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PubMed2003

"Honeycomb Golgi" in pituitary adenomas: not a marker of gonadotroph adenomas.

The vacuolar change in Golgi complexes known as "honeycomb Golgi" has been described as the ultrastructural hallmark of a specific tumor that has been called the "female gonadotroph" adenoma of the human pituitary. Recently, a few adenomas presenting with Cushing's disease have been reported to exhibit this feature. To clarify the significance of a "honeycomb Golgi" in the classification of pituitary adenomas, we studied clinically nonfunctioning adenomas with or without "honeycomb Golgi" using immunohistochemistry for adenohypophysial hormones and RT-PCR for the cell-specific transcription factors Tpit that identifies corticotrophs and SF-1 that identifies gonadotrophs. All adenomas were from women. Among 20 adenomas with complete "honeycomb Golgi" change, gonadotrophin subunits were totally immunonegative, but ACTH was positive in a few cells of 12 adenomas. Among eight adenomas with partial vacuolar change of the Golgi complex, five were positive for gonadotrophins and two were positive for ACTH. A subgroup of these lesions were examined by RT-PCR and among eight adenomas with typical "honeycomb Golgi" one case expressed both Tpit and SF-1, probably due to contamination with normal pituitary and another expressed neither Tpit nor SF-1. Of the remaining six cases, Tpit was expressed in two cases and SF-1 in four. These findings indicate that "honeycomb Golgi" change can been seen in corticotroph adenomas as well as gonadotroph adenomas. The reason why this vacuolar change occurs only in females remains to be clarified.

Adenoma↗
PubMed2000

Adenoma size and number are predictive of adenoma recurrence: implications for surveillance colonoscopy.

BACKGROUND: Three-year colonoscopic surveillance after initial polypectomy may not be required for all patients. Those with multiple baseline polyps and large adenomas, implicated as predictors of colon cancer, merit close observation. Conversely, patients with single small adenomas may be subjected to early endoscopic surveillance unnecessarily. METHODS: From our Adenoma Registry we evaluated patient and adenoma characteristics in 697 patients. All had an adenoma recurrence within 3 years of a positive baseline colonoscopy. Potential risk factors studied were age, gender, number of adenomas, size of largest adenoma and histology. We defined a significant outcome as size of 1 cm or greater, tubulovillous or villous histology, high-grade dysplasia, carcinoma in situ, invasive cancer, or 4 or more adenomas. RESULTS: Having 3 or more adenomas on initial colonoscopy with at least 1 measuring 1 cm or larger greatly increased the chance of a significant finding on the first surveillance colonoscopy. Conversely, patients with 1 or 2 adenomas all measuring less than 1 cm were at extremely low risk of an important outcome within 3 years. CONCLUSIONS: Patients with 1 or 2 adenomas all measuring less than 1 cm are an identified low risk group and their first surveillance examination may be delayed beyond the standard 3 years.

Adenomatous Polyps↗
PubMed1996

A case of pituitary somatotroph adenoma with concomitant secretion of growth hormone, prolactin, and adrenocorticotropic hormone--an adenoma derived from primordial stem cell, studied by immunohistochemistry, in situ hybridization, and cell culture.

Somatotroph adenomas often secrete prolactin (PRL) besides growth hormone (GH) and are sometimes immunostained for other anterior pituitary hormones or their subunits, such as thyroid-stimulating hormone (TSH) beta-subunit and glycoprotein hormone alpha-subunit (alpha SU). However, somatotroph adenomas showing hypersecretion of adrenocorticotropic hormone (ACTH) are extremely rare. There have been, to our knowledge, only five published reports on somatotroph adenomas accompanied by excessive ACTH secretion. Here we report a case of intracavernously invading somatotroph macro-adenoma with high serum GH, PRL, and ACTH levels. We examined the case using immunohistochemistry (IHC), in situ hybridization (ISH), and cell culture, and confirmed GH, PRL, and ACTH, as well as alpha SU, production, and the expression of Pit-1 protein by the adenoma, which is known as a transcriptional factor for GH, PRL, and TSH, not for ACTH. Therefore, the presence of unknown transcriptional factor other than Pit-1, common to GH, PRL, and ACTH, may be speculated to be expressed in this adenoma. In our previous study, we had found plurihormonal mRNA expression, especially for ACTH, the beta-subunit of follicle-stimulating hormone and luteinizing hormone in some somatotroph adenomas, using non-radio-isotopic ISH, and suggested that these adenomas might be derived from plurihormonal primordial stem cells. Our present case is significant from the viewpoint of histogenesis of pituitary adenomas, because it further supports the cell origin of somatotroph adenomas from plurihormonal primordial stem cells, and moreover it suggests the presence of unknown transcriptional factor other than Pit-1, common to GH, PRL, and ACTH.

