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)

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

Pure protoplasmic astrocytomas are a group of rarely encountered low grade astrocytic neoplasms. Relatively few studies have specifically examined this subset of tumors. A series of 18 protoplasmic astrocytomas in 14 males and four females (age range 2.5-52, mean 22 years) were studied in order to examine MIB1 (a marker of cell proliferation) and p53 (a tumor suppressor gene) immunoreactivity. All patients presented with seizures (mean duration 94 months) and three with headaches also. Eight tumors were located in the temporal lobe and six in the frontal lobe. All tumors were characterized by a proliferation of astrocytes with round nuclear contours arranged against a microcystic background. Only rare foci of mild vascular proliferation (3 tumors), rare mitotic figures (1 tumor), and mild nuclear atypia (3 tumors) were observed. Most tumors were primarily cortical in location. Necrosis was not seen in any of the tumors. MIB1 indices (number of MIB1 positive tumor cells/1000 tumor cells evaluated x 100) ranged from 0 to 4.3 (mean 0.7); in five tumors, no MIB1 staining was observed. p53 immunoreactivity was noted in 5 of 18 tumors (28%). Five patients received adjuvant radiation therapy and one adjuvant chemotherapy. At last known follow-up, 11 patients are alive with no evidence of residual tumor (mean 70 months), six patients are alive with evidence of residual tumor (mean 58 months), and one patient died of complications unrelated to the tumor (36 months) postoperatively. Based on these findings, the conclusions presented are as follows: (i) MIB1 indices are generally low in these tumors, corroborating the clinical impression of a slow growing neoplasm; and (ii) p53 immunoreactivity is observed in a minority of protoplasmic astrocytomas.
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PMID:MIB1 and p53 immunoreactivity in protoplasmic astrocytomas. 897 Jan 95

Tumors of mixed glioneuronal type are well recognized in the central nervous system. The most common examples of these lesions include gangliogliomas and dysembryoplastic neuroepithelial tumors. Recently, unusual examples of these lesions have been described, including the papillary glioneuronal tumor. This report describes a histologically similar-appearing lesion arising in the left parieto-occipital lobe of an 18-year-old man who presented with headaches and difficulties with vision. Imaging studies noted a large cystic neoplasm marked by a peripheral rim of enhancement. The patient underwent gross total resection of the tumor, which histologically was marked by a mixture of glial (glial fibrillary acidic protein-positive) and neural (synaptophysin-positive) components. Architecturally, the tumor was notable for a focal pseudopapillary pattern. Papillae were lined by predominantly glial cells, with intervening areas occupied by neurally differentiated cells. Mitotic activity, vascular proliferation, and necrosis were not noted. A MIB-1 labeling index of 1.1% was seen. p53 immunoreactivity was not observed. This report adds further evidence supporting the existence of this unusual mixed glioneuronal tumor of the central nervous system.
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PMID:Papillary glioneuronal tumor. 1110 65

Mixed glioneuronal neoplasms are relatively uncommon tumors in the central nervous system. Recently, an unusual glioneuronal tumor arising in adults marked histologically by neuropil-like islands was described. We present a similar case arising in a 23-year-old woman who presented with headaches and seizures and on imaging studies was noted to have a frontal-temporal lobe mass. The patient underwent partial resection of the tumor, which histologically resembled anaplastic astrocytoma, and received a course of radiation therapy and chemotherapy. Increasing seizure frequency and expanding size on neuroimaging prompted a re-excision of the tumor. The second resection was marked by islands of tissue resembling gray matter with slightly atypical neuronal and glial cells situated in the white matter. These islands stained positively with synaptophysin and did not stain with glial fibrillary acid protein. Mild vascular proliferation and moderate nuclear pleomorphism also characterized the tumor. Areas of necrosis were not noted. A MIB-1 labeling index of 18.1% was noted. P53 immunoreactivity was observed in approximately 40% of tumor cell nuclei. This lesion is felt to represent a clinically aggressive glioneuronal neoplasm with an unusual and distinctive histologic phenotype. HUM PATHOL 31:1435-1438.
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PMID:Glioneuronal tumor with neuropil-like islands. 1111 23

