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)

A series of 26 malignant peripheral nerve sheath tumours (MPNST) and 24 benign peripheral nerve sheath tumours (BPNST) were analysed immunocytochemically for p53 expression and the cell proliferation markers proliferating cell nuclear antigen (PCNA) and Ki67 (with MIB1). In 23/26 MPNST, 5%-65% of the tumour cell nuclei were immunoreactive for Ki67 with MIB1 while none of the 24 BPNST had nuclear staining exceeding 5%. Greater than 50% nuclear PCNA staining was detected in 25/26 MPNST compared with 8/24 BPNST; 17/26 MPNST showed 5-100% nuclear staining for p53 (13/26 > 20%), whereas none of the BPNST had nuclear staining exceeding 1%. The Ki67, PCNA and p53 immunostaining results correlated significantly with benign versus malignant (P < 0.001, P < 0.001 and P < 0.005, respectively) as well as mitotic rate (P < 0.001, P < 0.05 and P < 0.05). Ki67 immunostaining results correlated significantly with PCNA and p53, as did p53 and Ki67 and PCNA (P < 0.001 in both). Stepwise (logistic regression forward) multivariate analysis of the variable, benign versus malignant, revealed the strongest correlations with PCNA (P = 0.007) and Ki67 (P = 0.021). Direct confirmation of the presence of p53 protein was obtained by western blot analysis of 3 MPNST and 5 BPNST. Two MPNST, showing 90% and 30% immunoreactivity, were positive for p53, while one MPNST with 5% immunoreactivity and all 5 BPNST were negative. Southern blot analysis performed on the two MPNST with high p53 protein levels revealed no amplification of the MDM2 gene, suggesting that high p53 levels in MPNST are likely to be due to mutation. The results also indicate that PCNA and Ki67 are potentially useful in distinguishing BPNST from MPNST, particularly in problematic cases of cellular schwannoma versus MPNST. The detection of p53 in a large percentage of cells of a plexiform neurofibroma giving rise to MPNST and Ki67 in 5% and 25% of cells of two similar cases suggests that malignant transformation may be detected in some cases by p53 and proliferation markers prior to overt histological evidence of malignancy.
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PMID:Immunohistochemical and molecular analysis of p53, MDM2, proliferating cell nuclear antigen and Ki67 in benign and malignant peripheral nerve sheath tumours. 755 41

Germinal centre cell lymphomas (GCCL) show a wide range of clinical outcomes from persistent indolent disease to large cell transformation. To investigate possible mechanisms of this heterogeneity, a combined morphometric and immunohistological study of p53, bcl-2 and cell proliferation was carried out. There was wide variation in p53 expression between biopsies and between individual follicles in the same tumour. A similar pattern of variation was seen using the cell-cycle marker MIB1, but this did not correlate with p53 expression. Even in cases in which a t(14;18) was demonstrated by PCR, variation occurred in the number of cells expressing bcl-2. On the basis of these results, we suggest that the probability of the clonal expansion of GCCL tumour cells carrying additional genetic abnormalities depends on a complex interaction of cell proliferation with p53 and bcl-2 expression, and that this may account for variation seen in the clinical behaviour seen in this group of tumours.
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PMID:Heterogeneity in cell proliferation and expression of p53 and bcl-2 during the indolent phase of germinal centre cell lymphoma: an explanation for clinical variability. 766 61

The expression of p53 protein was studied in formalin-fixed paraffin-embedded specimens of 41 well-differentiated adenocarcinomas of the gall-bladder, six cases of acute cholecystitis and 23 cases of chronic cholecystitis, using a monoclonal p53 (PAb 1801) antibody and streptavidin-biotin. p53 staining was divided into diffuse, focal or sporadic patterns. The relationship between the p53 Labeling Index (p53 LI) and cellular proliferation was also investigated using monoclonal Ki-67 (MIB1) antibody. Twenty-four of the 41 carcinomas (58.5%) had a diffuse staining pattern with a high p53 LI (47-93%) and 9.8% (4/41) had a focal staining pattern with an intermediate p53 LI (22-34%), with no relation to pT stage, tumor size, histologic type or grade of cytologic atypia. The p53 LI was higher than the Ki-67 LI in these tumors except for one. On the other hand, p53 staining was completely sporadic in the non-neoplastic specimens with a low p53 LI (0.2-2.8%). The p53-positive cells in these specimens were located only within areas of Ki-67-positive cells. In conclusion, p53-protein overexpression occurs as an early event in approximately 70% of well-differentiated adenocarcinomas of the gall-bladder, and this alteration is maintained during progression from intramucosal to invasive carcinoma. p53 immunostaining can distinguish malignant from benign lesions of the gall-bladder.
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PMID:p53 immunostaining distinguishes malignant from benign lesions of the gall-bladder. 770 45