Adenoma↗
PubMed2003

Metanephric adenoma lacks the gains of chromosomes 7 and 17 and loss of Y that are typical of papillary renal cell carcinoma and papillary adenoma.

Metanephric adenoma has morphologic similarities to papillary renal cell neoplasms. Cytogenetic studies of papillary renal cell carcinoma and papillary adenoma have shown frequent gains of chromosomes 7 and 17 and loss of the Y chromosome. Some cytogenetic studies have supported the hypothesis that metanephric adenoma is related to papillary renal cell neoplasia; others have not. Seven metanephric adenomas were studied with fluorescence in situ hybridization in paraffin sections using centromeric probes for chromosomes 7, 17, and Y diluted 1:100 with tDenHyb1 buffer. The signals in 100 to 200 nuclei were counted in each tumor. Samples of histologically normal renal cortical tubule epithelium were used as controls. In all seven metanephric adenomas, the results for chromosomes 7 and 17 were similar: a high percentage of nuclei with two signals (range, 75 to 85%; median, 79%). Normal kidney showed similar results (range, 78 to 88%; median, 84%). The Y chromosome was present in all three of the tumors from males (range, 86 to 89% of nuclei; median, 87%). Normal kidney gave similar results (range 82% to 91%, median 84%). The presence of chromosomes 7, 17, and Y in metanephric adenomas is similar to their presence in normal kidney. Metanephric adenoma lacks the frequent gains of chromosomes 7 and 17 and losses of the Y chromosome that are typical of papillary renal cell neoplasms, supporting the notion that metanephric adenoma is not related to papillary renal cell carcinoma and papillary adenoma. Genetic analysis of chromosomes 7, 17, and Y may facilitate discrimination of metanephric adenoma from papillary renal cell carcinoma in difficult cases.

Adenoma↗
PubMed2006

TRAIL induces apoptosis in human colorectal adenoma cell lines and human colorectal adenomas.

PURPOSE: Recombinant human (rh) tumor necrosis factor-related apoptosis-inducing ligand (TRAIL) is a potential new anticancer drug which can induce apoptosis in colorectal cancer cell lines. The aim of this study was to investigate whether it is possible to induce apoptosis in human adenoma cell lines and human adenomas using rhTRAIL. EXPERIMENTAL DESIGN: Two human adenoma cell lines were exposed to 0.1 microg/mL of rhTRAIL for 5 hours. Apoptosis and caspase activation in cell lines were evaluated using immunocytochemistry, fluorimetric caspase assays, and Western blotting. Short-term explant cultures were established from freshly removed human adenomas (n = 38) and biopsies of normal colon epithelium (n = 15), and these were incubated for 5 hours in the presence or absence of 1 microg/mL of rhTRAIL. Apoptosis was determined in paraffin-embedded tissue using morphologic criteria and cleaved caspase-3 staining. RESULTS: In the adenoma cell lines, rhTRAIL induced up to 55% apoptosis. This coincided with caspase-8 and caspase-3 activation and could be inhibited by a pan-caspase inhibitor. rhTRAIL induced caspase-dependent apoptosis in adenomas with high-grade dysplasia (n = 21) compared with the paired untreated counterparts (apoptotic index, 34 +/- 5% versus 17 +/- 2%, mean +/- SE; P = 0.002), but not in adenomas with low-grade dysplasia (n = 17) or in normal colon epithelium (n = 15). CONCLUSIONS: Colorectal adenoma cell lines and adenomas with high-grade dysplasia are sensitive to rhTRAIL-induced apoptosis, whereas normal colon epithelium is not. This suggests the potential application of rhTRAIL in the treatment of adenomas with high-grade dysplasia.

