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PubMed1996

Analysis of the in vitro secretory activity of human pituitary adenomas: modification of corticotropin release from adenoma tissue explant cultures by addition of a human plasma ultrafiltrate bioactive fraction.

The lack of control of tumour behaviour is manifested in different ways, depending primarily on the type of tumour. This results in numerous problems of tumour diagnosis and therapy. In the case of "benign" tumours, like pituitary adenomas, in vitro studies are often used for evaluation of the tumour. The use of tissue explant cultures of human pituitary adenomas and the comparison of the feature of cultured tumours with their behaviour in vivo showed that corticotropin is released not only from the tumours associated with Cushing's disease, but also from clinically non-functioning tumours. Hence, it was supposed that the release of corticotropin in vivo from non-secreting tumours is probably under the influence of certain neuroendocrine and/or systemic humoral factors. To test this possibility, samples of 22 tumours were cultured in plain culture medium or in the presence of the "human plasma ultrafiltrate bioactive fraction" (tentatively termed as TBP) prepared by anion-exchange chromatography. In the presence of TBP the release of corticotropin was strongly inhibited in adenomas showing relatively high spontaneous secreting activity in vitro (> 200 ng/l in 24 hours), while immunohistochemistry of these tumours indicated accumulation of corticotropin inside the cells. In contrast, TBP stimulated corticotropin release from tumours that showed relatively low basic corticotropin release (< 200 ng/l in 24 hours), with no obvious change in cellular corticotropin immunoreactivity. Such a dual activity of TBP was not observed for 8 samples of adenomas cultured in the presence of surrounding pituitary tissue, probably because TBP did not affect corticotropin secretion by the normal pituitary cells (as indicated by immunohistochemistry). From these results, it appears that TBP could be one of the humoral factors involved in the regulation of corticotropin release from pituitary adenoma tissue. Its possible involvement in the regulation of corticotropin release from normal pituitary tissue, however, is uncertain.

Adenoma↗
PubMed1993

The Funen Adenoma Follow-Up Study. Characteristics of patients and initial adenomas in relation to severe dysplasia.

Between 1978 and 1992 a total of 1689 colorectal adenomas were removed in 1042 patients with no history of previous colorectal neoplasms. One hundred and eighteen patients had at least one adenoma with severe dysplasia. A 'clean colon' was ensured by total colonoscopy in 97% of the patients. A multiple logistic model was used to assess the independent risk factors associated with severe dysplasia. The size of largest adenoma and the extent of villous component were identified as independent patient risk factors associated with high risk of severe dysplasia. The results indicated that the risk of severe dysplasia is high in patients with large and/or villous adenomas and the risk is even higher when the adenomas are found in the sigmoid colon or rectum.

Adenoma↗
PubMed1993

The Funen Adenoma Follow-up Study. Incidence and death from colorectal carcinoma in an adenoma surveillance program.

The results of a prospective randomized study of 1056 patients with colorectal adenomas are presented. After initial polypectomy from 1978 to 1992, patients were allocated at random to different follow-up intervals varying from 6 to 48 months, except 53 patients who were allocated to intervals of 6 months. The examinations were mainly done by colonoscopy. Ten patients developed colorectal carcinoma, a number similar to that expected (7.96), when compared with a sex- and age-matched normal Danish population. The expected number of carcinomas was also calculated from adenoma to carcinoma conversion rates estimated in other studies and compared with that observed. If all carcinomas develop in large (> or = 10 mm) adenomas or adenomas with severe dysplasia, the expected number of carcinomas would have been 62 and 110, respectively, indicating a significant reduction of carcinomas in the present study. One patient died of colorectal carcinoma, which is significantly lower than the number expected (7.58). Two patients died of complications from therapeutic and diagnostic colonoscopy--that is, 2 deaths in 3959 colonoscopies. In conclusion, the follow-up strategy has resulted in a mortality from colorectal carcinoma which is reduced when compared with the normal population, in spite of an apparently similar incidence of carcinoma. However, previous suggested adenoma-carcinoma conversion rates indicate that a major reduction of incidence actually has taken place.

Adenoma↗
PubMed1994

[Cytogenetic subtyping of salivary gland pleomorphic adenoma and carcinoma in pleomorphic adenoma].