Atypical alveolar hyperplasia (AAH) has recently been described in human lungs in association with primary lung cancer, particularly adenocarcinoma. Unlike proximal bronchogenic carcinoma, peripheral (parenchymal) adenocarcinoma of the lung does not have a well-recognized progenitor lesion. Epidemiological morphometric, and cytofluorometric data in the literature suggest that AAH is a candidate premalignant entity. In this study, 97 AAH lesions were found in lungs resected from 29 patients (1-13 lesions per case, mean 3.5) being treated for presumed carcinoma (25/29 had adenocarcinoma). From a study case-load of 285 adenocarcinoma-bearing lungs, the AAH incidence was 8.8 per cent. Sections of 67 AAH lesions from 19 patients were stained using monoclonal antibodies against Ki67 (MIB1), p53 (DO7), and c-erbB-2 (NCL-CB11). Ki67 was expressed in up to 10 per cent of AAH nuclei. Thirty-nine lesions (58 per cent) showed stainable p53 protein, while five (7 per cent) expressed membrane c-erbB-2 oncoprotein. These latter five lesions were all strongly positive for p53, and both p53 and c-erbB staining was associated with increased cellular crowding and pleomorphism in AAH. These data demonstrate that AAH exhibits some genetic changes associated with malignancy and thereby support the hypothesis that AAH is premalignant.
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PMID:Atypical alveolar hyperplasia: relationship with pulmonary adenocarcinoma, p53, and c-erbB-2 expression. 788 86

A 77-yr-old man presented with a right inguinal mass. At herniotomy, an enlarged inguinal lymph node was also removed. Gross examination revealed a firm gray tumorous nodule measuring 3 cm in maximum diameter. On histological examination, the lymphatic tissue was found to have been almost completely replaced by spindle-shaped tumor cells arranged in whorls and bundles. In Giemsa-stained sections, about one-third of the tumor cells were seen to be strongly metachromatic tissue mast cells. The other tumor cells reacted only with a monoclonal antibody against vimentin out of a broad panel of antibodies directed against various antigens expressed by leukocytes, mesenchymal cells, and epithelial cells. A small fraction of the nonmetachromatic tumor cells reacted with the proliferation-associated antibody MIB1. Immunostaining with an antibody against p53 tumor-suppressor gene products was negative. Electron-microscopic examination revealed mast cells containing abundant granules, which were intermingled with fibroblasts that had bizarre, elongated nuclei. No myofibroblasts, desmosomes, or basement membrane material were detected. Clinical examination revealed no abnormalities, and blood and bone marrow findings were completely normal. A diagnosis of solitary (apparently benign) fibromastocytic tumor was established on the basis of the relative tumor cell numbers, the cytological features, and the clinical data. To the authors' knowledge, this is the first description of a solitary spindle cell tumor arising in a lymph node and simulating mastocytosis.
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PMID:Solitary fibromastocytic tumor arising in an inguinal lymph node: the first description of a unique spindle cell tumor simulating mastocytosis. 789 67

