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PubMed1995

Proliferative activity in colonic adenomas as a predictor of metachronous adenomas as assessed by proliferating cell nuclear antigen immunohistochemistry.

OBJECTIVES: The aim of this study was to determine whether cell proliferation in colonic adenomas, as estimated by proliferating cell nuclear antigen (PCNA), predicts the development of metachronous colonic adenomas. METHODS: Forty patients who underwent prior endoscopic polypectomy for colonic adenomas were reevaluated by colonoscopy 2 yr later. The expression of PCNA was studied in all adenomas that were removed. A five-point semiquantitative scale of 1-5 was used to estimate the PCNA score by the percentage of positively stained cells. RESULTS: Among the 40 patients studied, 16 developed recurrent adenomas (group A) and 24 were free of adenomas (group B). At initial colonoscopy, a total number of 51 adenomas (25 in group A and 26 in group B), were found. The median PCNA score in group A and group B index adenomas was 4 (interquartile range, 3-5) and 2 (interquartile range, 1-3), respectively (p < 0.01, Mann-Whitney U-test). A stepwise logistic regression analysis showed that PCNA score is a significant risk factor (p = 0.007, odds ratio 15.8, 95% confidence interval 2.2-112.4) in predicting adenoma recurrence. The median PCNA score in metachronous adenomas was 2 (interquartile range, 1-3). The difference in the PCNA score between group A index and metachronous adenomas was again statistically significant (p < 0.01, Mann-Whitney U-test). CONCLUSIONS: We conclude that the increased expression of PCNA in colonic adenomas may be a predictor for metachronous adenomas.

Adenoma↗
PubMedDate not supplied

Differences in the distribution of acidic mucins between flat tubular adenomas and flat serrated adenomas of the colorectal mucosa.

Two consecutive sections from 72 endoscopically detected flat colorectal polyps (flat tubular adenomas n = 40, flat serrated adenomas n = 18, flat hyperplastic polyps n = 7 and normal colonic mucosa n = 7) were stained with Alcian blue pH 2.5 (AB) or with high iron diamine (HID) without counterstain, to evidence the most important attribute of the colorectal cells i.e. their capacity to produce acidic mucins (sialomucins and sulphomucins respectively). Intense AB and HID staining (++) was found in the upper part of the crypts of all (100%) sections with normal colonic mucosa or with flat hyperplastic polyps, in 13 of the 18 (72%) flat serrated adenomas (with low grade dysplasia = LGD, n = 16; or high grade dysplasia = HGD, n = 2) but in none (0%) of the 40 tubular adenomas. Slight (+) or negative staining of the upper part of the crypts were recorded in all 40 (100%) flat tubular adenomas (LGD n = 32; HGD, n = 8), but in only 5 of the 18 (27,7%) flat serrated adenomas (LGD n = 3; HGD n = 2) and in none (0%) of the sections with normal colonic mucosa or with flat hyperplastic polyps. Intense AB and HID staining (++) was found in the lower part of the crypts in all sections (100%) with normal mucosa or with flat hyperplastic polyps, in 36 of the 40 flat (90%) tubular adenomas (LGD n = 32; HGD n = 8), but in none (0%) of the flat serrated adenomas. Slight (+) or negative stainings in the lower part of the crypts were recorded in all 18 (100%) flat serrated adenomas, but in only 4 of the 40 (10%) flat tubular adenomas and in none of the sections (0%) with normal mucosa or with flat hyperplastic polyps. Thus, the mucosal localization of the depletion of mucin production differs in flat serrated adenomas and in flat tubular adenomas. The difference in topographic distribution of the depletion of acidic mucins in epithelial cells is a new argument in favour of the identity of flat serrated adenomas as an independent neoplastic phenotype in the colorectal mucosa.

Adenoma↗
PubMed1997

Computer-Assisted Microscope Analysis of Feulgen-Stained Nuclei in Gonadotroph Adenomas and Null-Cell Adenomas of the Pituitary Gland.