Current research on salivary gland pleomorphic adenoma is aimed at grouping the cases by cytogenetical aberrations into several subtypes. In this report, 21 cases of pleomorphic adenomas were analysed cytogenetically and divided into 4 subtypes following Bullediek's method; normal karyotype (6 cases), 8q12 rearrangement (8 cases), 12q13-15 rearrangement (5 cases) and other aberrations (2 cases). The average occurrence age of each group was examined. The 8q12 rearrangement group (37.2 y.o.) was younger than the normal karyotype (49.2 y.o.) and 12q13-15 rearrangement groups (52.4 y.o.). Histological subtyping based on Seifert's classification was made and its relationship with the above cytogenetic subtypes was studied. In the 8q12 rearrangement group, Seifert's type-1 was predominant (88%), while in the normal karyotype and 12r13-15 rearrangement groups, Seifert's type-2 was the most common (50% and 80% respectively). We also examined 2 cases of carcinoma in pleomorphic adenoma. Although both showed some cytogenetic abnormalities, no aberrations specific to pleomorphic adenoma (8q12 or 12q13-15 rearrangement) were found. This suggests that original adenomas of these carcinomas showed a normal karyotype or other types of aberrations.

Adenocarcinoma↗
PubMed2004

Effects of expression of hRFI on adenoma formation and tumor progression in colorectal adenoma-carcinoma sequence.

For colorectal carcinomas as well as colonic polyps we investigated the expression of a newly discovered gene, hRFI, which is isolated by the yeast two-hybrid screening using hTid as a bait and expressed highly in esophageal carcinomas. Immunohistochemical staining was performed on 48 colorectal carcinomas and 77 colorectal polyps consisting of 70 adenomas and 7 hyperplastic polyps using the antibody of hRFI. We analyzed the expression of hRFI and the correlation between the percentage of staining of each and their clinico-pathological characteristics. Protein coding by hRFI was specifically and diffusely expressed in most of the cancerous regions of the colorectum. Also, in the early stage of colorectal adenomas, staining of hRFI was focal, and the percentage area of diffuse staining increased as the degree of dysplasia progressed. Although all normal colorectal glands and most hyperplastic polyps (71.4%) showed no staining of hRFI, most colorectal adenomas and carcinomas (93.2%) showed a focal or diffuse staining (P<0.001). Furthermore, the percentage of diffuse staining in carcinomas (81.3%) was significantly higher than in adenomas (5.7%) (P<0.001). hRFI is highly expressed in colorectal carcinomas. In the adenoma-carcinoma sequence, hRFI is involved at the initial tumor formation and its diffuse expression is associated with colorectal carcinogenesis. This evidence suggests that hRFI may act as an oncogenic molecule affecting the apoptotic pathway.

Adenoma↗
PubMed2006

Sessile serrated adenomas of the large bowel. Clinicopathologic and immunohistochemical study including comparison with common hyperplastic polyps and adenomas.

Sessile serrated adenoma (SSA) is a newly characterized type of the large bowel adenoma. It arises in hyperplastic polyp (HP) and represents a precursor lesion of colorectal carcinoma with microsatellite instability. SSAs differ from common HPs by abnormal proliferation of the crypt epithelium and by nuclear atypia. We examined 15 SSAs from 15 patients. The age range was 25-80 years (average 60 years). Six patients were females and 9 were males. For comparison, we examined 10 conventional tubular adenomas and 10 common HPs with vesicular cells. The sites of SSAs were as follows: 8 in rectum, 4 in rectosigmoid colon, 1 in transverse colon, 1 next to mucinous carcinoma of ascending colon, 1 in anastomosis after resection of the transverse colon adenocarcinoma. The diameter of the lesions ranged from 5 to 12 mm. Histologically, SSAs showed asymmetrical proliferation of the epithelium, irregular shape of the crypts with their branching and some crypt dilatations especially in the basal parts of the crypts. Cellular atypia (dysplasia) was usually low. In 5 cases the nuclei were focally stratified and localized in the lower part of the cells. High-grade dysplasia was found only in SSA adjacent to mucinous adenocarcinoma. Immunohistochemically, SSAs showed secretion of gastrointestinal mucin expressing MUC2 and MUC5A. Both MUC2 and MUC5A were also positive in mucinous carcinoma. In previous studies these expressions were considered specific for serrated type of carcinogenesis. However, our study found positivity of MUC2 and MUC5A also in conventional adenomas. Expression of p53 in SSAs was minimal. SSAs have malignant potential comparable with conventional adenomas and for this reason they must be distinguished from HPs.

Adenoma↗
PubMed1991

Differential sensitivity of human colonic adenoma and carcinoma cells to transforming growth factor beta (TGF-beta): conversion of an adenoma cell line to a tumorigenic phenotype is accompanied by a reduced response to the inhibitory effects of TGF-beta.

