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Query: UMLS:C0001430 (adenoma)
 21,222 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

To answer the question why some gastric cancers make elevation while others make depression in their early stage, and why polypoid cancers grow larger than their benign counterpart adenomas, the distribution of proliferating cells and apoptotic cells was compared between these lesions. Proliferating cells and apoptotic cells were detected with anti Ki-67 antibody (MIB-1) and with the in situ nick end labeling (ISNEL), respectively. A total of 62 gastric tumors, taken by the endoscopic mucosal resection method, was assessed. They consisted of 14 adenomas and 48 mucosal carcinomas (27 polypoid and 21 depressed type). Overall positive rates of Ki-67 were 27.5 +/- 9.0% in adenoma, 40.1 +/- 11.1% in polypoid cancer and 47.5 +/- 9.7% in depressed cancer. Proliferating cells were preferentially found in the cripts of metaplastic mucosa, in the middle to upper layer of adenomas, and in the whole layer including their surface of adenocarcinomas. Within cancers the polypoid type had more positive cells in the upper layer, so did the depressed type in the lower layer. ISNEL positive nuclei showed sphere, fragmented, ringed forms, or the same form as neighboring tumor nuclei. Apoptotic cells lay scattered throughout tumor glands. Apoptotic cell counts per 1000 tumor cells were 26.0 +/- 9.7 in adenoma, 36.3 +/- 32.1 in polypoid cancer, and 52.5 +/- 19.3 in depressed cancer. Depressed type cancers and a few polypoid cancers rich in non-tumor tissues showed higher numbers of apoptotic cells than adenomas and usual polypoid cancers. (ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Cell proliferation and cell death (apoptosis) in epithelial tumors of the stomach--analysis of tumor tissues by the endoscopic mucosal resection]. 772 65

To clarify relation between macroscopic appearance and the mode of tumor growth in the superficial lesion of colorectal neoplasms, we compared their colonoscopic findings with histological architecture of tumor cells. Macroscopic type was classified into the superficial elevated lesion (II a, n = 42, mean 5.14mm) and the superficial depressed lesion (n = 42, mean 3.84mm). The latter was further divided into 3 subtypes; subtype A, an irregular depression with high marginal elevation (Dep (A), n = 20); subtype B, an irregular depression with irregular marginal elevation (Dep (B), n = 7); subtype C, a clear and wide depression without marginal elevation (Dep (C), n = 15). Histological architecture was evaluated by the transmucosal growth index (TGI) of tumor cells, which is a ratio of tumor width contacting with the muscularis mucosae against that of tumor surface, and by the distribution of proliferating cells detected by Ki-67 antibody (MIB-1). In adenomas TGI increased with a degree of central depression (IIa < Dep(A) < Dep(C)). In carcinomas TGI was high irrespective of their macroscopic forms. Ki-67 labeling indices tended to increase with histological atypia. Adenomas with severe atypia showed a high labeling consistent with carcinomas. In both adenomas and carcinomas, Ki-67 positive cells were mainly noted in upper third of neoplastic glands in II a, Dep (A) and Dep (B) neoplasms. By contrast, Dep (C) neoplasms lost a preferential distribution of proliferating cells, which reached the whole neoplastic glands. These results suggest that Dep (C) adenomas and carcinomas have a unique histopathological architecture in terms of a high TGI and an enlarged distribution of proliferating cells, implying a high malignant potential.
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PMID:[Macroscopic classification and kinetic alternations in the superficial lesion of colorectal neoplasms]. 781 19

Samples of normal, hyperplastic, and neoplastic parathyroid tissues were analyzed for proliferative activity to determine (1) whether a higher number of proliferating cells were detectable in adenoma and hyperplasia versus normal tissues; (2) whether there was a difference in the number of proliferating cells in adenoma versus hyperplasia; and (3) whether there was a relationship between nodularity and proliferative rate in both adenoma and hyperplasia. Formalin-fixed, paraffin-embedded tissue from 21 patients with parathyroid adenoma and 10 patients with hyperplasia (two primary, six secondary, and two tertiary) was analyzed by immunohistochemistry with the monoclonal antibody PC10 to proliferating cell nuclear antigen (PCNA) and, in a subset of cases, with Ki-67 (MIB 1) as markers of cell proliferation. The results were that (1) no proliferating cells were found in normal glands or residual rim of "suppressed" parathyroid tissue; (2) the most intense proliferative activity was confined to nodular areas in both adenomas (57% nodular) and hyperplasias (80% nodular); (3) when fields of highest number of labeled nuclei were chosen, PCNA counts were higher in adenomas than in hyperplasia in both nodular and diffuse areas (P < .05); and (4) the number of nuclei immunoreactive for Ki-67 (MIB-1) was consistently and proportionally lower (range, 13% to 45%; mean, 32%) than the number of those immunoreactive for PCNA, although the nodular pattern was maintained. These findings demonstrate that nodules within parathyroid adenomas and hyperplasias contain subpopulations of cells with a consistently higher proliferative rate than nonnodular areas. Cells within these nodules may be more likely to develop genetic abnormalities that have been observed in hyperplastic and neoplastic parathyroid tissues.
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PMID:Nodular foci in parathyroid adenomas and hyperplasias: an immunohistochemical analysis of proliferative activity. 792 9

