia than did the adenomas with numerical changes only or those with a normal karyotype. All adenomas with a tubulovillous or villous architecture had structural rearrangements. Our findings confirm that a subset of colorectal adenomas exists that have only numerical chromosome aberrations. They also support our previous conclusion that loss of material from distal 1p is an early event in colorectal tumorigenesis, but that other cytogenetic aberrations follow and typically are present already at the adenomatous stage.(ABSTRACT TRUNCATED AT 250 WORDS)

Adenoma↗
PubMed1992

[Cystic parathyroid gland adenomas: pathologic-anatomic variants of parathyroid gland adenomas or a separate disease entity?].

Between 01.01.1987 and 31.12.1990 a primary operation was performed on 126 patients in the Dept. of General Surgery, University of Marburg Hospital for primary hyperparathyroidism due to a parathyroid adenoma. Their clinically relevant data were prospectively documented. In 6 patients (4.8%) a total of 7 cystic parathyroid adenomas was found. While there was no difference in age- and sex-distribution, patients with cystic adenomas were found to have markedly higher serum parathormone and alkaline phosphatase levels than patients with solid adenomas. Calcium levels were similar in both groups. Cystic adenomas were much heavier than solid adenomas. A significant number of cystic adenomas was found to be displaced into the posterior mediastinum. The property of cystic parathyroid adenomas to be frequently located away from their usual anatomical position can make the intraoperative search for them difficult.

Adenoma↗
PubMed1991

Lung adenoma structure among inbred strains of mice: the pulmonary adenoma histologic type (Pah) genes.

Urethane-induced, lung adenoma multiplicity and histologic type vary among mouse strains. We asked whether the Pas genes which control multiplicity also determine adenoma structure. Lung adenomas from inbred mice, F1 hybrids, and recombinant inbred mice were classified by growth pattern as either solid or papillary. Since no correlation was observed between adenoma multiplicity and histologic type, no linkage apparently exists between the Pas genes and adenoma morphology. We propose the name Pah (Pulmonary Adenoma Histologic type) for the genes controlling lung adenoma growth patterns. Genetic analysis indicated dominance of the papillary phenotype, and that two or more Pah genes determine adenoma structure.

Adenoma↗
PubMed1997

Distal hyperplastic polyps do not predict proximal adenomas: results from a multicentric study of colorectal adenomas.

BACKGROUND: The association between distal hyperplastic polyps and proximal adenomas is still a matter of debate. We investigated this association while taking into account patient characteristics. METHODS: After exclusion of patients with inflammatory bowel diseases, familial adenomatous polyposis, or any cancer, 3088 eligible consecutive subjects aged 18 to 69 years underwent total colonoscopy in four gastroenterology units. The odds ratios (OR) of having proximal adenomas according to patient characteristics (age, sex, medical center, year of endoscopy, reasons for referral, and distal findings) were estimated in univariate and multivariate analyses. RESULTS: Patients with distal polyps of any type showed an adjusted OR of 2.5 (95% CI [1.9, 3.1] p < .001) of having proximal adenomas as compared with those without distal polyps. When distal adenomas and distal hyperplastic polyps were included in the multivariate model as independent factors, the presence of adenomas significantly increased the risk of proximal adenomas (OR = 2.8: 95% CI [2.2, 3.6] p < .001), whereas the presence of hyperplastic polyps did not (OR = 1.1: 95% CI [0.8, 1.5] p = .64). No association with number, size, or location of distal hyperplastic polyps was seen. CONCLUSIONS: Our data show that the presence of hyperplastic polyps should not be the sole indication for total colonoscopy because they are not associated with proximal adenomas when adjusting for patient characteristics and presence of distal adenomas.

Adenoma↗
PubMed2001

Immunohistochemical aspects of basal cell adenoma and canalicular adenoma of salivary glands.