The growth of three non-tumorigenic human colonic adenoma cell lines, designated AA/C1, RG/C2 and RR/C1, was inhibited by low concentrations of transforming growth factor beta (TGF-beta) (0.05-0.5 ng ml-1). However, the growth of five human colon cancer cell lines under identical conditions was resistant to high concentrations of TGF-beta (2-10 ng ml-1). This is the first report of well-characterized premalignant human colonic cells showing sensitivity to TGF-beta. The TGF-beta-sensitive adenoma cell line AA/C1 was derived from a relatively large adenoma with a K-ras gene mutation and represents a relatively late-stage adenoma, indicating that loss of response to TGF-beta occurs at a relatively late stage in colorectal carcinogenesis and that the presence of a ras gene mutation does not necessarily confer resistance to TGF-beta. Of further interest, the RG/CZ cell line has a p53 mutation showing that p53 mutations do not necessarily lead to TGF-B insensitivity. Furthermore, in this paper we show that the conversion of the AA/C1 adenoma cell line to a tumorigenic phenotype [Williams et al., (1990) Cancer Res., 50, 4724] is accompanied by a reduced response to the growth-inhibitory effects of TGF-beta up to 10 ng ml-1. Reduced responsiveness to the inhibitory effects of TGF-beta may be an important event in the loss of growth control in colorectal carcinogenesis.

Adenoma↗
PubMedDate not supplied

[Immunohistochemical study of monomorphic adenoma (clear cell and basal cell) and pleomorphic adenoma of the parotid gland].

The present paper reports the results of an immunohistochemical study of 6 cases of monomorphic (2 clear cell, 4 basal cell) and 12 cases of pleomorphic adenomas in the parotid gland. The surgical specimens, embedded in paraffin, were tested by antisera vs. epithelial cell markers with epithelial membrane antigen (EMA) and cytokeratins (CK). They were also tested vs. myoepithelial and non-epithelial markers with S-100 protein and Glial Fibrillary Acidic Protein (GFAP). In pleomorphic adenomas, positive cells were found for all the tested antigens. Positive cell distribution showed a marked variability from case to case and even within each area, depending on cell morphology. In particular, areas showing tubular structures were constantly EMA-positive and CK-positive in more than 50% of the cases. In epithelioid areas EMA was negative while many cells were variably positive for CK, S-100 and GFAP. At times, the same cell proved positive to two different antigens. In those fuso-stellate (myxoid) cell areas considered to be of myoepithelial origin, cells were slightly CK-positive and widely GFAP and S-100 positive. In basal cell adenomas, widespread CK positivity was uniformly present while rare, focal positivity was evidenced for EMA and widespread non reactivity was found for S-100 and GFAP. In clear cell adenomas focal CK expression was found in the tubular lumina while clear cells, of myoepithelial origin, were steadily S-100 positive and GFAP-negative. It was noted that a sort of S-100/GFAP positive myoepithelial cell with fuso-stellate morphology was present in pleomorphic adenomas.(ABSTRACT TRUNCATED AT 250 WORDS)

Adenoma↗
PubMed1995

Tubular apocrine adenoma with eccrine and apocrine immunophenotypes or papillary tubular adenoma?

A case of papillary tubular adenoma is reported. On microscopic examination the lesion, located on the scalp, showed a tubular-branching pattern, opening on the skin surface, and features of decapitation secretion. Immunohistochemical evidence of both eccrine and apocrine differentiation was found. This case, which on a clinicopathological basis alone could be classified as tubular apocrine adenoma, illustrates the difficulties in contrasting the latter to its eccrine counterpart (papillary eccrine adenoma) and suggests that the terms papillary tubular adenoma or tubulopapillary hidradenoma more accurately describe these lesions.

Adenoma↗
PubMed2002

Clinicopathologic study of 123 cases of prolactin-secreting pituitary adenomas with special reference to multihormone production and clonality of the adenomas.