Adenoma↗
PubMed2002

Expression of Pit-1 and growth hormone-releasing hormone receptor mRNA in human pituitary adenomas: difference among functioning, silent, and other nonfunctioning adenomas.

We analyzed the expression of Pit-1 and growth hormone-releasing hormone receptor (GHRH-R) mRNA in various types of functioning and nonfunctioning adenomas using a quantitative reverse transcriptase polymerase chain reaction (RT-PCR) method. Among clinically nonfunctioning adenomas, tumors considered as silent adenomas were reclassified on a pathologic basis. Competitive RT-PCR showed that the levels of Pit-1 and GHRH-R mRNA expression in silent somatotroph adenomas and silent prolactinomas were similar to those in the corresponding functioning adenomas. In silent thyrotroph adenomas, both mRNAs showed high levels of expression that were similar to those in functioning and silent somatotroph adenomas. The results suggest that the cause of the silence in these tumors seems to be in the downstream to transcription of Pit-1 gene in the signaling pathway leading to hormone secretion. Competitive RT-PCR assay could distinguish silent adenomas of the Pit-1 group from the other nonfunctioning adenomas in the expression levels of Pit-1 and GHRH-R mRNAs. In the future, precise diagnosis of various adenomas may become possible by assaying transcription factors such as steroidogenic factor-1 and thyrotroph embryonic factor, which are thought to be related to adenohypophyseal cytodifferentiation.

Adenoma↗
PubMed1996

Prognostic model for patients treated for colorectal adenomas with regard to development of recurrent adenomas and carcinoma.

OBJECTIVE: To quantify the risk of developing recurrent adenomas or colorectal cancer for patients who had already had colorectal adenomas removed. DESIGN: Retrospective study. SETTING: University hospital, Denmark. SUBJECTS: 479 patients who had colorectal adenomas removed between 1958-80. INTERVENTIONS: All patients were followed up by rectoscopy and double contrast barium enema. The survival data were analysed by Cox's proportional hazards model. MAIN OUTCOME MEASURES: Variables of significant prognostic importance for recurrence of adenomas and the development of cancer were identified. Results. For the long term risk of recurrence of the adenoma (more than 1.5 years after removal of the first adenoma), two variables were of prognostic significance: The occurrence of synchronous adenomas or recurrent adenomas, and the sex of the patient. The model for development of colorectal cancer identified two variables of prognostic significance: the grade of dysplasia and the size of the first adenoma. CONCLUSION: We suggest that these variables can be used in the management of patients with adenomas, particularly in developing individual follow-up regimens.

Adenoma↗
PubMed1998

[Immunohistochemical studies in depressed type adenomas of the stomach--comparison with protruded type adenomas and depressed type well differentiated mucosal gastric cancers].

In this study, we performed immunohistochemical studies using p53 and Ki-67 immunostaining in 48 depressed type adenomas, and compared with protruded type adenomas (n = 28) and depressed type well differentiated mucosal gastric cancers (mcancer: n = 46). Focal and diffuse p53 staining patterns were not noticed in depressed type adenomas and in protruded type adenomas, but were noticed in mcancers (focal: 4.3%, diffuse: 41.3%). Ki-67 positive cells were noticed in surface epithelium in 24.4% of depressed type adenomas, in 21.4% of protruded type adenomas and in 87.0% of mcancers. Ki-67 positive rate in foveolar epithelium (superior, middle, inferior) were noticed in (31.1%, 12.9%, 6.1%) of depressed type adenomas, in (33.4%, 15.4%, 6.9%) of protruded type adenomas and in (33.4%, 31.4%, 20.4%) of mcancers. These results suggest that from the point of immunohistochemistry, depressed type adenomas were similar to protruded type adenomas, but were different from mcancers.

