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)

Using the polymerase chain reaction and single-strand conformation polymorphism analysis, p53 gene mutations were examined in 24 cases of ovarian tumor including 14 ovarian carcinomas and 2 borderline cases of common epithelial type, 7 germ cell tumors, and one stromal tumor. Abnormal bands indicating mutations were detected in 12 (50%) of the cases examined, being present most frequently in common "epithelial" ovarian carcinoma (71%, 10/14). One case each of squamous cell carcinoma originating in a dermoid cyst and anaplastic dysgerminoma were positive for mutation. Direct sequencing confirmed 12 mutations and revealed G-->A and G-->C nucleotide changes in 5 and 3 cases (42% and 25%), respectively. The mutation was localized at the CpG site of the gene in 3 cases. Immunohistochemical examination of p53 protein in 21 cases and DNA flow-cytometrical analysis in 17 cases were also performed. Nuclear accumulation of the p53 protein and DNA aneuploidy pattern were detected in 11 (52%) and 9 (53%) cases, respectively. These were significantly correlated with p53 gene mutation (P < 0.01 and P < 0.05, respectively; Fisher's exact test). Neither mutation of the p53 gene, nuclear accumulation of p53 protein nor DNA aneuploidy was detected in borderline cases of common "epithelial" type, typical dysgerminoma and immature teratoma. These results suggest that p53 gene mutation, nuclear accumulation of the protein and the DNA aneuploidy pattern are events occurring almost simultaneously in the progression of ovarian tumors, and that p53 abnormalities seem to be correlated with a high grade of malignancy.
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PMID:High incidence of p53 gene mutation in human ovarian cancer and its association with nuclear accumulation of p53 protein and tumor DNA aneuploidy. 142 9

Intratubular germ cell neoplasia (ITGCN) and mature teratoma of the testis are uncommon findings in children. We report a case of a 3-year-old boy with both ITGCN and mature teratoma--a unique finding in our experience. Immunohistochemical markers, including placental alkaline phosphatase (PLAP), 43-9F, p53, and proliferating cell nuclear antigen (PCNA), as well as the periodic acid-Schiff (PAS) stain, were applied to the ITGCN. PLAP and 43-9F were not detected, whereas p53 and PCNA nuclear expression was detected in approximately 5% of atypical germ cells. Abundant clumped intracytoplasmic glycogen deposits were identified within atypical germ cells. Our findings indicate that both PCNA and p53, in addition to a PAS stain, may be useful markers in detecting malignant intratubular germ cells.
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PMID:Intratubular germ cell neoplasia (ITGCN) with p53 and PCNA expression and adjacent mature teratoma in an infant testis. An immunohistochemical and morphologic study with a review of the literature. 769 57

We describe the case of a pregnant mother and her fetus who both carried teratomas during the pregnancy. The fetus was diagnosed at 38 weeks' gestation to have an intracranial mass, which was later determined to be an immature teratoma. During a cesarean section delivery, an ovarian tumor was found in the 27-year-old mother that was also diagnosed to be an immature teratoma. Because of the similar histology of the tumors carried by both mother and child, a single clonal origin was suspected. Using polymerase chain reaction (PCR) and electrophoresis of highly polymorphic DNA satellite sequences, we determined that the origin of the intracranial teratoma carried by the child was independent of the mother's tumor. We also examined the p53 tumor suppressor gene in constitutional cells from both mother and child for the possible presence of a cancer-predisposing inherited mutation, but none was found. To our knowledge, this is the first report of the simultaneous occurrence of independent malignant immature teratomas in a mother and child during pregnancy.
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PMID:Immature teratomas of different origin carried by a pregnant mother and her fetus. 826 78

A rare case with a metastasizing teratocarcinoma of the lung is presented. The 51-year-old man developed a central tumour mass in the left lung. Bronchoscopy and intraoperative sections of an involved lymph node supplied histomorphologic findings that are indicative for an epidermoid carcinoma. Further detailed analysis resulted in the final classification as a malignant teratoma. This rare tumour was further analyzed for the expression of various cellular characteristics, namely binding sites for various carbohydrates including sequences such as saccharides of the ganglioside GM1, for erythropoietin, tumour necrosis factor-alpha, and epidermal growth factor. Immunohistochemistry was used to determine the expression of neuron-specific enolase, carcino-embryonic antigen, calcyclin, epidermal growth factor, beta-HCG, AFP, p53 protein, and heparin-specific lectin. The results revealed similarities to a case with a pulmonary blastoma, and remarkable differences to that of epidermoid carcinoma cases. Similar results were seen in the DNA- and syntactic-structure analysis. The tumour reported on here should, therefore, be considered as a rare, specific entity of primary lung malignancies.
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PMID:Malignant teratoma of the lung with lymph node metastasis of the ectodermal compartment: a case report. 831 68