BACKGROUND: Prolactinoma is the most invasive type of pituitary adenoma and is generally believed to be well-differentiated adenoma and to produce only prolactin (PRL). The factors related to the various biologic behaviors occurring in patients of different ages and sexes await clarification. Since different immunophenotypes of adenoma may show different biologic behaviors and responses to medical agents, the authors examined hormone production and tried to clarify the clonality of plurihormonal prolactinoma. METHODS: Clinicopathologic factors were studied in 123 patients with prolactinomas (40 males and 83 females). The specimens were fixed in either 10% neutral buffered formalin or 70% alcohol and used for light microscopy. Alcohol-fixed tissue was used to extract DNA from 26 samples obtained from female patients for human androgen receptor gene (HUMARA) assay. RESULTS: Sixty one cases (50%) were pure prolactinoma and 62 cases (50%) were plurihormonal prolactinoma. Spearman rank correlation analysis revealed a significant relationship between age and serum PRL level (P = 0.0002), age and tumor volume (P < 0.0001), and tumor volume and serum PRL level (P < 0.0001). Multiple regression analysis showed a significant correlation only between tumor volume and serum PRL level. The Mann-Whitney U test revealed that prolactinomas associated with higher PRL levels, larger adenomas, and higher ages were significantly more invasive to the cavernous sinus and that male patients had significantly higher PRL levels and larger adenomas. The HUMARA assay disclosed that 11 of 13 plurihormonal prolactinomas (85%) were compatible with monoclonal origin. CONCLUSIONS: The current results suggest that not only can various hormones other than PRL be secreted by prolactinoma, but also that most multihormone-producing prolactinomas are monoclonal in origin.

Adolescent↗
PubMed1999

Expression of P27kip1 and Ki-67 in pituitary adenomas: an investigation of marker of adenoma invasiveness.

Mirroring the ambiguities noted with other endocrine tumours, histology is a poor predictor of the invasiveness of pituitary adenomas. Accordingly, the proteins p27Kip1 (p27) and Ki-67, which respectively block cell-cycle progression and reflect proliferative activity of cells, were studied immunohistochemically in 123 specimens of pituitary adenomas including 57 clinically verified invasive cases. Only Ki-67 had a significant association with invasiveness; only p27 differed significantly between functioning and nonfunctioning adenomas, with a higher frequency of cell labelling in the former. No relationship between Ki-67 and p27 was obtained. Ki-67 detected by MIB-1 is thus an important marker related to the invasive potential of adenomas, and thereby may be helpful in planning postoperative management of patients with pituitary adenomas.

Adolescent↗
PubMed1993

[A case of adrenal adenoma with radiologic "cystic" appearance associated with hypophyseal adenoma].

Expansive lesions of the adrenal glands without signs of hormonal hypersecretion are usually discovered "incidentally", and are therefore called "incidentalomas". Since the silent adrenal masses constitute a heterogeneous group of lesions, the most important issue raised by the identification of these masses is their possible malignant potential. Therefore, the age and sex of the patients, the size of the mass, its imaging characteristic and its histologic features are the most important factors in the assessment of nonfunctioning adrenal masses. We report here the case of a women, aged 43 years mild hypertension, harbouring a great adrenal mass of 8 cm diameter, with cystic appearance at CT scan and ultrasonography, it did not show any uptake after 75Se-Seleniumcholesterol or 131I-Metaiodobenzyl-guanidine. The patient was also affected by mild hyperprolactinemia caused a small pituitary adenoma. After selective venography, she underwent the surgical removal of the left adrenal gland with its mass, which showed a hystological picture of adrenal adenoma. The postoperative course was clinically normal. The interest of this case resides: in the dimensions of the adrenal tumor (the presence of adenomas greater than 6 cm diameter is extremely rare); in the radiographic findings, showing a cystic appearance, probably related to a fluid component, in the association of adrenal and pituitary adenoma, as a possible variant of multiple endocrine neoplasia (MEN) of type I.(ABSTRACT TRUNCATED AT 250 WORDS)

Adenoma↗
PubMedDate not supplied

Hereditary nonpolyposis colorectal cancer and colonic adenomas: aggressive adenomas?

Hereditary nonpolyposis colorectal cancer (HNPCC) results from an inherited defect in one of the genes responsible for repair of errors that occur during DNA replication. Affected individuals have high risk for cancers of the colon and certain extracolonic sites. It appears that HNPCC patients form adenomas at about the same rate s the general population and there is some circumstantial evidence that adenoma is the precursor to colorectal carcinoma in the syndrome. It is hypothesized that HNPCC features accelerated progression from colonic adenoma to carcinoma, a process theoretically driven by the inability to repair DNA mismatches. Evidence in support of the "Aggressive Adenoma" in HNPCC is provided. We discuss our recommendations for colonoscopic surveillance on an annual basis for HNPCC gene-positive individuals, and for genetic counseling.

Adenoma↗
PubMed2002

Pyloric gland-type tubular adenoma superimposed on intraductal papillary mucinous tumor of the pancreas. Pyloric gland adenoma of the pancreas.