Basal cell adenoma is a benign epithelial neoplasm with a uniform histologic appearance dominated by basaloid cells. Those cells may be distributed in various arrangements as solid, trabecular, tubular and membranous. Canalicular adenoma is also a benign neoplasm composed by columnar cells arranged in branching and interconnecting cords of single or double cell thick rows. There is some disagreement among investigators about whether canalicular adenoma should be included within the basal cell adenoma histologic spectrum. In the present study we compared the expression of cytokeratins (CK), vimentin and muscle-specific actin, utilizing immunohistochemical technique, in three cases diagnosed as basal cell adenomas predominantly of the solid type, and three cases of canalicular adenomas. The results obtained showed a distinct immunoprofile for both neoplasms. Solid areas of basal cell adenomas did not stain for any of the tested antibodies; only when there was tubular differentiation, those structures expressed CKs 7, 8, 14, and 19 in luminal cells and vimentin in non-luminal cells. On the other hand, canalicular adenomas strongly expressed CKs 7 and 13. The panel of antibodies utilized supports the separation of the two entities.

Actins↗
PubMed2006

Immunonegative "null cell" adenomas and gonadotropin (Gn) subunit (SUs) immunopositive adenomas share frequent expression of multiple transcription factors.

The differentiation of pituitary cells and human pituitary adenomas follow three cell lineages: GH-PRL-TSH, ACTH, and FSH/LH, which are regulated by a combination of various transcription factors and co-factors. We have used RT-PCR and immunohistochemistry to show that immunonegative, "null cell" adenomas are equipped with multiple transcription factors and co-factors. The "null cell" adenomas showed similar frequencies of transcription factors as did the gonadotropin subunit (GnSU)-positive adenomas, with the exception that there were fewer instances of SF1 in the former. We speculate, therefore, that null cell adenomas and GnSU-positive adenomas share common molecular mechanisms in functional differentiation, even though the former do not produce hormones. From the high frequency of various transcription factors, we also speculate that both null cell adenomas and GnSU-positive adenomas are derived from "committed" pituitary progenitor stem cells. The questions, why a certain proportion of these pituitary tumor groups lack hormone production and why they are molecularly more committed to Gn transcription, remain to be further investigated.

Adenoma↗
PubMed1995

In vivo and in vitro evidence for the production of inhibin-like immunoreactivity in human adrenocortical adenomas and normal adrenal glands: relatively high secretion from adenomas manifesting Cushing's syndrome.

To clarify whether adrenal gland secretes inhibin in vivo in physiological or pathological conditions, we measured the levels of inhibin-like immunoreactivity (inhibin-LI) in adrenal veins (A-vein) and compared them with those in inferior vena cava (IVC) using blood samples obtained at catheterization of adrenal vein in the patients with adrenal adenoma manifesting Cushing's syndrome (Cs), aldosterone-producing adenoma, clinically non-functioning adenoma and normal adrenal gland. The tumor sides of A-veins in the patients with adenomas and also both sides of A-veins in subjects with normal adrenal glands showed significantly higher contents of inhibin-LI than their IVC. When the inhibin-LI secretion rate from adrenal gland was estimated by the difference between the levels of A-vein (tumor side) and IVC, Cs adenomas showed the highest secretion rate. Similarly, the tissue inhibin-LI content and the basal secretion rate of inhibit-LI from primary cultured cells were the highest in Cs adenomas. These findings indicated that normal adrenal glands and adrenocortical adenomas produced and secreted inhibin-LI into the general circulation in vivo and Cs adenomas have relatively high capacity for secreting inhibin-LI, and the present study provided the first in vivo evidence for adrenal inhibin-LI production in pathological conditions.

Adrenal Cortex Neoplasms↗
PubMed1994

[A case of normotensive primary aldosteronism in association with non-functioning adenoma and aldosterone producing adenoma in ipsilateral adrenal gland].

A case of normotensive primary aldosteronism in association with non-functioning adenoma and aldosterone producing adenoma in ipsilateral adrenal gland is reported. Fourteen cases of normotensive primary aldosteronism were previously reported and our case was considered as the fifteenth case. Furthermore, its association with non-functioning adenoma and aldosterone producing adenoma is very rare. Only four cases of such association were reported, and in these four cases non-functioning adenoma existed in contralateral side of aldosterone producing adenoma. In our case, its association with non-functioning adenoma and aldosterone producing adenoma was seen in the ipsilateral adrenal gland. The report of this kind of association has not been seen in the literature so far.

Adenoma↗
PubMed1999

Beta-catenin mutations are more frequent in small colorectal adenomas than in larger adenomas and invasive carcinomas.