The current classification of clinically nonfunctioning pituitary adenomas is based on immunocytochemical and ultrastructural studies. However, a number of cases have less distinctive features that cannot be easily conformed with the prevailing morphologic classifications. The diagnostic information contributed by the determination of the nuclear DNA content (DNA ploidy level) and quantitative chromatic pattern description as opposed to the morphofunctional diagnosis in clinically nonfunctioning adenomas was consequently investigated in a series of 71 pituitary adenomas, including 31 null-cell adenomas, 35 gonadotropin adenomas, and 5 nonfunctioning adenomas that were not examined by electron microscopy. DNA ploidy level (8 variables) and quantitative chromatin pattern description (30 variables) were carried out by means of the computer-assisted microscope analysis of 80-1600 Feulgen-stained nuclei analyzed/case. The diagnostic information contributed by the 38 quantitative variables was determined by multifactorial statistical analysis (i.e., Discriminant Analysis). This computer-assisted classification significantly differentiated nulLcell adenomas from gonadotropin adenomas (p = 0.0025). In addition, it was able to differentiate three major subtypes of nonfunctioning adenomas on the basis of their immunohistochemical profiles. These were the immunonegative adenomas, the follicle-stimulating hormone (FSH)-positive adenomas, and the a-subunit (a) and/or luteiwizing hormone (LH)-positive adenomas (p < 0.0001 to p < 0.001). We thus suggest that the cytometric image analysis of Feulgen-stained nuclei can contribute on the discrimination of subtypes of clinically nonfunctioning pituitary adenomas.

Journal Article↗
PubMed2002

Size-dependent expression of cyclooxygenase-2 in sporadic colorectal adenomas relative to adenomas in patients with familial adenomatous polyposis.

Several studies have indicated that administration of non-steroidal anti-inflammatory drugs (NSAID) to patients with familial adenomatous polyposis (FAP) results in a regression of colorectal adenomas through inhibition of cyclooxygenase-2 (COX-2). It is thought that sporadic colorectal adenomas might also be useful targets for the chemoprevention of colorectal cancer, but a marked effect of NSAID on the regression of sporadic adenomas has not been observed. We investigated the immunohistochemical expression of COX-2 in sporadic tubular adenomas (n = 100) from 63 patients and in tubular adenomas (n = 121) from 12 patients with FAP, in order to determine if chemoprevention might be more successful in sporadic adenomas once they have reached a certain size. COX-2 scores were significantly lower (P < 0.0001) in small (< 5 mm in diameter) adenomas than in large (> or = 5 mm) adenomas. This was observed in both sporadic cases and in cases involving patients with FAP. With regard to small (< 5 mm) adenomas, significantly higher (P = 0.02) COX-2 scores were obtained in adenomas resulting from FAP than sporadic adenomas. The variation in COX-2 expression observed among sporadic adenomas of different sizes should be taken into account when making decisions regarding attempts at chemoprevention using NSAID. Sporadic adenomas 5 mm or larger with upregulated COX-2 expression are potentially useful targets for the antiproliferative effects of NSAID.

Adenomatous Polyposis Coli↗
PubMed1999

Immunohistochemical staining patterns of MUC1, MUC2, MUC4, and MUC5AC mucins in hyperplastic polyps, serrated adenomas, and traditional adenomas of the colorectum.

We studied the distribution of the four human apomucins MUC1, MUC2, MUC4, and MUC5AC in hyperplastic polyps, serrated adenomas, and traditional adenomas of the colorectum using immunohistochemical techniques, with the aim of comparing and contrasting their patterns of expression. A series of 12 hyperplastic polyps, 27 serrated adenomas, and 20 traditional adenomas was studied. No significant change in apomucin expression was observed in traditional adenomas compared with normal colorectal epithelium, except for MUC5AC, which was present in 12 of the adenomas (60%) and only 20% of the normal samples. In both hyperplastic polyps and serrated adenomas, MUC2 and MUC5AC mucin expression was consistently and markedly increased. In 50% of the hyperplastic polyps, MUC4 was reduced but in the remaining cases was similar to normal. Loss of MUC4 expression was observed in all serrated adenomas. MUC1 was not increased in the hyperplastic polyps but increased expression was seen in 17 of the serrated adenomas (63%). Similar altered distribution patterns of MUC2, MUC4, and MUC5AC were seen in hyperplastic polyps and serrated adenomas, whereas traditional adenomas showed little change from normal patterns of expression. Although hyperplastic polyps are commonly defined as benign lesions without neoplastic potential, the similar phenotypes of hyperplastic and serrated adenomas and the existence of mixed polyps suggest that these lesions may represent a histogenetic continuum.