Recent reports have shown that gamma-knife radiosurgery provides a safe and effective strategy for the management of brain tumors. To evaluate the role of stereotactic radiosurgery in the management of meningiomas, we investigated the histopathology of two patients. The patients, a 37-year-old man and a 54-year-old woman, presented with visual field disturbance or headache. Imaging studies demonstrated intracranial meningiomas--tentorial and sphenoid ridge, respectively. Each patient undewent subtotal surgical resection (more than 90% in both patients), followed by gamma-knife radiosurgery of the remnant tumor marginal doses of 15 Gy. Pathological examination of the original tumors revealed a meningothelial meningioma and an atypical meningioma, respectively. Enlargement of the remnant tumors 4 months after radiosurgery resulted in total surgical resection in both patients. Thirteen months later, the patient with the atypical meningioma underwent a third operation for early recurrence of the tumor. Histopathology was investigated, and MIB-1, p53, and bcl-2 labeling indexes (LI) were analyzed immunohistochemically. Histopathologically, the specimens showed necrosis and intratumoral vessel obliteration after radiosurgery in both cases. However, more remnant tumor cells survived in the atypical meningioma. Immunohistochemically, increased wild-type p53, decreased bcl-2 expression, and decreased MIB-1 LI were observed in the benign meningioma. In the atypical meningioma, on the contrary, MIB-1 LI was decreased and mutant-type p53 and bcl-2 expression were unchanged. The specimen from the third operation revealed an anaplastic meningioma, and MIB-1 LI was markedly increased. These findings suggest that the efficacy of radiosurgery may differ between benign and atypical meningiomas.
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PMID:Different responses of benign and atypical meningiomas to gamma-knife radiosurgery: report of two cases with immunohistochemical analysis. 1190 75

Few studies have examined the role of cell proliferation and apoptotic markers in chordomas. This study retrospectively reviews the clinicopathologic features of 26 chordomas and examines MIB-1, p53, bcl-2, and cyclin D1 immunoreactivity in these neoplasms. Patients ranged in age from 34 to 78 years (mean, 60.7 years) and included 14 females. The most common presentations included lower back pain (N = 15) and headaches (N = 10). Sixteen tumors arose in the lumbosacral region and 10 in the clivus. Initial surgery included biopsy (N = 17), subtotal resection (N = 4), and gross total resection (N = 5). The single highest mitosis count per 10 high power fields ranged from 0 to 6 (mean, 1). Marked nuclear pleomorphism was identified in seven tumors. Marked hypercellularity was seen in two tumors. Focal necrosis was identified in seven tumors. MIB-1 labeling indices (LI) in 22 tumors ranged from 0 to 3.8 (mean, 0.5). Cyclin D1 LI ranged from 0 to 82.4 (mean, 35.6). Seven tumors had positive p53 immunostaining and three demonstrated focal positive staining with bcl-2 antibody. Five tumors locally recurred; two patients developed metastatic disease. Thirteen patients received adjuvant chemotherapy and/or radiation therapy. At last known follow-up, seven patients died with tumor (12 to 132 months follow-up). Five additional patients died, two without tumor at 36 and 72 months follow-up and three patients in whom the tumor status at death was not known. Seven patients were alive with evidence of tumor (1 to 120 months) and five patients were alive without evidence of tumor (12 to 84 months). Clinical follow-up was not available in one patient. In conclusion, the low MIB-1 LIs and the lack of p53 and bcl-2 staining is in keeping with the low-grade nature of most chordomas. High cyclin D1 LIs may be reflective of a tendency to accumulate cyclin D1 protein; however, there appears to be a block in the effect of cyclin D1 on cell proliferation in these tumors. Cyclin D1, MIB-1, p53, and bcl-2 immunostaining does not appear to improve one's ability to predict behavior versus routine light microscopy.
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PMID:Apoptotic and proliferative markers in chordomas: a study of 26 tumors. 1217 Apr 53