We report an autopsy case of true malignant histiocytosis that developed during chemotherapy for mediastinal immature teratoma. The patient was a 14-year-old boy who exhibited hepatosplenomegaly while receiving chemotherapy for a mediastinal immature teratoma that had been resected 11 months before. The spleen and liver of the excisional biopsy displayed infiltration of multinucleated giant atypical cells with prominent erythrophagia in massive aggregations. These atypical cells expressed CD68, alpha1-antitrypsin, alpha1-antichymotrypsin, lysozyme, and vimentin, suggesting that the tumor cells may have been derived from macrophages. Immunocytochemistry showed p53 expression in the tumor cells of the malignant histiocytosis, as well as in the elements of the immature teratoma. Direct sequence analysis showed the p53 mutation in the tumor cells of the immature teratoma to be a mutation at codon 175 (exon 5), whereas the mutation in the malignant histiocytosis occurred at codon 285 (exon 8), ie, polyclonality was exhibited and these features suggested that the malignant histiocytosis arose independently from the immature teratoma during the chemotherapy.
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PMID:True malignant histiocytosis developed during chemotherapy for mediastinal immature teratoma. 889 99

This study investigates the extent of apoptosis in 53 testicular and ovarian germ cell tumors by using the in situ 3'-end DNA labeling technique on tumor sections. The tumors were also immunostained with antibodies to the p53 and bcl-2 proteins. The extent of apoptosis was highest in embryonal carcinoma (mean, 2.9%) followed by seminoma (mean, 1.1%), choriocarcinoma (mean, 0.7%) and immature teratoma (mean, 0.7%). In individual components of the mixed germ cell tumors the apoptotic index was in the same range as in the corresponding pure germ cell tumors. Mature teratomas rarely contained any apoptotic cells. Sixty-two percent of all the tumors expressed p53 protein. p53 expression was quantitatively strongest in embryonal carcinomas which also showed the highest level of apoptosis. Bcl-2 positivity could only be detected in some mesenchymal and epithelial components of the immature and mature teratomas; embryonal carcinomas, seminomas, or choriocarcinomas did not express bcl-2 at all. Our results show that the level of apoptosis in germ cell tumors associates with the histological type of the neoplastic component independent of whether it is singly present or a component of a mixed germ cell tumor. The results suggest that the quantity of p53 expression may contribute to the level of apoptosis in different tumor groups.
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PMID:Extent of apoptosis in relation to p53 and bcl-2 expression in germ cell tumors. 891 34

Congenital sacrococcygeal teratoma (SCT) is the most common germ cell tumor of infancy and childhood with a female preponderance. Most SCTs are diagnosed at birth, are benign, and consist of fully differentiated, mature tissues. Tumorigenesis of SCTs remains poorly understood. Almost nothing is known about possible oncogene activation or tumor suppressor inactivation in these rare tumors. We describe the presence of various oncoproteins and tumor suppressor proteins in eight cases of congenital SCT. The following oncogenes were examined: ras family (c-H-, c-N-, and c-K-ras), early genes (fos, jun), and tumor suppressor genes (p53 and nm23-H-I). There was no relationship between the intensity of expression of these oncoproteins and tumor suppressor genes and the following parameters: tumor size, age, and survival of the patients. We did not observe any difference, however, between the expression of the examined oncogenes and tumor suppressor genes nm23 and p53 in immature and mature teratomas. Our findings suggest that the ras family of oncogenes, fos and jun oncogenes, and nm23 and p53 tumor suppressor genes are present in congenital SCT, indicating a possible role in genesis and development of these tumors.
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PMID:Oncoproteins and tumor suppressor proteins in congenital sacrococcygeal teratomas. 905 59

