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 myoepithelial carcinoma, a rare malignant salivary gland neoplasm, arose in a pleomorphic adenoma of the parotid gland. The initial tumour was a pleomorphic adenoma with epithelial and myoepithelial elements. Subsequently the tumour recurred twice and was characterised by invasion of the mandible. Histological examination of the second recurrence showed a malignant spindle cell neoplasm with an infiltrative growth pattern and a high mitotic rate. There was involvement of local lymph nodes. The immunophenotype was characteristic of myoepithelial differentiation: tumour cells stained positively with anticytokeratin antibodies, S-100 protein, alpha smooth muscle actin, and vimentin. Electron microscopy confirmed myoepithelial differentiation, with small foci of keratinocytic phenotype. Large numbers of tumour cell nuclei were reactive with the anti-p53 antibody, DO-7, in contrast to the two previous resections. Thus malignant transformation of a pleomorphic adenoma may involve myoepithelial as well as epithelial elements. Accumulation of p53 protein, perhaps through mutational events, may have played a role in this malignant transformation.
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PMID:Myoepithelial carcinoma (malignant myoepithelioma) of the parotid gland arising in a pleomorphic adenoma. 1007 Mar 44

This study was designed to identify the immunophenotypic characteristics of malignant soft tissue tumours, induced experimentally with benzo(a)pyrene (BaP), and to evaluate the immunohistochemical expression of the ras oncogene family and p53 onco-suppressor gene in these tumours, in association with prognostic factors. Seventy-five male Wistar rats were subcutaneous injected, dorsally, with a single dose of 10.08 mgr BaP. A solid, well-circumscribed tumour was formed at the injection site, in 70 of the animals, 80-100 days after the carcinogen's administration. The tumour as well as selected main organs were excised and studied after the animals' death. All the specimens were fixed in formalin 10%, embedded in paraffin and stained with H + E. The immunohistochemical avidin-biotin method was performed in the tumour sections, using the following monoclonal or polyclonal antibodies: vimentin, desmin, muscle specific actin (MSA), a-smooth muscle actin (SMA), myoglobin, smooth muscle myosin, a-1-antitrypsin, a-1-antichymotrypsin, S-100 protein, epithelial membrane antigen (EMA), K-ras, H-ras, Pan-ras and p53. The induced tumours of the animals were almost well-circumscribed, with a partly storiform cut surface. Histologically, their appearance was more conventional with high grade leiomyosarcomas; about half of them showed highly anaplastic areas, resembling other pleomorphic undifferentiated sarcomas. Pulmonary metastatic foci were detected in 37 animals. Immunohistochemically, all the tumours displayed positive expression of vimentin, MSA and SMA. Desmin was positively expressed in 40 tumours, smooth muscle myosin in 57 tumours and EMA in 12 tumours. All the tumours were negative for myoglobin, a-1-antitrypsin, a-1-antichymotrypsin and S-100 protein. In addition, five tumours showed a positive reaction for K-ras p21, 37 for H-ras p21, 41 for Pan-ras p21 and 14 for p53 protein. The overexpression of the oncoproteins H-ras p21 and Pan-ras p21 in these tumours was significantly associated with a non-advanced tumour stage (absence of metastatic focus). In conclusion, the histological as well as the immunophenotypic features of the induced tumours are more conventional with leiomyosarcomas mostly of high grade; many of them are "dedifferentiated". The identification of both ras and p53 gene products in these tumours indicates that alterations of these genes are common but not specific events, implicated in the tumourigenesis, which may become prognostic markers for this subtype of soft tissue sarcomas.
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PMID:Immunophenotype, ras oncogenes and p53 onco-suppressor gene in benzo(a)pyrene induced malignant soft tissue tumours in Wistar rats. 982 59

Carcinosarcoma of the esophagus is a rare malignant tumor with both carcinomatous and sarcomatous components. We present 3 cases of carcinosarcoma of the esophagus and discuss the histogenesis of the tumors. We performed immunohistochemical studies using various antibodies: anti-cytokeratin, anti-vimentin, anti-smooth muscle actin, anti-p53, and MIB 1 reacting with Ki-67 nuclear antigen.
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PMID:Carcinosarcoma of the esophagus: three cases with immunohistological examination. 995 93

Although gastric carcinoma is one of the most common cancers worldwide, only a few histologic proximate precursors have been demonstrated. Several authors have found that foci of misplaced gastric mucosa with cystic dilatations (s.c. heterotopic mucosa) are often associated with gastric adenocarcinomas. However, adenocarcinomas originating within heterotopic gastric mucosa have never been reported. In present work, the review of 213 consecutive gastrectomy specimens in Japanese patients showed heterotopic gastric mucosa in 20.1% (n = 43). Up to 18 foci per gastrectomy were present. The heterotopic mucosa was surrounded by invaginations of the muscularis mucosae which showed strong positivity for smooth muscle actin. In 3 of the 213 specimens, an adenocarcinoma was found within a focus of heterotopic gastric mucosa. All 3 adenocarcinomas had cystic dilatations lined by neoplastic columnar epithelium with polymorphic nuclei, irregular nuclear membrane, large irregular nucleoli and pathological mitosis. The tumors had lateral bundles of smooth muscle (smooth muscle actin positive), regarded as invaginations of the muscularis mucosae. The p53 protein was strongly overexpressed in all 3 tumors. The heterotopic gastric mucosa may be one mucosal locus from which gastric adenocarcinomas may originate.
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PMID:Gastric adenocarcinomas in displaced mucosal glands. 1047 61