Adenoma↗
PubMed1995

p53 overexpression in flat serrated adenomas and flat tubular adenomas of the colorectal mucosa.

The expression of the p53 protein was investigated in flat serrated neoplasias as well as in other histological phenotypes of flat or exophytic hyperplasias or neoplasias of the colorectal mucosa. A total of 104 such lesions were analyzed: 24 were flat serrated neoplasias (22 flat serrated adenomas and 2 flat serrated adenocarcinomas), 26 flat tubular adenomas, 17 flat hyperplastic polyps, 29 exophytic tubular and/or villous neoplasias (23 adenomas and 6 exophytic adenocarcinomas) and the remaining 8, exophytic hyperplastic polyps. Deparaffinized, rehydrated sections were treated immunohistochemically to detect those overexpressing the p53 protein. Lesions having slight (+), moderate (++) or intense ( ) staining were considered immunoreactive. The results showed that 50% of the flat serrated adenomas with low-grade dysplasia (LGD) and 66.7% of those with high-grade dysplasia (HGD) had p53 immunoreactivity. None of the flat tubular or of the exophytic adenomas with LGD expressed p53, but immunoreactivity was present in 61.5% of the flat tubular adenomas with HGD and in 52.3% of the exophytic adenomas with HGD. All adenocarcinomas had an intense p53 reaction. Weak p53 expression was demonstrated by 11.7% of the flat hyperplastic polyps but none of the exophytic polyps reacted. The occurrence of p53 expression in flat serrated adenomas with LGD suggested that, despite its low histological profile, one-half of those lesions could be biologically already committed to independent growth. The occurrence of p53 expression in nearly 12% of the flat hyperplastic polyps was totally unexpected and deserves further investigation. Flat serrated adenoma emerges as a novel, independent histological entity among the various phenotypes of flat neoplasias of the colorectal mucosa.

Adenocarcinoma↗
PubMed1990

Morphometrical analysis of gall-bladder adenoma and adenocarcinoma with reference to histogenesis and adenoma-carcinoma sequence.

In order to examine whether our subdivision of gall-bladder adenoma and adenocarcinoma into non-metaplastic and metaplastic types is reasonable from the viewpoint of their cytological features, a morphometrical analysis was conducted on 17 adenomas and 59 adenocarcinomas. The morphometrical parameters used were nucleo-cytoplasmic ratio (N/C ratio) and nuclear areas (NA). N/C ratio in the metaplastic type of both adenoma and adenocarcinoma was significantly larger than that in the non-metaplastic. This result shows that the different tumour types are associated with a different N/C ratio. Continuous measurement of N/C ratio and NA in progressing from non-cancerous mucosa to the lesion was made and the data obtained were analysed by the Lowess method. In some adenomas the total area of polypoid lesions was serially measured and these data were also analysed by the Lowess method. The results showed different processes in non-metaplastic and metaplastic types of adenoma and adenocarcinoma from the standpoint of nuclear changes of N/C ratio and NA. These results indicate that our histogenetic classification of adenocarcinoma is reasonable in morphometrical nuclear analysis. We also investigated the adenoma-carcinoma sequence as a possible histogenesis for gall-bladder carcinoma. Eight (72.7%) of 11 metaplastic adenomas and two (33.3%) of six non-metaplastic adenomas had foci of atypical gland proliferation and were considered to be carcinomas. Moreover, these carcinomatous areas were surrounded by severe dysplasia. These findings indicate that adenoma-carcinoma sequence accounts for one of the histogenesis of gall-bladder carcinoma.

Adenocarcinoma↗
PubMed2006

Ganglion cell containing pituitary adenomas: signs of neuronal differentiation in adenoma cells.

