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)

We quantitatively analyzed the c-myc and p53 products using flow cytometry in 28 cases of resected lung cancer and one case each of chorio-carcinoma, plasmacytoma, malignant mesothelioma and sclerosing hemangioma. In the lung cancer cases, c-myc and p53 products were detected in 10 cases (35%) and 7 cases (21%), respectively. These rates are higher than the DNA abnormal expression rates of the c-myc and p53 genes (15% and 12%, respectively) in our own data. In the adenocarcinoma of lung cancer cases, c-myc and p53 products were detected in 9 cases (53%) and 5 cases (29%), respectively. Among the squamous cell carcinoma cases, there were one case (11%) of c-myc expression and one case (11%) of p53 expression. DNA content analysis of the lung cancer patients revealed 7 cases of DNA diploidy and 21 cases of DNA aneuploidy. All 10 c-myc-positive cases showed DNA aneuploidy; thus the positive rate for c-myc products in the DNA aneuploidy cases was significantly different compared with the DNA diploidy cases (p < 0.05). In the sclerosing hemangioma case, we detected both c-myc and p53 products. Sclerosing hemangioma has been thought to be a benign tumor, but it may be a malignant tumor.
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PMID:[DNA content analysis and detection of c-myc and p53 products using flow cytometry in resected lung cancer cases]. 820 22

The c-myc and p53 genes are thought to be an oncogene and a tumor suppressor gene, respectively. These genes' products are characteristic of malignant tumors. We quantitatively analyzed the c-myc and p53 products by flow cytometry in two cases of pulmonary sclerosing hemangioma. In case 1, 32.3% of the tumor cells were found to have the c-myc product, and 8.9% were found to have the p53 product. In case 2, 6.7% of the tumor cells were found to have the c-myc product and 15.5% were found to have the p53 product. The percentages in both cases were twice as high as those in a negative control lymphocytes stained with c-myc and p53 products. Therefore, these two cases showed positive expression of the c-myc and p53 products. In addition DNA from six other patients with sclerosing hemangioma was analyzed with paraffin-embedded sections. All six had DNA diploidy, with DNA indexes ranging from 0.91 to 1.03 and coefficients of variation ranging from 3.0 to 5.5. We suggest that pulmonary sclerosing hemangioma is a very weakly malignant tumor.
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PMID:[Positive expression of c-myc and p53 products in two cases of pulmonary sclerosing hemangioma]. 882 86

Infantile capillary haemangioma (ICH) is a well-established clinicopathological entity which often regresses spontaneously. To elucidate the cause of spontaneous involution of ICH, the apoptotic and proliferative activities in seven cases of ICH were compared with those in five cases of lobular capillary haemangioma (LCH), using formalin-fixed paraffin-embedded tissue sections. The number of apoptotic cells detected by the modified in situ end-labelling method was significantly higher in ICH than in LCH, while the proliferative activities evaluated with mitosis and Ki-67 antigen expression did not differ significantly. Lewisy (Ley) antigen, an apoptosis-associated marker, was expressed in all cases of ICH but in none of LCH, while labelling for p53 protein and bcl-2 protein was almost completely negative in both tumours. These findings clearly demonstrate a much higher apoptotic activity in ICH than in LCH and suggest that apoptosis might be a cause of the spontaneous involution of ICH.
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PMID:High frequency of apoptosis in infantile capillary haemangioma. 886 88

The clinicopathologic, immunohistochemical, and ultrastructural features of soft tissue angiosarcomas are not well defined. Eighty cases of angiosarcoma that involved the deep subcutis, skeletal muscle, retroperitoneum, mesentery, and mediastinum are reported. The lesions occurred in 50 male and 30 female patients who were 5-97 years of age; the peak incidence was in the seventh decade of life. A variety of associated conditions were documented in 20 of these cases, including a history of other neoplasms (some irradiated), synthetic vessel grafts, heritable conditions, and prior trauma or surgery. The angiosarcomas occurred in the extremities (n = 43 cases), trunk (n = 28), and the head and neck (n = 9) regions, with the thigh and the retroperitoneum being the most common sites. They often were characterized as enlarging, painful masses of several weeks' duration and were occasionally associated with acute hemorrhage, anemia, or a coagulopathy. The tumors measured 1-15 cm in diameter (median 5 cm) and frequently were hemorrhagic and multinodular. There was a wide morphologic spectrum within and between cases, including areas similar to cavernous and capillary hemangioma, Dabska tumor, spindle cell and epithelioid hemangioendothelioma, various spindle cell sarcomas, or carcinoma. Histologically, epithelioid angiosarcoma was the most frequently observed pattern; 70% of cases had epithelioid cells that were arranged in nests, clusters, papillae, and gaping vascular channels. Hemorrhage tended to obscure the diagnosis in several cases and often was associated with papillary endothelial hyperplasia-like areas. All 42 cases studied immunohistochemically stained at least focally for Factor VIII-related antigen, and nearly all stained strongly for vimentin, which accentuated the endothelial cells and vessel lumen formation. CD34 antigen was detected in 74% of cases, BNH9 in 72%, and cytokeratins in 35%. Epithelial membrane antigen, S-100 protein, and HMB45 were not detected. Fifty-five percent of the tumors had intracytoplasmic aggregates of laminin. Immunostains for alpha-smooth muscle actin demonstrated a prominent pericytic component in several tumors (24%). Ki67 immunostains with MIB1 indicated high proliferative activity (> or =10%) in 72% of cases. p53 immunoreactivity (>20% nuclear staining) was observed in 20% of cases. Ultrastructural studies performed on poorly differentiated areas of 12 cases showed groups of cells, which were frequently epithelioid, surrounded by basal lamina, and closely associated with pericytes, along with intercellular and intracellular lumina with or without red blood cells. Whorls of abundant intermediate filaments, occasional tonofilamentlike structures, and pinocytotic vesicles also were noted. In contrast to the findings of others, Weibel-Palade bodies were not seen. Follow-up in 49 cases (61%) showed that 53% of patients were dead of disease at a median interval of 11 months, whereas 31% had no evidence of disease at a median interval of 46 months. The remaining patients were either alive with disease (14%) or alive but disease status was unknown (2%). There were local recurrences in 20% of cases and distant metastases in 49%, most frequently to the lungs, followed by the lymph nodes, soft tissues, bone, liver, and other sites. These results indicate that angiosarcoma of soft tissue is a high-grade sarcoma. Older patient age, tumor location in the retroperitoneum, and larger tumor size as well as detection of MIB1 in > or =10% of the tumor cell population were all associated with a poorer prognosis.
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PMID:Angiosarcoma of soft tissue: a study of 80 cases. 963 Jan 75