Adenoma↗
PubMed1995

Natural history of minute sessile colonic adenomas based on radiographic findings. Is endoscopic removal of every colonic adenoma necessary?

PURPOSE: With the development of colonoscopy and double-contrast barium enema, detection of minute sessile colonic adenomas has increased. We evaluated progression of these lesions radiologically and attempted to clarify the natural history. METHODS: A total of 125 minute sessile adenomas (< or = 5 mm in size) with histologic confirmation were examined by double-contrast barium enema at an interval of more than one year. The average follow-up period was 24 (range, 12-36; standard deviation, 9.4) months. To allow for differences in magnification, adenomas increasing in size by 2 mm or more were defined as growing, and the other lesions were defined as unchanged. RESULTS: Eighty-six adenomas showed no interval change in size. Four adenomas decreased 1 mm in size, and 27 adenomas increased 1 mm in size. The remaining eight adenomas (6 percent) increased by 2 or 3 mm in size. None of the adenomas showed any morphologic changes. There was also no difference in degree of histologic atypia between growing and unchanged adenomas. None of the adenomas developed into carcinomas during the follow-up period. CONCLUSIONS: These data show that most minute sessile adenomas remain unchanged in size and morphology over the long term. Accordingly, these adenomas probably should be followed up radiologically or endoscopically to avoid excessive polypectomy.

Adenoma↗
PubMed1998

Adenoma characteristics at first colonoscopy as predictors of adenoma recurrence and characteristics at follow-up. The Polyp Prevention Study Group.

BACKGROUND & AIMS: All patients with colorectal adenomas may not require identical follow-up. We aimed to determine if adenoma characteristics at initial colonoscopy could predict adenoma recurrence or characteristics at follow-up. METHODS: The number of adenomas and the size, type, and degree of atypia in 479 patients in a polyp prevention trial were evaluated as predictors of the same characteristics at follow-up using odds ratios (ORs) with 95% confidence intervals (CIs). Multiple logistic regression analysis was performed to determine if several baseline characteristics were simultaneously associated with outcome. RESULTS: Although several characteristics were significant predictors of recurrence univariately, by multivariate analysis, multiple adenomas at follow-up were more likely when patients had > or = 3 baseline adenomas (OR, 2.25; 95% CI, 1.20-4.21) or at least 1 tubulovillous adenoma (OR, 2.12; 95% CI, 1.12-4.02). No specific characteristic was associated with recurrence of high-risk polyps (> or = 1 cm, villous, severe atypia). Seventy percent of patients with 1 or 2 baseline adenomas had no recurrence, and only 3.3% had any adenomas of clinical concern. CONCLUSIONS: Number and type of baseline adenomas predict recurrent adenomas, but the recurrence is rarely of clinical concern. Patients with 1 or 2 tubular adenomas constitute a low-risk group for whom follow-up might be extended beyond 3 years.

Adenoma↗
PubMed2004

High frequency of colorectal adenoma in patients with duodenal adenoma but without familial adenomatous polyposis.

BACKGROUND: Duodenal adenomas are extremely common in patients with familial adenomatous polyposis. However, it is uncertain whether patients with duodenal adenomas without familial adenomatous polyposis are at greater risk for colorectal neoplasia and, therefore, should routinely undergo surveillance colonoscopy. The aim of this study was to determine whether there is a correlation between non-papillary duodenal adenoma without familial adenomatous polyposis and colorectal adenoma. METHODS: Twenty-five patients with non-papillary duodenal adenomas without familial adenomatous polyposis, seen from January 1990 to April 2003, were retrospectively evaluated. RESULTS: Non-papillary duodenal polyps were diagnosed by endoscopy in the 25 patients. Of these, 21 underwent colonoscopy and one underwent proctoscopy. The mean age of these 22 patients (12 women, 10 men) was 69 years (range 50-83 years). Sixteen of the 22 patients (72.7%) with duodenal adenomas had associated colorectal adenomas. A total of 38 adenomas and one colorectal cancer were detected. The mean size of the polyps was 6.2 mm (range 3-15 mm). The adenomas were removed by snare excision or with a biopsy forceps. CONCLUSIONS: Based on the results of this uncontrolled, retrospective study, the frequency of colorectal adenomas in patients with duodenal polyps without familial adenomatous polyposis appears to be increased compared with the general population. All patients with duodenal polyps should undergo surveillance colonoscopy for colorectal adenomas. A prospective study to definitively establish the frequency of colorectal adenomas in these patients is warranted.