Differently from conventional primary neuroectodermal tumors (PNETs), molecular features of undifferentiated lesions have been poorly studied. Medulloblastoma and PNET neoplasms showed a high incidence of loss of heterozygosity (LOH) on chromosome 17p13, in the region of tumor suppressor gene p53. Recent studies have shown a significant correlation between the presence of p53 Arg72Pro polymorphism and several undifferentiated carcinomas. We performed molecular analysis in an anaplastic tumor of posterior fossa in a patient with a constitutional maternal translocation [46,XX,t(5;19)] and a history of headache, nausea and vomiting. We identified the presence of LOH at 17p13 and Pro72Arg polymorphism in tumor DNA. These molecular findings helped us better characterize this undifferentiated tumor and led to a more aggressive therapy.
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PMID:Loss of heterozygosity and p53 polymorphism Pro72Arg in a young patient with medulloblastoma. 1268 57

A case of pleomorphic xanthoastrocytoma in a 10-year-old Malay boy is reported. The patient presented with headache and epilepsy. On computed tomography, a ring-enhancing low-density lesion was observed in the left fronto-temporal area. During surgery, a cystic tumour containing serous fluid was found and almost totally removed. Histologically, the tumour exhibited marked pleomorphism of oval and spindle-shaped cells intermixed with uni- and multinucleated giant cells, and xanthomatous cells with foamy cytoplasm. The tumour displayed pericellular reticulin and periodic acid-Schiff positive granules. Focally, six mitotic characters per 10 high-power fields were seen, and necrosis was confined only to the inner lining of the cyst. Mutational analysis showed that a frameshift mutation (a 4-bp deletion) in the p53 gene had occurred in codons 273 and 274 of exon 8. No mutation was detected in the p16 gene. No allelic loss and/or loss of heterozygosity were observed on chromosome 10 using microsatellite marker D105532. The patient was treated with postoperative radiotherapy because of histological anaplasia and the presence of residual tumour. The patient showed marked neurological recovery after a follow-up period of 2 years.
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PMID:Molecular genetic analysis of anaplastic pleomorphic xanthoastrocytoma. 1273 98

Gliosarcoma (GSa) is a rare primary central nervous system neoplasm (CNS) characterized by biphasic histological pattern with both glial and sarcomatous components. Our objective is to describe the clinical, morphological and immunohistochemical features of four cases of GSa and to discuss its pathogenetic mechanisms. The male:female ratio was 3:1. The mean age was 39 years, ranging from 19 to 48. Headache was the commonest clinical symptom. All patients underwent craniotomy with microsurgery and total resection of the tumor. Diagnosis was suspected due to microscopic architecture and confirmed by detection of reticulin fibers through histochemical techniques. Immunohistochemical analysis was positive for p53 in both glial and sarcomatous cells in all four cases. EGFR was focally positive in glial cells in one case. Our findings support monoclonal origin of GSa involving the TP53 tumor-suppressor gene. However, alternative pathways cannot be ruled out.
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PMID:Gliosarcoma: report of four cases with immunohistochemical findings. 1533 17

We describe a rare tumor site in a 46 year old man who presented with a two week history of headache. Physical examination revealed bilateral papilloedema with no other localizing signs. Computed Tomographic Scan as well as Magnetic Resonance Imaging of the brain revealed a lesion with a dura tail located adjacent to the falx cerebri of the right frontal lobe. This lesion was not invading the inner table of the skull base. A tumor blush was seen on angiogram. There were no abnormalities on CT scan of the abdomen and fundoscopy was normal. Intraoperatively a vascular tumor not attached to the dura was noted and removed totally. Histopathological examination was typical of a hemangioblastoma. Analysis revealed no mutations of the VHL gene in 5 regions, exon 5-8 of the p53 gene, exon 1-2 of the p16 gene and exon 5,6 and 8 of the PTEN gene. This is the first case report of a supratentorial hemangioblastoma in a non-Von Hippel Lindau patient with genetic evidence.
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PMID:Molecular genetic analysis of a supratentorial haemangioblastoma in a non-Von Hippel Lindau patient. 1637 93


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