The endothelium is one of the largest cellular compartments of the human body and has a high proliferative potential. However, angiosarcomas are among the rarest malignancies. Despite this interesting contradiction, data on growth and angiogenesis control mechanisms of angiosarcomas are scarce. In this study of 19 angiosarcomas and 10 benign vascular control lesions we investigated the sequence and expression of the p53 tumor suppressor gene and the expression of the mdm-2 proto-oncogene, which is a negative regulator of p53 activity and of the vascular endothelial growth factor (VEGF), whose expression, among other factors, is regulated by the p53/MDM-2 pathway. Ten sarcomas (53%) exhibited clear nuclear p53 protein accumulation. Two of these cases revealed mutations in the sequence-specific DNA binding domain of the p53 gene. Thirteen angiosarcomas (68%) showed an increased amount of MDM-2 protein. Elevated expression of p53 and MDM-2 protein correlated with increased VEGF expression, which was found in nearly 80% of the angiosarcoma cases. Negative or clearly lower immunostaining was obtained in cases from the benign control collective. Only one case of a juvenile hemangioma reached the cutoff value of p53 positivity coincidentally with high VEGF expression. Our data suggest that the p53/ MDM-2 pathway is impaired in about two-thirds (14/ 19) of the angiosarcomas. This may be a key event in the pathogenesis of human angiosarcomas. The increased VEGF expression observed supports this hypothesis.
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PMID:MDM-2 oncoprotein overexpression, p53 gene mutation, and VEGF up-regulation in angiosarcomas. 981 33

The role of p53 tumor suppressor gene in the pathomechanism of adrenal tumors was investigated by measuring p53 protein and its messenger ribonucleic acid (mRNA) in 12 normal human adrenals as well as in 56 adrenal tumors (7 aldosterone-producing adenomas, 5 adrenocortical adenomas causing Cushing's syndrome, 19 non-hyperfunctioning adrenocortical adenomas, 5 adrenocortical carcinomas, 12 pheochromocytomas, 3 myelolipomas, 4 ganglioneuromas and 1 hemangioma). The p53 protein concentration was significantly increased in aldosterone-producing adenomas (394+/-36 pg/mg cytosolic protein, mean+/-SE, vs 266+/-18 in normal human adrenals), whereas the concentration of this protein in Cushing's adenomas, non-hyperfunctioning adrenocortical adenomas, pheochromocytomas, and in all but one adrenocortical carcinomas was similar to that measured in normal human adrenal tissues. One adrenocortical carcinoma tissue showed very high p53 protein content (3000 pg/mg cytosolic protein). By contrast, myelolipomas (23+/-20) ganglioneuromas (43+/-15) and a hemangioma (11 pg/mg cytosolic protein) had very low p53 protein content. Northern blot analysis revealed the presence of p53 mRNA in each adrenal tissue examined with highest levels in aldosterone-producing and Cushing's adenomas. It is possible that the differences in p53 protein and/or mRNA contents reflect corresponding differences in the pathogenetic importance of p53 alterations in these types of adrenal tumors.
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PMID:p53 protein and its messenger ribonucleic acid in human adrenal tumors. 997 75