Adenoma, Villous↗
PubMed1999

Quantitative analysis of growth-related factors in human pituitary adenomas. Lowered insulin-like growth factor-I and its receptor mRNA in growth hormone-producing adenomas.

To elucidate the contribution of growth factors to the development, growth and behavior of human pituitary adenomas, the authors used competitive reverse transcription-polymerase chain reactions to quantify expression of mRNAs for growth factors extracted from pituitary adenomas. As previously diagnosed by endocrinologic evaluation, the pituitary adenomas in this study consisted of six prolactin-producing, six growth hormone (GH)-producing, four follicle-stimulating hormone producing and six nonfunctioning adenomas. The mRNAs examined included those for platelet-derived growth factor (PDGF) B-chain, transforming growth factor (TGF)-beta1, epidermal growth factor (EGF), basic fibroblast growth factor (bFGF) and insulin-like growth factor (IGF)-I and -II; proliferating cell nuclear antigen (PCNA) as an indicator of cell proliferation; and pituitary-specific transcription factor-1 (Pit-1) which is a nuclear transcription factor expressed in the anterior pituitary. All factors except the last were expressed in all adenomas, and expression of PDGF B-chain, TGF-beta1, EGF, bFGF and IGF-II did not differ between the four adenoma varieties. Pit-1 was expressed only in GH- and prolactin-producing adenomas. PCNA expression also showed no differences. However, IGF-I mRNA in GH-producing adenomas was significantly lower than in prolactin-producing and nonfunctioning adenomas despite high serum IGF-I levels (1121+/-253 ng/ml). The analysis on IGF-I receptor mRNA was significantly lowered in GH-producing adenoma compared with the other types of adenoma. These findings suggest that the attenuation of negative feedback through the pituitary GH-IGF-I axis may be involved in development of GH-producing adenoma.

Adenoma↗
PubMed2003

Bottom-up histogenesis of colorectal adenomas: origin in the monocryptal adenoma and initial expansion by crypt fission.

The adenoma:carcinoma sequence is well established. Understanding the molecular pathology of the adenoma is therefore important. There is great controversy within the field. The Vogelstein group champions the "top-down" theory (colorectal adenomas arise and grow across the mucosal surface and down into the crypts), whereas other studies, including our own, propose "bottom-up" spread. Serial sections of 40 small (<3 mm) sporadic colorectal adenomas were stained with H&E, MIB-1, and for beta-catenin. 10 early adenomas were Feulgen-stained and microdissected. We also examined the flat mucosa of three patients who had undergone colectomies for familial adenomatous polyposis (FAP) and specimens from a XO/XY individual with FAP, the latter using in situ hybridization for the Y chromosome. In the earliest sporadic adenomas, there were crypts entirely filled with adenomatous epithelium, which showed proliferative activity and nuclear localization of beta-catenin. There was a sharp cutoff between crypt epithelial cells showing nuclear beta-catenin and surface cells with membrane staining. In slightly larger lesions, adenomatous spread from above was seen. Microdissected adenomas showed multiple fission events, with proliferation distributed equally throughout. In FAP tissue, numerous isolated monocryptal adenomas, which were clonal in origin, were seen. Examination of adenomas in the XO/XY individual showed no instances of XY or XO adenomatous epithelium growing down into crypts of the other genotype. Both sporadic and FAP adenomas start as a unicryptal adenomas and grow initially by crypt fission--a bottom-up pattern. Later, in sporadic adenomas, there is evidence of growth down into adjacent crypts (top-down).

Adenoma↗
PubMed1991

Analysis of pituitary hormones and chromogranin A mRNAs in null cell adenomas, oncocytomas, and gonadotroph adenomas by in situ hybridization.