The proto-oncogene Bcl-2 encodes a protein that protects cells from programmed cell death (apoptosis). The protein is expressed in the proliferative compartment of several normal tissues, including normal colonic crypts. The aim of this study was to test Bcl-2 expression in colorectal neoplasms, assuming that, as a regulator of apoptosis, it might be involved in the progression from adenoma to carcinoma. To this end, Bcl-2 reactivity was tested by immunohistochemistry in hyperplastic polyps, colonic adenomas, and carcinomas and its expression was compared with staining for the proliferation-associated Ki-67 antigen, using the MIB-1 antibody. Bcl-2 expression occurred in 2 out of 10 hyperplastic polyps and in 31 out of 35 (tubular, villous, and tubulovillous) adenomas, irrespective of their degree of dysplasia. Of ten carcinomas, only three were focally Bcl-2-positive, all moderately to well differentiated. In two of four carcinomas in Bcl-2-positive adenomas, no Bcl-2 staining was observed. High numbers of MIB-1-positive cells were found in all hyperplastic and neoplastic lesions, without apparent correlation between proliferation and Bcl-2 expression. These findings suggest that in the pathogenesis of hyperplastic polyps, increased crypt cell proliferation is primarily involved, but in some lesions decreased apoptosis may play a role. Furthermore, the increased Bcl-2 expression in adenomas but not in the majority of the carcinomas suggests either that decreased apoptosis is not usually involved in the pathogenesis of these lesions or that the regulation of apoptosis in colorectal epithelia involves additional regulatory factors.
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PMID:Expression of Bcl-2 protein in hyperplastic polyps, adenomas, and carcinomas of the colon. 869 16

The relationship between invasiveness and proliferative potential was studied in 31 cases of pituitary adenomas. The invasiveness was determined by histological examination of sellar floor dura resected during transsphenoidal surgery. The proliferative potential of adenoma specimens was examined immunohistochemically using monoclonal antibody (MIB-1). There were 11 adenomas with histologically verified dural invasion out of 31 cases. These adenomas had a higher MIB-1- positive ratio than adenomas without dural invasion (p < 0.05). Pituitary adenomas with a high proliferative potential tend to be invasive.
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PMID:Dural invasion and proliferative potential of pituitary adenomas. 874 Dec 48

A case of tubular adenoma arising in the right ventricular choroid plexus of a 4-month-old boy is described. A basic pattern of neoplastic glandular epithelium and lack of papillary architecture distinguished this tumor from a papilloma. Coexpression of S -100 protein, transthyretin and cytokeratin identified the neoplastic cells as being of choroid plexus origin. Immunohistochemical detection of MIB-1 showed a proliferation rate (16%) similar to adenomas in more conventional locations, but not encountered in benign brain tumors. In situ detection of DNA-derived oligonucleosomal fragments by TUNEL analysis, on the other hand, detected apoptotic activity in 5-8% of tumor cells. The indolent course of the disease in the present case, thus, might suggest a compensatory elimination of proliferating cells by apoptosis. This possibly points to mechanisms of neoplastic transformation different from those involved in choroid plexus papillomas.
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PMID:Tubular adenoma of the choroid plexus: evidence for glandular differentiation of the neuroepithelium. 889 20

This study documents a pyloric gland type adenoma of the gallbladder with prominent spindle cell metaplasia arising in a 61 year-old woman. A pedunculated polyp, 1.5 x 1.0 x 1.0 cm, was histologically diagnosed as a tubular adenoma. Most glandular structures showed positivity for a monoclonal antibody M2 (2B5) which indicates a differentiation to pylotic gland type. The spindle cell component displayed no apparent epithelial structures but stained mostly positive for pancytokeratin and cytokeratin (CK) 18, and focally for CK 5 + 6, CKs 7 and 19, whereas CKs 8, 13, 20, and non-epithelial markers could not be demonstrated. This suggests that the spindle cells were immature epithelial cells differentiating towards squamous and/or glandular cells. Even in spindle cell areas, the nuclear atypia was mild, and proliferating cells positive for MIB-1 (Ki-67) antigen were infrequently seen. This unique phenomenon, of which only three cases have been previously reported, is considered to represent benign squamoid spindle cell metaplasia.
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PMID:Pyloric gland type adenoma of the gallbladder with squamoid spindle cell metaplasia. 895 Jul 64