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

Recurrence of basal cell carcinoma (BCC) following treatment is a common event and long-term follow-up of all patients presenting with a primary BCC has been recommended. Proliferation indices have been recognized as important prognostic factors in several tumour types in a variety of cancer systems, being significantly elevated in more aggressive lesions. We have examined 51 BCCs (17 non-recurrent tumours [group 1], 17 original tumours which later recurred [group 2-O], and the corresponding 17 recurrent specimens [group 2-R]) for Ki67 antigen expression, a proliferation-associated antigen using immunohistochemistry with the monoclonal antibody MIB1. There was a significant increase in the percentage positive for MIB1 in the Group 2-O as compared with the group 1 BCCs (P < 0.05). p53 protein expression, as assessed by immunohistochemistry with the monoclonal antibody DO7, was similar in each group. These results show that Ki67 antigen expression differs between BCCs which later recur and BCCs that do not recur.
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PMID:Prognostic value of Ki67 antigen expression in basal cell carcinomas. 855 26

The objective of this study was to evaluate conjunctival nevi for p53 gene mutations. We studied 11 conjunctival nevi by immunohistochemistry with the DO7 monoclonal p53 antibody as well as the cell proliferation marker, MIB1. Of the 11 cases, 2 were negative, 2 had less than 1%, and 7 had more than 2% p53 immunopositive nuclei with no direct correlation with MIB1 positivity. Our results suggest altered expression of p53 in conjunctival nevi.
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PMID:Expression of p53 in conjunctival melanocytic nevi. An immunohistochemical study. 861 50

Malignant meningiomas are rarely encountered neoplasms. Few studies have examined MIB1 (marker of cell proliferation) or p53 (tumor suppressor gene) immunoreactivity in these tumors. This study retrospectively examines 23 malignant meningiomas (defined by the presence of either unequivocal brain invasion or metastasis) including MIB1 and p53 immunohistochemistry. The patients included 13 women and 10 men who ranged in age from 22 to 82 years (mean 63 years). Initial clinical presentation included weakness or numbness in 10 patients, visual signs or symptoms in 7 patients, and headaches in 6 patients. Histologically, nuclear pleomorphism was present in 23 of 23 tumors, disorganized architecture in 22 of 22, necrosis in 20 of 23, prominent nucleoli in 17 of 23, and hypervascularity in 4 of 23. One to 18 mitotic figures per 10 high power fields (HPF) (mean 6.1) were observed. Metastases were present in six patients (bone: 3 patients; lung: 2 patients; skin: 2 patients; kidney: 1 patient; and liver: 1 patient). MIB1 indices (positive tumor cells per 1,000 tumor cells evaluated x 100) in 20 tumors ranged from 1.3 to 24.2 (mean 11.7). p53 nuclear staining was observed in only 2 of 20 tumors. Follow-up information was available in 21 patients: 6 died of tumor (mean 27 months); 9 are alive with residual tumor (mean 35 months); 5 are alive with no evidence of tumor (mean 12 months); and 1 died 13 days postoperatively. There was no obvious correlation of the MIB1 index and tumor behavior. The majority of malignant meningiomas are characterized by nuclear pleomorphism, architectural disorganization, necrosis, prominent nucleoli, and increased mitoses. MIB1 labeling in most malignant meningiomas was high, consistent with the generally rapid growth of these tumors. Only a rare malignant meningioma demonstrated p53 alteration by immunostaining.
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PMID:Malignant meningioma: a clinicopathologic study of 23 patients including MIB1 and p53 immunohistochemistry. 865 46

Gliofibromas are rarely encountered astrocytic neoplasms characterized by an admixture of astrocytic and fibroblastic cell components. The exact nature of these rare tumors are still a matter of considerable debate. This article reports a case of gliofibroma occurring in a 3-month-old boy. The astrocytic component of the tumor stained diffusely positive for glial fibrillary acidic protein (GFAP) and S-100 protein. Prominent reticulin staining was observed within the fibroblastic component of the tumor. The MIB1 labeling index (positive number of tumor cells divided by total tumor cells counted X 100) was low (0.9), supporting the general slow growth of these tumors. Immunohistochemical staining with antibody against p53 protein was negative. Gliofibromas seem to be a low-grade variant of an astrocytoma that shares many features with other desmoplastic astrocytic neoplasms (desmoplastic infantile astrocytoma, desmoplastic infantile ganglioglioma) including a generally favorable prognosis.
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PMID:Gliofibroma: a distinct entity or a subtype of desmoplastic astrocytoma? 866 74


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