To study the relationship between null cell adenomas, oncocytomas and gonadotroph adenomas, we analyzed 32 surgically removed formalin-fixed paraffin-embedded pituitary tumors for the expression of pituitary hormone messenger RNAs (mRNAs) by in situ hybridization (ISH). Most tumors were also analyzed for chromogranin A mRNA. To identify the cell type constituting the tumors and to assess hormone content, all tumors were investigated by histology, transmission electron microscopy and immunohistochemistry. Most null cell adenomas (6/11) and gonadotroph adenomas (9/10) expressed the mRNAs for alpha-subunit of glycoprotein hormones whereas only 2/11 oncocytomas expressed alpha-subunit mRNA. FSH beta and/or LH beta mRNA were present in most null cell and gonadotroph adenomas but only in a few oncocytomas. Prolactin (PRL) mRNA was detected in two null cell tumors and in one gonadotroph adenoma, whereas GH and POMC mRNA were present in one null cell adenoma. Chromogranin A mRNA, which codes for the major secretory granule protein, was present in 25/26 tumors including all tumors that were negative for pituitary hormone mRNAs, indicating adequate preservation of specific mRNA transcripts in the paraffin-embedded sections of tumor cells. These results indicate that null cell adenomas and gonadotroph adenomas are closely related neoplasms and that oncocytomas may represent a functionally defective form of null cell adenoma characterized by mitochondrial abundance, which has retained the capacity to synthesize the major secretory granule protein chromogranin A. Although the cytogenesis of null cell adenomas and oncocytomas is not clear, it can be suggested that these two tumor types are derived from a pluripotential precursor cell that is capable of undergoing multidirectional differentiation and synthesizing various hormones, mainly glycoproteins.

Adenoma↗
PubMed1993

Minute adenomas of the depressed type in familial adenomatous polyposis of the colon. A pathway to ordinary polypoid adenomas.

BACKGROUND: It has been thought that colorectal adenomas are polypoid from their beginning. Although depressed adenomas have been described, they have been considered an unusual form and have not been studied systemically. METHOD: More than 5000 colorectal adenomas in 24 resected large intestines of patients with familial adenomatous polyposis were examined by dissecting microscopic study. These adenomas were classified by their surface appearance as depressed, flat, or polypoid type. The frequencies and sizes of the three types were determined. RESULTS: In addition to ordinary polypoid adenomas, many adenomas of the depressed type were found. Of the 5287 adenomas detected, 635 (12.0%) were depressed, 967 (18.3%) were flat, and 3685 (69.7%) were polypoid. Depressed adenomas constituted approximately 15% of all adenomas smaller than 1.5 mm diameter. However, they were rare in those of 1.5-2.0 mm diameter and were not found among those of more than 2.0 mm in diameter. CONCLUSION: These findings suggest that some ordinary polypoid adenomas originate from minute depressed adenomas.

Adenoma↗
PubMed2002

[Differentiated papillary kidney tumors. Differentiation between metanephric adenoma and papillary adenoma].

Metanephric adenoma of the kidney is a well described tumor entity. The differential diagnosis between papillary adenoma or papillary carcinoma type 1 and metanephric adenoma of the kidney can be challenging in single cases. We report two cases of metanephric adenomas and compare their immunophenotype with a papillary adenoma. The analysis of these metanephric adenomas and a review of the literature shows that CD-57 positivity and lack of EMA expression are helpful in distinguishing metanephric adenoma from papillary adenoma and papillary carcinoma. Glomeruloid structures, Psammoma bodies, necrosis or expression of cytokeratin 7 and vimentin are common features in metanephric adenoma and papillary adenoma or papillary carcinoma. The knowledge of the immunohistochemical constellation is important, because metanephric adenoma can be very large and often have some necrosis.

Adenoma↗
PubMed2003

Telomerase activity in pituitary adenomas: significance of telomerase expression in predicting pituitary adenoma recurrence.

