Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UNIPROT:P04637 (p53)
 77,613 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The effects of treatment in a hydrated autoclave (121 degrees C, 2 atm for 20 min), microwave oven (in water), and simple heating (60 degrees C overnight in distilled water or 90 degrees C for 10 min in ZnSO4) on the stainability of 56 antigens by commercially available antibodies in formalin-fixed paraffin-embedded tissue sections were evaluated. The detectability of nuclear antigens, glycoprotein, lymphocytic surface markers, and chromogranin A was significantly and reproducibly improved by these treatments, whereas the detectability of viral antigens and peptide hormones was attenuated or unchanged. This enhancement includes not only the distinctiveness of the positive staining, but also the number of positive cells, as revealed by comparing serial sections. Among these four heating procedures, microwave heating and autoclaving were more effective than the others on p53, c-erbB-2, and CA125, whereas simple heating was best for smooth-muscle actin (HHF35 and CGA7). Generally the effects of the heating procedures for these antigens were consistent among the cases, but the effects on GFAP varied with the case. The alterations we observed could significantly influence the interpretation of immunohistochemical staining of currently popular tumor markers such as p53 in terms of their prevalence (28% vs 64% in gastric cancer; 36% vs 82% in metastatic liver cancer) and other diagnostically important markers.
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PMID:Alteration of immunoreactivity by hydrated autoclaving, microwave treatment, and simple heating of paraffin-embedded tissue sections. 751 73

Colorectal adenocarcinomas may display features of endocrine differentiation, shown by argyrophil stains and by the expression of endocrine markers such as chromogranin A. We investigated chromogranin A and secretogranin II immunoreactivity in a series of 208 carcinomas of the large bowel to assess the prevalence and clinical significance of endocrine differentiation. Tumors expressing endocrine markers were classified as low expressors (< than 1 immunoreactive tumour cell/mm2) and high expressors (> than 1 immunoreactive tumour cell/mm2). There were 33 (16%) carcinomas showing both chromogranin A and secretogranin II immunoreactivity: 11 tumours (5%) were high expressors. Endocrine differentiation was not related to the disease stage, tumour location, grade, DNA ploidy and p53 protein accumulation. In the entire series chromogranin A immunoreactivity did not provide prognostic information using univariate and multivariate analysis. A worse overall survival (P = 0.048) was demonstrated for the stage III patients with high expressor tumours, but there were only five patients in this group. The results of our investigation suggest that chromogranin A immunoreactivity is not a useful variable in the prognostic assessment of colorectal adenocarcinomas.
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PMID:The prevalence and clinical significance of chromogranin A and secretogranin II immunoreactivity in colorectal adenocarcinomas. 765 39

Bcl-2 expression has been evaluated immunocytochemically in a series of 33 medullary thyroid carcinomas (MTC) with long-term (mean, 10.3 years) follow-up. Twenty-six of 33 cases showed intense bcl-2 immunoreactivity in more than 25% neoplastic cells. Bcl-2 immunoreactivity did not correlate with several clinicopathologic parameters including sex and age of the patients, sporadic or familial disease, tumor size and stage, amount of amyloid stroma, and immunoreactivity for calcitonin, chromogranin A, proliferating cell nuclear antigen (PCNA), N-myc, and p53. Lack of bcl-2 immunoreactivity, however, correlated significantly (P = .0001) with a shorter survival. Indeed, the seven patients with tumors devoid of bcl-2 immunoreactivity all died of disease within 8 years from the diagnosis. In multivariate analysis, lack of bcl-2 immunoreactivity was an independent predictor of worse prognosis (P = .001 for disease-free survival and P = .0001 for overall survival). None of the other clinicopathologic variable investigated proved to be an independent prognostic parameter. It is concluded that down-regulation of bcl-2 expression in MTC may identify a subset of tumors with a more aggressive clinical course.
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PMID:Prognostic value of bcl-2 immunoreactivity in medullary thyroid carcinoma. 767 94