Ganglion cell containing pituitary adenomas are rare. They represent tumors originating in the sella turcica which are composed of adenomatous and neuronal components. Recently accumulated information suggests a common origin for their neuronal and pituitary constituents. The objective of this study was to report the clinical and morphologic findings of pituitary gangliocytomas and study their immunoprofile using neuronal markers. Seven cases of pituitary gangliocytomas retrieved from 1,322 sellar lesions were studied. All tumors were removed from patients with mild acromegaly. Histologically they were biphasic composed of pituitary adenoma and clusters of ganglion cells embedded in a variably dense neuropil substrate. All adenomas belonged to the category of sparsely granulated somatotroph adenoma and were positive for growth hormone, whereas in five tumors, a few adenoma cells were also positive for prolactin. Ganglion cells were immunoreactive for NSE, synaptophysin and neurofilament protein (NFP). NFP-reactive fibrils were observed in the neuropil substrate and varied in number among the cases. Interestingly, all tumors contained varying numbers of adenoma cells with NFP-positive, dot-like areas of cytoplasmic reactivity, mostly tiny paranuclear, a finding not previously reported in human pituitary gangliocytomas. The presence of NFP in pituitary adenomas indicates neuronal differentiation in adenoma cells, suggesting a common origin for neuronal and pituitary adenoma cell elements in gangliocytomas.

Acromegaly↗
PubMed1995

Expression of plurihormonal mRNAs in somatotrophic adenomas detected using a nonisotopic in situ hybridization method: comparison with lactotrophic adenomas.

We used a nonisotopic in situ hybridization (ISH) method to investigate the expression of pituitary hormone, including glycoprotein hormone mRNAs in 17 somatotrophic and four lactotrophic adenomas. Our ISH studies of lactotrophic adenomas showed that their hormonal gene expression was confined to prolactin, whereas those of somatotrophic adenomas showed that some of them expressed plurihormonal genes. In some somatotrophic adenomas that were immunohistochemically negative for pituitary hormones, positive reactions, mainly for adrenocorticotropic hormone (ACTH), follicle-stimulating hormone beta subunit (FSH beta), and luteinizing hormone beta subunit (LH beta) mRNAs, were observed in our ISH studies. These results suggest that some somatotrophic adenomas may originate from plurihormonal primordial stem cells, which we have presumed serve as precursors for various hormone-expressing cells. It is unclear why some somatotrophic adenomas derived from plurihormonal primordial stem cells manifest clinically only as the acromegalic hyperfunction syndrome or gigantism. Additional translational factors or some other somatic mutations may play important roles in the clinical manifestations of such adenomas. In conclusion, some somatotrophic adenomas appear to be derived from plurihormonal primordial stem cells, whereas lactotrophic adenomas are well differentiated tumors that originate from lactotrophic cells, which represent the final stage of acidophilic cell line differentiation.

Adenoma↗
PubMed2002

Utility of MMP-1, p53, E-cadherin, and collagen IV immunohistochemical stains in the differential diagnosis of adenomas with misplaced epithelium versus adenomas with invasive adenocarcinoma.