Hemangiomas and hemangiosarcomas are uncommon in rodents and humans and, as such, the mechanisms giving rise to these tumors are poorly understood. Inactivating mutations in the p53 gene have been detected in sporadic and chemically induced human and rodent hemangiosarcomas. Additionally, experimental ablation of p53 function in mice by targeted gene disruption increases the incidence of both spontaneous and carcinogen-induced vascular tumors. These findings implicate p53 disruption in vascular tumor development. In this study, we characterized p53 inactivation immunocytochemically and by gene sequencing in a large number of vascular tumors that developed in B6C3F1 mice during a long-term (2-year) study of the thiazolidinedione troglitazone. For comparative purposes, a murine hemangiosarcoma induced by polyoma middle-T antigen, which transforms endothelial cells via a p53-independent mechanism, five spontaneous human hemangiosarcoma specimens, and species-specific positive control tissues were also evaluated by immunocytochemistry for p53 inactivation. While 20% of the human hemangiosarcomas and all positive control tissues expressed significant levels of nuclear p53, indicating functional inactivation of the protein, none of the 161 mouse vascular tumors studied expressed detectable p53 protein. The absence of inactivating mutations was confirmed in eight of the histologically most malignant mouse hemangiosarcomas by sequencing exons 5 to 8 of the p53 gene. These results demonstrate that p53 inactivation did not play a role in development of the vascular tumors seen in the long-term study of troglitazone, and they indicate that loss of p53 function is not essential for vascular tumor development in mice.
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PMID:p53 is not inactivated in B6C3F1 mouse vascular tumors arising spontaneously or associated with long-term administration of the thiazolidinedione troglitazone. 1019 75

In the study the expression of Ki-67, p53, bcl-2 and apoptotic index in ten cases of lobular capillary hemangioma (LCH), ten of capillary hemangioma (CH), and five of epithelioid hemangioma (EH) was examined. The expression of Ki-67, p53 and bcl-2 did not differ significantly between each group of lesions. Instead, significant differences in apoptotic index between LCH and CH were found. The expression of bcl-2 was positively correlated with that of Ki-67 in LCH and CH group, but negatively correlated in the EH group. Our results confirm that LCH, EH and CH, which are histologically similar, are different in terms of proliferation/apoptosis balance. This reflects their different biology, and presumably pathogenesis.
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PMID:Proliferation and apoptosis within the oral mucosa "hemangiomas". 1097 33

Xeroderma pigmentosum is an inheritable autosomal recessive DNA repair deficient syndrome characterized by a high predisposition to skin cancers. An elevated proportion of tumors from xeroderma pigmentosum patients harbor ultraviolet-induced mutations (CC:GG > TT:AA tandem transitions) of the p53 and/or the INK4a-ARF genes. Here, we report the clinical and molecular features of a 12 y old xeroderma pigmentosum patient who, in addition to severe cutaneous clinical symptoms, also had three unusual tumors, a mediastinal lymphoblastic lymphoma, an atypical fibroxanthoma, and an epithelioid hemangioma. Single strand conformation polymorphism and sequencing analysis of the p53 and INK4a-ARF genes were carried out in DNA from normal skin and different tumors (four actinic keratosis, two microinvasive squamous cell carcinomas, one basal cell carcinoma, and one atypical fibroxanthoma) from the patient. After characterization of the xeroderma pigmentosum C complementation group, we found unexpectedly that this patient also carried a germline mutation of the INK4a-ARF locus affecting the p16INK4A reading frame. Three different somatic mutations that all harbor the signature of ultraviolet light (two of p16INK4A and one of p53) were also detected in the basal cell carcinoma. We hypothesize that the germline mutation of p16INK4A, in association with the nucleotide excision repair defect, could explain the patient's unusual phenotype. Furthermore, this study confirms that concomitant somatic mutations of INK4a-ARF and p53 occur in some xeroderma pigmentosum associated tumors, and seem to accumulate during tumor progression rather than the initiation step.
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PMID:Germline and somatic mutations of the INK4a-ARF gene in a xeroderma pigmentosum group C patient. 1248 39

Alveolar adenoma is a rare and benign tumour of the lung that usually presents in asymptomatic patients as a coin lesion on chest radiography. Only 25 cases have been reported in the English medical literature. Alveolar adenoma has a characteristic multicystic histology and often resembles the normal lung parenchyma. Ultrastructural studies indicate that the epithelial cells lining the cysts are type-II pneumocytes. Immunohistochemical analysis may aid in the characterization of alveolar adenoma and discriminate this condition from other types of benign lesions of the lung. An indolent clinical progression and absence of recurrence and metastasis after complete resection are the most important characteristics indicative of the benign nature of alveolar adenoma. Few studies have been conducted at the molecular level, such as by flow cytometry, with the objective of characterizing the biological nature of alveolar adenoma. Differential diagnoses include sclerosing hemangioma, papillary adenoma, lymphangioma, atypical adenomatous hyperplasia and bronchioloalveolar carcinoma. In this article we describe the immunohistochemical and flow cytometric features of this neoplasm in two male patients. Both the tumours showed a diploid DNA pattern with a low proliferation index. p53 test was found to be negative, and post-operative follow-up examinations at 22 and 32 months proved uneventful.
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PMID:Alveolar adenoma of the lung. Immunohistochemical and flow cytometric characteristics of two new cases and a review of the literature. 1818 18


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