Loss of serine or threonine phosphorylation sites from exon 3 of beta-catenin has been identified in approximately half of colorectal tumors which lack adenomatous polyposis coli (APC) mutations, but the overall contribution of beta-catenin mutations to sporadic colorectal tumorigenesis is unclear. We therefore used PCR to amplify and sequence exon 3 of beta-catenin from 202 sporadic colorectal tumors. Exon 3 beta-catenin mutations were identified in 6 of 48 small (< 1 cm) adenomas, 2 of 82 large (> or =1 cm) adenomas, and 1 of 72 invasive carcinomas. Eight of the nine mutations, including all of those in the small adenomas and the invasive cancer, involved loss of serine or threonine phosphorylation sites. The percentage of beta-catenin mutations in small adenomas (12.5%) was significantly greater than that in large adenomas (2.4%) and invasive cancers (1.4%; P = 0.05 and P = 0.02, respectively). We conclude that mutation of beta-catenin can be an early, perhaps initiating, event in colorectal tumorigenesis. Small adenomas with beta-catenin mutations do not appear to be as likely to progress to larger adenomas and invasive carcinomas as other adenomas, however, with the result that beta-catenin mutations are only rarely seen in invasive cancers. This suggests that APC and beta-catenin mutations are not functionally equivalent, and that the APC gene may have other tumor suppressor functions besides the degradation of beta-catenin.

Adenoma↗
PubMed1986

[Three-dimensional analysis of colonic adenoma and of carcinoma in adenoma with scanning electron microscope and sequential serial sectioning].

Three-dimensional structures were analyzed on 32 human colonic adenomas, 5 hyperplastic polyps, 4 normal colonic mucosa and 5 advanced colonic carcinomas with Scanning Electron Microscope (SEM) and with sequential serial sectioning. After SEM observation, the samples were softened with 2% NaHCO3 and observed with histological serial sectioning. By combining both techniques, that is combined analysis of outer structures for SEM and inner structures for serial sectioning, three dimensional analysis of the colonic adenoma and carcinoma in adenoma were successfully completed. The colonic adenomas were classified into 6 types based on the surface structure observed by SEM as Type I (circular type), Type II (long-elliptical type), Type III (branched type), Type IV (gyral type), Type V (wrinkle type) and Type VI (complicated type). Classified Types I, II, III and IV were observed in tubular adenoma, and grades of atypia seemed to be increased as increasing type numbers. Type V, in tubulo-villous adenoma and villous adenoma, were found out and showed severer atypia than observed in Type IV. Among 32 adenomas, 3 portions of focal cancers were detected, and the surface structures of them had highly complicated patterns as shown with Type VI.

Adenoma↗
PubMed1999

Adenomas and adenoma-like DALMs in chronic ulcerative colitis: a clinical, pathological, and molecular review.

Dysplasia in chronic ulcerative colitis (CUC) is categorized as either flat or associated with a raised lesion or mass (dysplasia-associated lesion or mass [DALM]). One specific subtype of DALM consists of an isolated discrete "adenoma-like" polypoid dysplastic lesion that is difficult to distinguish from a sporadic adenoma that occurs coincidentally in patients with CUC. Sporadic adenomas are, by definition, also polypoid dysplastic lesions, but their development is unrelated to the underlying colitis. The clinical distinction between CUC-associated polypoid dysplastic lesions and sporadic adenomas is important because the former is an indication for colectomy whereas the latter is usually treated by simple polypectomy. This review focuses on the clinical, pathological, and molecular aspects of polypoid dysplastic lesions and sporadic adenomas in CUC. There are a variety of clinical and pathological features that can be used to distinguish these lesions, but none of these features are entirely specific for either type of neoplasm. Furthermore, there is recent evidence to suggest that the molecular pathogenesis of CUC-associated polypoid dysplasia is different, in terms of the order and timing of genetic events, in comparison to sporadic adenomas and, thus, this information may be used to distinguish these lesions in the near future. Few studies have evaluated the natural history of CUC-related polypoid dysplastic lesions and sporadic adenomas. However, recent reports indicate that the majority of these lesions will follow a relatively benign course with a low risk of progression to flat dysplasia or adenocarcinoma. This review also summarizes the current provisional treatment recommendations for CUC patients with an adenoma-like polypoid dysplastic lesion.

Adenomatous Polyps↗