Adenomas with misplaced epithelium in the submucosa of the polyp stalk ("pseudoinvasion") may be difficult to distinguish from adenomas that harbor invasive adenocarcinoma by morphologic analysis. Recently, several epithelial and stromal proteins, such as matrix metalloproteinase-1 (MMP-1), p53, E-cadherin, and collagen IV, have been shown to be altered in colonic adenocarcinomas in comparison with adenomas and normal colonic mucosa. Therefore, the purpose of this study was to evaluate the diagnostic use of several epithelial (p53, E-cadherin) and stromal (MMP-1, collagen IV) markers in distinguishing adenomas with misplaced epithelium from those with invasive adenocarcinoma. Routinely processed polypectomy specimens from 23 patients with an adenoma with misplaced epithelium (male/female ratio 12/11; mean age 65 years) and 23 patients with an adenocarcinoma arising in an adenoma (male/female ratio 13/10; mean age 63 years) were immunohistochemically stained (avidin-biotin complex method) for monoclonal antibodies to MMP-1 (epithelial and stromal cell collagenase), p53 (tumor suppression gene), E-cadherin (intercellular adhesion protein), and collagen IV (basement membrane collagen component), and the results were compared between the two polyp groups. Where appropriate, immunopositivity was evaluated in the epithelium (MMP-1, p53, E-cadherin), stroma (MMP-1), and/or basement membrane (collagen IV). Cases were considered positive if an increase (MMP-1, p53) or decrease (E-cadherin, collagen IV) in either the intensity or proportion of cells staining was noted in the submucosal epithelial component compared with the intramucosal portion of the polyp head for each individual polyp. In adenomas with invasive adenocarcinoma, MMP-1 staining of the stroma surrounding submucosal epithelium and p53 nuclear staining within the epithelium were increased in 21 (91%) and 14 (61%) cases, respectively, whereas decreased or discontinuous E-cadherin and collagen IV staining was noted in 15 (65%) and 22 (96%) cases, respectively. All these values were significantly different (p < 0.005) from those observed in adenomas with misplaced epithelium [MMP-1, 11 of 23 (48%); p53, 1 of 23 (4%); E-cadherin, 0 of 23 (0%); collagen IV, 0/23 (0%)]. Furthermore, in three diagnostically difficult cases that contained foci of misplaced epithelium with high-grade dysplasia, the immunohistochemical results confirmed the impression that the lesions represented epithelial misplacement rather than invasive adenocarcinoma. In conclusion, the degree and/or pattern of MMP-1, p53, E-cadherin, and collagen IV staining in the submucosal epithelial elements in comparison with the intramucosal adenomatous tissue may help distinguish adenomas with misplaced epithelium from those with invasive adenocarcinoma.

Adenocarcinoma↗
PubMed1995

Flat serrated adenomas and flat tubular adenomas of the colorectal mucosa: differences in the pattern of cell proliferation.

In the present work we have investigated the cell proliferation pattern of flat serrated adenomas and flat tubular adenomas. For this purpose tissue sections from 23 consecutive flat serrated adenomas and 22 consecutive flat tubular adenomas of the colorectal mucosa were challenged with MIB1, a monoclonal antibody directed against a proliferation-related antigen. The results (including semi-quantitative studies) demonstrated that, whereas flat serrated adenomas had a high cell proliferation at the lower part of the crypts, flat tubular adenomas had a high cell proliferation in the upper part of the crypts. In serrated adenomas with invasive adenocarcinoma, high cell proliferation was demonstrated both at the lower portion of the crypts and in the subjacent submucosa. This suggests that the cells of the lower portion of the crypts in serrated adenomas are truly neoplastic, with the capacity to evolve into invasive growth. The difference in cell proliferation between the two types of flat lesions reported here is a new argument in favor of the classification of flat serrated adenomas as a novel and independent type of neoplastic change of the colorectal mucosa.

Adenoma↗
PubMed1983

Follicle-stimulating hormone-secreting pituitary adenomas: correlation of reduction of adenoma size with reduction of hormonal hypersecretion after transsphenoidal surgery.

Ten men who had FSH-secreting pituitary adenomas were evaluated before and 4-6 weeks after transsphenoidal surgery to determine whether reduction of adenoma mass would ameliorate the hormonal abnormalities associated with these adenomas. Nine of the 10 men exhibited marked reduction in adenoma size, as judged by computerized tomography, an 7 had improvement in vision. The same 9 men also had decreases in basal serum FSH concentrations to within the normal range after surgery. The 1 man who had no reduction in adenoma size by computed tomographic scan and whose serum FSH concentration did not decrease to normal after surgery was also the only patient whose abnormal FSH and LH responses to TRH did not improve after surgery. Another man, who had a reduction in adenoma size and serum FSH concentration after surgery, subsequently had regrowth of the adenoma and concomitant resurgence of the FSH concentration. Two men had increases in their serum testosterone concentrations from subnormal to well within the normal range after surgery, suggesting that gonadotroph cell adenomas may impair LH secretion from normal gonadotroph cells. We conclude that the correlation of reduction in adenoma size with reduction in hormonal hypersecretion after surgery suggests that the hormonal hypersecretion is a direct consequence of the adenomatous tissue.

Adenoma↗
PubMed1998

Hyperfunctioning thyroid adenoma concomitant with papillary thyroid carcinoma, follicular thyroid adenoma and primary hyperparathyroidism.