Lymphoepithelial carcinoma (Schmincke's tumor) is a relatively common malignancy in the upper respiratory tract (nasopharynx), but it rarely occurs at other sites. We describe here the first case of a vaginal neoplasm that closely resembled lymphoepithelial carcinoma in its histological features and immunophenotype. The tumor was detected in an 81-year-old woman who presented with recurrent vaginal bleeding. On colposcopy, an ulcerated polypoid tumor mass was seen in the posterior wall of the middle portion of the vagina. Histologic examination revealed an undifferentiated spindle-cell carcinoma (KL1+, chromogranin A-, vimentin-) with abundant lymphocytes (mostly UCHL1+ T cells), plasma cells, and macrophages (CD68+) in and around the tumor cell nests. A minority of the tumor cells exhibited overexpression of p53 protein and a quarter of the tumor cells reacted with the antibody MIB1, that is, were in a proliferate state. The tumor cells did not react with the monoclonal antibody DAKO-EBV, which detects a latent membrane protein (LMP-1) encoded by the Epstein-Barr virus. The tumor underwent regression after radiotherapy. No signs of recurrence or dissemination of the carcinoma have been detected clinically during the 6 months since treatment.
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PMID:Lymphoepithelioma-like carcinoma of the vagina: a case report with special reference to the immunophenotype of the tumor cells and tumor-infiltrating lymphoreticular cells. 800 41

Multiple carcinomas of the pancreatico-biliary tree are rare. A 53 year old Japanese man was diagnosed as having an adenocarcinoma in the papilla of Vater. During the operation, he was also found to have a polypoid mass in the common bile duct. While cutting the operative specimen into stepwise sections, a small tumor was also detected incidentally in the main pancreatic duct of the pancreatic head. Histologically, all three tumors proved to be papillary adenocarcinomas and were restricted to the mucosa. Immunohistochemically, all three tumors were positive for carcinoembryonic antigen, carbohydrate antigen 19-9, chromogranin A and serotonin, while they were negative for somatostatin. Immunoreactivity to the tumor suppressor gene p53 protein (PAb 1801) was found in all three tumors. A flow cytometric analysis of the cellular DNA content revealed all three tumors to be aneuploid. The above results suggested that these three tumors from different sites all had the same histological, immunohistochemical and flow cytometrical characteristics.
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PMID:Three synchronous carcinomas of the papilla of Vater, common bile duct and pancreas. 804

In a series of 22 pancreatic acinar cell carcinomas, including two acinar cystadenocarcinomas, cellular differentiation was analyzed by immunocytochemistry and electron microscopy. In addition, overexpression of p53 protein and Ki-ras codon 12 mutation was studied. Four of the 20 noncystic acinar cell carcinomas showed a pure acinar pattern, nine an acinar-solid, and seven a solid pattern. All tumors stained for at least one of the following pancreatic acinar markers: trypsin (21 of 22), lipase (19 of 22), chymotrypsin (13 of 22), phospholipase A2 (nine of 22), and pancreatic stone protein (19 of 22). One-third of the tumors expressed neuroendocrine markers (synaptophysin, eight of 22; chromogranin A, six of 21) and duct cell markers (CA19.9, nine of 21; B72.3, six of 21). Cellular coexpression of trypsin and synaptophysin was demonstrated in one tumor. Electron microscopy revealed zymogen granules (nine of nine). In only one of 16 tumors a Ki-ras mutation at codon 12 was found, whereas in none of 19 tumors could overexpression of p53 protein be demonstrated. The results suggest that acinar cell carcinomas show obvious capacity to differentiate into several directions, but nevertheless constitute an entity different from ductal adenocarcinomas or endocrine tumors.
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PMID:Pancreatic acinar cell carcinoma. An analysis of cell lineage markers, p53 expression, and Ki-ras mutation. 836 71

We examined over-expression of p53 protein and proliferative activity of neoplastic endocrine and Paneth cells in cancer or dysplasia of ulcerative colitis (UC). The labeling index of p53 or Ki-67 of endocrine cells was counted with double immunostaining of p53 or Ki-67 and chromogranin A (CGA). 540 CGA-positive cells and 65 Paneth cells were all negative for p53. 5.1% of CGA-positive cells and none of 56 Paneth cells were positive for Ki-67 reaction. These observation suggest that even in cancer or dysplasia of UC cell-differentiation to neoplastic endocrine and Paneth cells decrease proliferative activity, and that these types of cell-differentiation suppress over-expression of p53 protein.
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PMID:[Overexpressed p53 protein and cell-proliferative activity disappear or remarkably decrease in neoplastic CGA-positive endocrine and Paneth cells in cancer or dysplasia of ulcerative colitis]. 855 76