Cytoplasmic carcinoembryonic antigen (CEA) positivity assists in the distinction of benign and malignant glandular lesions of the cervix, but some cases remain problematic. The accumulation of p53 protein and an increased proliferative index, as measured by the expression of Ki-67 antigen, have not been used as adjuncts to the diagnosis of these lesions. Immunohistochemical stains for CEA, p53 protein, and Ki-67 antigen were performed on 31 formalin-fixed, paraffin-embedded endocervical lesions including invasive adenocarcinoma, adenocarcinoma in situ, adenoma malignum, tunnel clusters, florid microglandular hyperplasia, mesonephric remnants, florid glandular hyperplasia, atypical glandular hyperplasia, and normal controls. Ki-67 antigen expression was quantitated as negligible, low, moderate, or high on the basis of the percentage (< 5%, 5-10%, 11-40%, > 40%, respectively) of glandular nuclei that were positive with MIB-1 antibody. Strong staining of more than 10% of the glandular epithelial nuclei was interpreted as positive for p53 protein overexpression. CEA positivity was determined by either diffuse or focal cytoplasmic staining of columnar epithelial cells equalling glycocalyceal staining in intensity. The combination of CEA positivity and a moderate-to-high proliferative index was limited to cases of invasive adenocarcinoma, adenoma malignum, and adenocarcinoma in situ, as compared with benign glandular lesions (P = 0.005). A high Ki-67 proliferative index and/or CEA positivity were features of malignant lesions rather than benign mimickers; there were no false positives or false negatives. Similarly, only malignant neoplasms shared a combination of p53 overexpression and CEA positivity (P = 0.043). The combination of cytoplasmic CEA positivity in glandular cells and a moderate-to-high Ki-67 proliferative index is diagnostic of malignancy in endocervical lesions. With the exception of florid microglandular hyperplasia, p53 expression is only seen in neoplastic lesions of the endocervix. An immunohistochemical battery consisting of MIB-1 (Ki-67), p53 protein, and CEA is useful in discriminating between benign and malignant endocervical lesions.
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PMID:Immunohistochemical staining for Ki-67 antigen, carcinoembryonic antigen, and p53 in the differential diagnosis of glandular lesions of the cervix. 907 23

Herein we present a group of rare tumors of the sella region that have not been previously recognized. Although clinically and radiographically the tumors resemble nonfunctioning pituitary adenomas, their histologic, immunohistochemical, and ultrastructural features differ and indicate a salivary gland origin. The lesions cover a morphologic spectrum that includes cellular pleomorphic adenoma, monomorphic adenoma, oncocytoma, and low-grade adenocarcinoma of the salivary gland. All tumors except the oncocytoma were immunoreactive for cytokeratin and were negative for pituitary hormones and synaptophysin. Ultrastructural characteristics in the cases examined include hypodense stromal material, basal lamina, and tonofilament bundles. The single oncocytoma was packed with mitochondria and lacked membrane-bound secretory granules. DNA ploidy based on image analysis and MIB-1 labeling indices showed diversity within this group of tumors, with labeling indices ranging from 0.06% to 15%. The presumed origin of these rare neoplasms is from salivary gland rests related to the normal pituitary gland. Despite their varied morphology, such tumors are easily confused with pituitary adenoma. Although rare, tumors of salivary gland origin should be considered in the differential diagnosis of unusual adenohypophyseal tumors.
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PMID:Salivary gland-like tumors of the sellar region. 913 Sep 89

A retrospective study on 22 cases of parathyroid adenoma, 9 cases of primary parathyroid hyperplasia and 14 specimens of normal suppressed glandular tissue was undertaken to determine the usefulness of proliferative index (PI) for discriminating adenoma from hyperplasia, as an adjunct to the existing histological criteria. PI was determined by avidin-biotin-complex immunostaining after high temperature microwave antigen retrieval in paraffin sections, using monoclonal MIB-1 antibody which detects paraffin resistant analogue of cell cycle-associated Ki-67 antigen. PI expressed as percentage positive cell nuclei, was 1.36 +/- 0.62 (range 0.04-2.72) in adenoma, 1.17 +/- 0.83 (0.02-1.98) in hyperplasia and 0.03 +/- 0.02 (0.00-0.06) in normal suppressed glandular tissue. While the difference between normal suppressed glandular tissue and adenoma and hyperplasia was significant (P < 0.001), that between adenoma and hyperplasia was not. We conclude that although PI could distinguish between normal suppressed glandular tissue versus glands with primary hyperparathyroidism, it failed as an additional useful parameter for discriminating between adenoma and hyperplasia, both of which have low but similar proliferative activity.
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PMID:MIB-1 proliferative index in parathyroid adenoma & hyperplasia. 918 80


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