A case of 67-year-old woman with hyperthyroidism due to functioning thyroid adenoma is reported. The patient had concomitant follicular thyroid adenoma and primary hyperparathyroidism in addition to functioning adenoma. Histological examination of the excised thyroid tissue revealed occult papillary carcinoma within a functioning adenoma. Genetic analysis of such tumors indicated that functioning adenoma and papillary carcinoma may be etiologically independent. There have been a number of case reports on the coexistence of functioning thyroid adenoma and thyroid cancer or hyperparathyroidism, but none of the studies had examined the etiologic relationship of these lesions on a genetic basis. Furthermore, to our knowledge, this is the first report of the concurrence of four tumors in the neck, functioning thyroid adenoma, papillary thyroid carcinoma, follicular thyroid adenoma and parathyroid adenoma.

Adenoma↗
PubMed2002

Comparison of ACTH secretion in Cushing's adenoma and clinically silent corticotroph adenoma by cell immunoblot assay.

Immunocytochemical staining and cell immunoblot assay (CIBA) were performed in adenoma tissue from five patients with Cushing's disease and three patients with clinically silent corticotroph adenomas. All five patients with Cushing's disease showed hypersecretion of ACTH (130, 190, 331, 120, and 130 pg/ml), high levels of serum cortisol (26.6-44.0 micrograms/dl), and symptoms of Cushing's disease. All three patients with silent corticotroph adenoma showed hypersecretion of ACTH (110, 140, and 160 pg/ml) and normal levels of serum cortisol (11.4-26.8 micrograms/dl). The size of the pituitary adenoma on magnetic resonance imaging was smaller in patients with Cushing's disease (mean 8.2 mm) than in patients with silent corticotroph adenoma (mean 26.7 mm) (p = 0.001). Transsphenoidal surgery was performed to totally resect the adenoma tissue. Immunostaining for ACTH showed diffuse ACTH-immunopositive cells in all eight adenomas. CIBA technique showed a good correlation between percentage of ACTH-immunopositive cells and level of plasma ACTH in patients with Cushing's disease but no correlation between the two parameters in patients with silent corticotroph adenoma. The percentage of ACTH-secreting cells and the amount of hormone secreted by a single cell are too low in silent corticotroph adenomas to cause an increase in plasma ACTH level corresponding to the large tumor size.

Adenoma↗
PubMedDate not supplied

Adenoma and tiny carcinoma in adenoma of the papilla of Vater--p53 and PCNA.

BACKGROUND/AIMS: Adenomas develop only rarely in the small bowel mucosa. We particularly tried to clarify the histologic change in atypia of ampullary adenomas which are not familial polyposis. METHODOLOGY: Four adenomas, 4 adenocarcinomas, and 4 normal mucosal regions of the ampulla of Vater were investigated in this study. All cases were characterized in paraffin sections for the presence of p53 protein using the anti-p53 monoclonal antibody (DO7, Dako Corp., Glostrup, Denmark) and proliferating cell nuclear antigen using the anti-PCNA antibody (PC 10, Dako A/S, Copenhagen, Denmark). To obtain the percentages (labeling index) of PCNA, a dual wavelength imaging microdensitometer (CAS 200, Elmhurst, IL) was used. RESULTS: Transition of adenoma into adenocarcinoma was recognized in 2 of 4 cases. Labeling index of PCNA was 12.2% in normal mucosa, 41.3% in adenomas, and 66.0% in adenocarcinoma, respectively. In 2 cases with carcinoma in adenoma, labeling index was higher in carcinomatous lesion than in adenomatous lesion. p53 Protein was positive in all cases of adenocarcinoma of the ampulla of Vater, and not in any case of normal mucosa or adenoma. CONCLUSIONS: The adenoma-carcinoma sequence was morphologically recognized especially in tiny carcinoma in adenoma of the papilla of Vater. Both p53 mutation and high proliferative activity play important roles for the histogenesis of invasive adenocarcinoma.

Adenocarcinoma↗