We report on two patients in whom osteosarcoma occurred as second malignancy of childhood cancer. One patient had a malignant teratoma and the other adrenocortical carcinoma as the primary cancer. The emergence of cancer in cured cases and long-term survival cases of childhood cancer may result in an increase in the number of osteosarcomas seen in adolescence occurring as second malignancy. Anti-cancer drugs in large does were used for the treatment of a malignant teratoma in the former. These anti-cancer drugs may be involved in the occurrence of the second malignancy. In the latter, the patient has the germ-line mutation of p53 tumor suppressor gene, so genetic factors are presumably related to the occurrence of the second malignancy.
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PMID:Two cases of osteosarcoma occurring as second malignancy of childhood cancer. 1069 17

Prognosis of infants born with sacrococcygeal teratomas (SCTs) correlates with gestational age (GA). The survival rate after 30 weeks of gestation is 75%, compared to 7% before 30 weeks of gestation. Studies correlating GA with size, morphologic composition of teratomas, ploidy or expression of cell cycle control proteins such as p53, and ret [a tyrosine kinase receptor of the GDNF (glial cell line-derived neurotrophic factors)] receptor family may provide information explaining differences in survival. Seven SCTs (GA 21 to 41 weeks), ranging in size from 5 to 15 cm, were evaluated for morphologic composition. DNA ploidy was assessed in mature and immature neural elements. Immunohistochemical reactivity with monoclonal antibodies recognizing p53, and ret was quantitated and correlated with morphological pattern and GA. Relative size of teratomas to infants' weight and content of immature neural tissues correlated inversely with advancement of GA. Yolk sac tumor (YST) and immature tissues showed aneuploid cell populations. Nuclear p53 reactivity was apparent in the teratoma with YST in the microcystic patterns, the neuroectodermal rosettes, and the glandular patterns. Ret reactivity was seen in osteoclasts adjacent to bone formation surrounding developing teeth in an immature teratoma, and in rare mature neural cells of one SCT of 35 weeks GA. The rapid growth of SCT (GA <30 weeks) correlates with increase in immature neural tissues. Our study confirms aneuploidy in YST and suggests aneuploid populations within immature tissues. p53 accumulates in a variety of patterns of YST and may be seen in immature components of SCTs. To understand the possible role of ret, further studies comparing ret expression in immature human tissues are needed.
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PMID:Congenital sacrococcygeal teratomas: effect of gestational age on size, morphologic pattern, ploidy, p53, and ret expression. 1074 11

Chromosomal information on germ cell tumors of the infantile testis, ie, teratomas and yolk sac tumors, is limited and controversial. We studied two teratomas and four yolk sac tumors using comparative genomic hybridization (CGH) and in situ hybridization. No chromosomal anomalies were found in the teratomas by any of the methods, not even after CGH on microdissected tumor cells. All yolk sac tumors showed aneuploidy, loss of parts of 4q and 6q, and gain of parts of 20q. Underrepresentation of parts of 8q and overrepresentation of parts of 3p, 9q, 12p, 17, 19q, and 22 were detected in most cases. In addition, one recurrent yolk sac tumor after a sacral teratoma was studied, showing a highly similar pattern of imbalances. While CGH demonstrated loss of 1p36 in one testicular yolk sac tumor, in situ hybridization revealed loss of this region in all yolk sac tumors. High-level amplification of the 12q13-q14 region was found in one yolk sac tumor. MDM2, of which the encoding gene maps to this chromosomal region, was found in all cases using immunohistochemistry, whereas no p53 could be detected. Accordingly, no mutations within exons 5 to 8 of the p53 gene were observed. These data prove the absence of gross chromosomal aberrations in teratomas of the infantile testis and show a characteristic pattern of gains and losses in the yolk sac tumors. Besides confirmation of previously found anomalies, recurrent losses of 1p21-31 and 4q23-33 and gains of 9q34 and 12p12-13 have not been reported before. While genetic inactivation of p53 seems unimportant in the pathogenesis of these tumors, biochemical inactivation by MDM2 might be involved. These data support the existence of three entities of germ cell tumors of the human testis: teratomas and yolk sac tumors of infants, seminomas and nonseminomas of adolescents and young adults, and spermatocytic seminomas of the elderly, each with its own specific pathogenesis.
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PMID:Comparative genomic and in situ hybridization of germ cell tumors of the infantile testis. 1090 50


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