We report a rare case of pyloric gland-type tubular adenoma of the main pancreatic duct. It was a grossly visible polypoid nodule and was composed of closely packed pyloric-type glands. This adenoma was present within an intraductal papillary mucinous adenoma (IPMA). In this IPMA lesion, aggregations of pyloric-type glands were occasionally observed, and most of the cells including ductal lining cells expressed pyloric gland-type mucin. The IPMA of the present case showed more extensive pyloric gland metaplasia or differentiation than commonly noted in IPMAs. We consider this pyloric gland-type tubular adenoma to be derived from a selective growth of IPMA cells showing pyloric gland metaplasia.

Adenoma↗
PubMedDate not supplied

Somatotroph and corticotroph pituitary adenoma (double adenoma) in a cat with diabetes mellitus and hyperadrenocorticism.

A 9-year-old castrated male European shorthair cat with insulin-resistant diabetes was referred with the preliminary diagnosis of pituitary-dependent hyperadrenocorticism, based on measurements of urinary corticoids. Further studies revealed not only resistance of plasma concentrations of cortisol, adrenocorticotropic hormone (ACTH) and alpha-melanocyte-stimulating hormone (alpha-MSH) to suppression by a low dose of dexamethasone, but also elevated plasma concentrations of growth hormone (GH) and insulin-like growth factor I (IGF-I). Pituitary imaging with dynamic contrast-enhanced computed tomography demonstrated an enlarged pituitary gland and an adenoma. The cat underwent trans-sphenoidal hypophysectomy after which the insulin resistance disappeared. On histopathological and immunocytochemical examination of the surgical specimen a double adenoma was found, consisting of a corticotroph adenoma and a somatotroph adenoma separated by unaffected pituitary tissue.

Adenoma↗
PubMed2000

Decreased expression of the gut-enriched Krüppel-like factor gene in intestinal adenomas of multiple intestinal neoplasia mice and in colonic adenomas of familial adenomatous polyposis patients.

Gut-enriched Krüppel-like factor (GKLF) is a zinc finger-containing transcription factor, the expression of which is associated with growth arrest. We compared Gklf expression in intestinal and colonic adenomas to normal mucosa in multiple intestinal neoplasia (Min) mice and familial adenomatous polyposis (FAP) patients, respectively, using semi-quantitative RT-PCR. In Min mice, the level of Gklf transcript is highest in normal-appearing intestinal tissues and decreases as the size of the adenoma increases. In FAP patients, the level of GKLF transcript is lower in adenomas compared to paired normal-appearing mucosa from the same patient or normal colonic mucosa from control individuals without FAP. The possibility of DNA methylation as a cause for the decreased expression of Gklf in adenomas of Min mice was investigated by methylation-specific PCR. Results indicate that the Gklf gene is not methylated in either normal or tumorous tissues. The findings of our study are therefore consistent with the potential role of GKLF as a negative growth regulator of gut epithelial cells.

Adenoma↗
PubMed1994

[Parathyroid adenoma encapsulated in a thyroid adenoma: an anatomical curiosity].

We describe a primitive hyperparathyroid in a old woman due to a parathyroid adenoma localized by Technetium 99m, Thallium 201 scintigraphy within the thyroid gland. During surgery, this adenoma was found inside a thyroid adenoma. It is the second case reported on the literature in a such localization. We underline the interest of the scintigraphy Technetium 99m, Thallium 201, for the detection of ectopic parathyroid adenoma.

Adenoma↗
PubMed1995

Truly benign "bronchial adenoma". Report of 10 cases of mucous gland adenoma with immunohistochemical and ultrastructural findings.

Mucous gland adenoma of the bronchus (MGAB) is a rare, solitary, benign, well-circumscribed, multicystic, predominately exophytic bronchial tumor. Mucous gland adenoma arises from the submucosal seromucous glands and ducts of proximal airways; since the location, signs and symptoms, and bronchoscopic findings are similar to those of other tumors arising in the bronchus, diagnosis depends on tissue biopsy. We herein report 10 patients with MGAB. Patients ranged in age from 25 to 67 years old (mean, 52). In two thirds of patients, the tumor was located in the middle or lower lobes. Tumors ranged in size from 0.8 to 6.8 cm (mean, 1.8). Cut surface was shiny, mucoid, cystic, and usually firm. Mucous gland adenomas are protean in their histologic patterns. They may appear glandular and tubulocystic or papillocystic, and they often show a mixture of these features. The tumors are rich in mucins and are immunopositive for epithelial markers. Mucous gland adenoma needs to be distinguished from low-grade malignant tumors of the bronchus--most notably, low-grade mucoepidermoid carcinoma. Complete removal of the tumor is curative.

Adenoma↗