In a 55-year-old man, a tumor about 3 cm in diameter was detected in the upper abdomen by abdominal ultrasound screening during follow-up of chronic hepatitis C discovered in 1990. There were no symptoms and no abnormalities on physical examination. Tests for tumor markers were negative. By barium meal and gastroscopy, submucosal tumor was found on the lesser curvature of the stomach, with bridging fold in the absence of central ulceration. Biopsy revealed no tumor tissue. Under the diagnosis of submucosal tumor of the stomach, either a leiomyoma or leiomyosarcoma, partial resection of stomach was performed. Direct invasion of the surrounding organs, lymph node metastasis or distant metastasis was not observed grossly in the operation. Histologic examination of the resected specimen revealed proliferation of spindle cells and oval cells in an interlacing pattern. Immunohistochemistry for CD34, vimentin and c-kit protein was strongly positive, while smooth muscle actin, S-100 protein, desmin and p53 protein were negative. The proliferating cell nuclear antigen index was about 50%, while the MIB-1 index was < or = 1%. From these findings, this tumor was diagnosed as a gastrointestinal stromal tumor of the uncommitted type.
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PMID:A case of gastrointestinal stromal tumor of the stomach. 1081 97

To evaluate the effect of hypercholesterolemia on apoptosis and proliferation after vascular injury, iliac arteries of hypercholesterolemic (HC) and normocholesterolemic (NC) rabbits were examined after balloon injury using TUNEL, immunohistochemical staining of PCNA, macrophages, smooth muscle actin and p53. In media, apoptosis occurred massively early after injury and then decreased. HC did not affect this early post-injury apoptosis but significantly increased apoptosis 14 days later (D14). Immediate apoptosis in media was followed by active proliferation. HC sustained a high activity of proliferation until D14. The changes of immunoreactivity to p53 over the same 14 day period parallel that of apoptosis. In intima, where cells were scarce initially, proliferative activity reached a peak at D7 and then decreased. HC significantly enhanced proliferation at D14. In intima proliferation was accompanied by a later low-level apoptosis. HC significantly enhanced this low-level apoptosis at D14. These effects of HC resulted in significantly increased areas of intima and media. The fundamental difference between HC and NC was the infiltration of macrophages in HC. In conclusion, balloon injury induces early massive p53-associated apoptosis followed by proliferation in media, whereas in intima, it induces active proliferation followed by a low-level apoptosis. Hypercholesterolemia does not affect the early post-injury apoptosis but enhances proliferation and low-level apoptosis at a later stage, which in turn results in intimal and medial hyperplasia.
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PMID:Effect of hypercholesterolemia on the sequential changes of apoptosis and proliferation after balloon injury to rabbit iliac artery. 1085 23

Salivary gland carcinosarcoma, or true malignant mixed tumor, is a very rare and extremely aggressive neoplasm. The clonality and clonal origin of this tumor are discussed controversially. We report a carcinosarcoma of the left parotid gland in a patient who subsequently died of cutaneous, lymphatic and pulmonary metastases. Immunohistochemical staining, electron micrograph analysis, loss of heterozygosity (LOH) analysis and sequence analysis were performed on this tumor with an adenocarcinomatous and a predominant spindle cell-like component. While smooth muscle actin was undetectable by immunohistochemistry, cytoplasmatic myoepithelial structures could be detected by electron microscopy. LOH analysis at 12 genomic locations detected complete deletion of one allele at 17p13.1, 17q21. 3, and 18q21.3 indicating allelic loss in both components of the tumor. Double strand sequencing of the remaining allele of the p53 tumor suppressor gene revealed a wild-type allele. Based on our results, we favor the hypothesis of monoclonal origin of this salivary gland carcinosarcoma with a common stem cell that could be the myoepithelial cell and an inactivated tumor suppressor gene on chromosome 17 other than p53.
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PMID:Salivary gland carcinosarcoma: immunohistochemical, molecular genetic and electron microscopic findings. 1089 75