A case is presented of pulmonary blastoma occurring in the right upper lobe of a 25-year-old man without distinct clinical features and laboratory abnormality. Light microscopic analysis revealed that the tumor was composed of branching glands and morulae embedded in a primitive but bland mesenchyme. Immunohistochemically the epithelial cells were immunoreactive for cytokeratins, S-100 protein, protein gene product 9.5, chromogranin A, calcitonin, and Ki-67 (MIB-1); the mesenchymal cells were immunoreactive for vimentin, actin, cytokeratins, and Ki-67; and all the tumor cells were negative for p53, estrogen receptor protein, and human chorionic gonadotropin beta. Characteristically, many epithelial cells contained optically clear nuclei which were immunoreactive for biotin (M743). Electron microscopic analysis revealed that the optically clearing change was due to replacement of the central area of the nuclei by a mass of parallel-arranged 7- to 10-nm filaments, and biotin-immunoreactive products were mainly localized in the nuclear matrix. Additionally, spherical bodies were identified in the cytoplasm of the nuclear filament-aggregated cells, suggestive of an intimate pathogenetic association of the two morphological abnormalities. The similarity of the aggregated nuclear filaments to those observed in gestational endometrium and ovarian endometrioid carcinoma implies that a similar mechanism plays a role in the pathogenesis of these abnormalities.
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PMID:Pulmonary blastoma: an ultrastructural and immunohistochemical study with special reference to nuclear filament aggregation. 859 6

The clinicopathologic features, including a detailed immunohistochemical, ultrastructural, and flow cytometric analysis, are described in three cases of atypical carcinoid tumor of the larynx. All patients had metastatic disease within cervical lymph nodes at presentation and eventually developed distant metastases. Special stains revealed focal intracytoplasmic mucin accumulation, and immunohistochemistry showed the tumors to be positive for CAM 5.2, CEA, chromogranin A, and calcitonin. In two cases, double-staining techniques revealed occasional cells that stained for both mucin and chromogranin A. The histochemical and immunohistochemical findings in these two cases were confirmed at the ultrastructural level, with most tumor cells containing many neurosecretory granules. Smaller numbers of cells contained mucin vacuoles and, in occasional cells, both mucin and neuroendocrine granules were identified. The three tumors exhibited positive staining with D07 (anti-p53), and flow cytometric analysis revealed DNA aneuploidy and polyploidy. The double-staining and ultrastructural features indicate that laryngeal atypical carcinoid qualifies for the designation of true amphicrine carcinoma. Further study is necessary to determine whether mutation of the p53 gene is important in the evolution of laryngeal neuroendocrine tumors and whether DNA aneuploidy or polyploidy identifies a subset of these tumors with a poor prognosis.
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PMID:Atypical carcinoid tumor of the larynx: an immunohistochemical, ultrastructural, and flow cytometric analysis. 927 73

Pancreatic ductal adenocarcinoma is one of the major causes of cancer mortality in the industrialized world, having among the poorest prognosis of any malignancy. Mutations or alterations in the p53 tumor suppressor gene/protein are observed in 50-70% of these cancers, yet little information is available regarding the phenotypic effects of restoration of wild-type (wt) p53 function in pancreatic ductal carcinoma cells. The consequences of stable reintroduction of wt p53 on apoptosis and differentiation was examined in a poorly differentiated pancreatic carcinoma cell line (Panc-1), possessing only mutant (mt) p53 (codon 273 mutation). Cells were transfected with a temperature-sensitive mouse p53val135 (tsp53) vector under additional control of a genetically-modified metallothionein promoter. This tsp53 has a 'mt' phenotype at 37.5 degrees C, and a 'wt' phenotype at 32.5 degrees C and the presence of 100 microM ZnCl2. Stable expression of wt p53 caused upregulation of the p21/WAF1 gene, and G1 growth arrest as shown by flow cytometry and BrdU labeling. Additionally, apoptosis was induced 8-12 post-induction in the majority of the cells (60-70%), as demonstrated by morphological changes, in situ TdT labeling and internucleosomal laddering. However, a subpopulation (30%) of the transfectants survived this apoptotic fate. Unlike the epithelial parental Panc-1 cells, these cells exhibited the appearance of a neuroendocrine-like phenotype with extensive branch-like processes, and marked cytoplasmic and cytoskeletal immunostaining for tau-2, synaptophysin, and chromogranin A. These studies suggest that stable and regulated expression of wt p53 can have multiple phenotypic consequences (apoptosis and altered differentiation to a neuroendocrine-like phenotype) in poorly-differentiated pancreatic carcinoma cells.
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PMID:Stable reintroduction of wild-type P53 (MTmp53ts) causes the induction of apoptosis and neuroendocrine-like differentiation in human ductal pancreatic carcinoma cells. 956 27


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