Clinical and histopathological evaluations are inadequate for assessing biological aggressiveness and regrowth potential in benign pituitary adenomas. To develop reliable and prognostically informative means of predicting behavior remains an intractable problem. Telomerase, a reverse transcriptase that extends telomere length, may facilitate tumorigenesis and tumor immortality. In the present study, we investigated the telomerase activity of pituitary adenomas, and attempted to assess the value of telomerase expression for predicting their clinical course. In total, 31 (30 patients) benign pituitary adenoma samples including 8 recurrent adenomas were studied. Telomerase expression was evaluated by polymerase chain reaction (PCR)-based telomeric repeat amplification protocol (TRAP) assay and telomerase activity levels were quantitated by improved PCR enzyme-linked immunosorbent assay (ELISA). The data were analyzed in relation to clinical course which was reviewed at 4-5.5 years (median follow-up time, 52.5 months) after surgery. The relative values of the telomerase expression for predicting the clinical course were compared with the MIB-1 antigen-based proliferative cell index (PCI) and p53 immunoreactivity which have recently been suggested to correlate with aggressive behavior in pituitary adenomas. Overall, telomerase expression was detected in 13% of the adenomas (4 tumor tissues, 3 patients). These adenomas comprised large, invasive, and functioning adenomas. The number of telomerase-positive adenomas was small; however, the PCI was higher in cases with telomerase expression (4 tumor tissues; mean, 4.2 +/- 2.4%) than in those without it (27 tumor tissues; 1.4 +/- 1.3%) (p = 0.01). One tumor with detectable telomerase expression, which did not undergo additional pharmacological or radiotherapeutic intervention after first surgery, recurred rapidly despite gross total surgical resection, although the PCI of both the primary and recurrent adenomas was not high. Detection of telomerase expression may represent an additional useful means of identifying aggressive behavior, complementing the histopathological evaluation of benign-appearing pituitary adenomas.

Adenoma↗
PubMed2001

Adenoma characteristics as risk factors for recurrence of advanced adenomas.

BACKGROUND AND AIMS: The link between adenoma characteristics at baseline colonoscopy and adenoma recurrence is poorly understood. We assessed whether the number, size, location, or histology of resected adenomas was related to the probability of recurrence of advanced lesions. METHODS: Analyses were based on 1287 men and women in the wheat bran fiber (WBF) study, a randomized, double-blind trial of WBF as a means of decreasing the probability of adenoma recurrence over a period of 3 years. Multiple logistic regression was used to calculate odds ratios (ORs) and 95% confidence intervals (CIs). RESULTS: Recurrence of advanced adenomas (>1 cm or tubulovillous/villous histology) was higher among individuals with adenomas >1 cm compared with those with adenomas <0.5 cm (OR, 2.69; 95% CI, 1.34-5.42) and among those with proximal than those with distal adenomas (OR, 1.65; 95% CI, 1.02-2.67). No association was observed for adenoma number or histology. A shift in location from the distal colon and rectum at baseline (54.6%) to more proximal recurrent adenomas (45.2%), including advanced lesions (42.8%), was observed. CONCLUSIONS: Large or proximally located adenomas are important indicators of recurrence of advanced lesions. Because most recurrences were detected in the proximal colon, careful surveillance of this area is warranted.

Adenoma↗
PubMed1994

Lower incidence of K-ras codon 12 mutation in flat colorectal adenomas than in polypoid adenomas.

In order to clarify genetic changes in flat adenomas, K-ras codon 12 point mutations were examined in 56 flat adenomas, 81 polypoid adenomas and 42 cancers of colon and rectum. The mutation frequency in flat adenomas was 23% (13/56), significantly lower than that in polypoid adenomas (67%: 54/81) and cancers (76%: 32/42). Even mildly dysplastic adenomas or small (less than 5 mm) adenomas showed higher mutation incidence in polypoid type (62%, 57%) than in flat type (23%, 19%). Among flat adenomas, flat elevated lesions exhibited relatively higher mutation frequency than completely flat or depressed ones. As for cancers, 14 tumors (33%) contained mutations only in a minor tumor cell population, indicating that these mutations occur at a late stage of tumorigenesis. These results suggest that the adenoma-carcinoma sequence through flat adenomas may be different from that through polypoid adenomas, and genetic changes may be heterogeneous in colorectal carcinogenesis.

Adenoma↗