The clinical histories of 10 women suffering from benign metastasizing leiomyoma (BML) after hysterectomy and information on lung lesions detected in these women are presented, together with corresponding data for 2 women with metastasizing leiomyosarcoma of the uterus for comparison: gross appearance, survival, and light microscopical, immunohistochemical and lectin-histochemical findings are reported. All patients with BML had undergone hysterectomy for uterus leiomyomatosus without any detection of sarcomatous lesions in the uterus wall. After a median period of 14.9 years intrapulmonary masses were detected by imaging techniques. On average, six nodules with a mean diameter of 1.8 cm were seen. Resection of the lesions was performed in all cases. The immunohistochemical and lectin-histochemical examination of the tumors included analysis of the proliferation-associated protein Ki-67, the p53 protein, estrogen and progesterone receptor, sarcolectin as an indicator of the presence of lymphokine macrophage migration inhibitory factor, antibodies and the labeled protein to assess galectin (galactoside-binding animal lectin)-dependent parameters, analysis of tumor vascularization (CD-34), and expression of bcl-2, vimentin, smooth muscle actin, desmin, and keratin. The lesions were characterized by low proliferation activity of 2.9% (measured with Ki-67), frequent hormone receptor expression (8 of the 10 cases presented hormone-specific receptors), low to moderate vascularization compared with metastases from the two uterine sarcomas, remarkable p53 overexpression and frequent expression of the lymphokine, the galectins and accessible binding sites. The median survival of the BML patients was 94 months after excision of the intrapulmonary lesions, and the maximum survival of the two sarcoma patients was 22 months. The results recorded in this patient sample with the methodology applied suggest that benign metastasizing leiomyomas are a slow-growing variant of leiomyosarcoma of the uterus, which becomes clinically apparent at a young age and progresses with low velocity.
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PMID:Benign metastasizing leiomyoma of the uterus: documentation of clinical, immunohistochemical and lectin-histochemical data of ten cases. 1103 49

The tumor suppressor p53 transcriptionally regulates a large number of target genes that may affect cell growth and cell death pathways. To better understand the role of p53 loss in tumorigenesis, we have developed a mouse mammary cancer model, the Wnt-1 TG/p53 model. Wnt-1 transgenic females that are p53-/- develop mammary adenocarcinomas that arise sooner, grow faster, appear more anaplastic, and have higher levels of chromosomal instability than their Wnt-1 transgenic p53+/+ counterparts. In this study, we used several assays to determine whether the presence or absence of p53 affects gene expression patterns in the mammary adenocarcinomas. Most of the differentially expressed genes are increased in p53+/+ tumors and many of these represent known target genes of p53 (p21WAF/C1P1, cyclin G1, alpha smooth muscle actin, and cytokeratin 19). Some of these genes (cytokeratin 19, alpha smooth muscle actin, and kappa casein) represent mammary gland differentiation markers which may contribute to the inhibited tumor progression and are consistent with the more differentiated histopathology observed in the p53+/+ tumors. Several differentially expressed genes are growth regulatory in function (p21, c-kit, and cyclin B1) and their altered expression levels correlate well with the differing growth properties of the p53+/+ and p53-/- tumors. Thus, while tumors can arise and progress in the presence of functioning wild type p53, p53 may directly or indirectly regulate expression of an array of genes that facilitate differentiation and inhibit proliferation, contributing to a more differentiated, slow growing, and genomically stable phenotype.
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PMID:Differential gene expression in mouse mammary adenocarcinomas in the presence and absence of wild type p53. 1114 50

The characterization of clinical, histopathological, immunohistochemical, and genetic features of intimal sarcomas arising in the pulmonary artery is presented in this study. Four resected lungs, one endarterectomy specimen and three biopsies from eight patients (four males and four females; median age 41 years) suffering from intimal sarcomas of the pulmonary artery using conventional stains, immunohistochemistry, and comparative genomic hybridization (CGH) were analyzed. The predominant clinical presentation was dyspnea (all eight patients) and febrile pulmonary disease (six of eight). Signs of embolic lung disease were present in all patients. One patient died postoperatively, six patients died of disease 8-35 months after presentation, and one patient was alive 6 months after surgery. Histopathological examination of the submitted material showed spindle cell, partially myxoid and pleomorphic sarcomas. Metastases were histologically confirmed in three patients (lung, pleura, and skull). Immunohistochemically, vimentin was strongly expressed in all tumors. Focal positivity was observed for alpha smooth muscle actin, CD117, CD68, p53, and bcl2. No reaction could be obtained for endothelial markers. The proliferation index Ki-67 was between 5% and 80%. Six examined tumors were positive for mdm2. In the CGH analysis, gains and amplifications in the 12q13-14 region were found in six of eight tumors (75%). Other, less consistent alterations, were losses on 3p, 3q, 4q, 9p, 11q, 13q, Xp, and Xq, gains on 7p, 17p, and 17q, and amplifications on 4q, 5p, 6p, and 11q. Intimal sarcomas of the pulmonary artery are tumors with an unfavorable prognosis and poorly differentiated morphology. A majority of tumors show a consistent genetic alteration (gains and amplifications in the 12q13-14 region) and overexpression of mdm2, implicating the mdm2/p53 pathway as a possible mechanism in the tumor pathogenesis.
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PMID:Gains of 12q13-14 and overexpression of mdm2 are frequent findings in intimal sarcomas of the pulmonary artery. 1121 36


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