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)

Sinonasal melanoma is a rare malignancy. We present the clinicopathologic review of 18 cases seen at the British Columbia Cancer Agency between 1976 and 1992: 13 men and five women, mean age 66 years (range 32-88). Patients presented with nasal obstruction and bleeding (n = 8), obstruction alone (n = 4), bleeding alone (n = 5) or pain (n = 1). Those with bleeding presented with a shorter duration of symptoms than those with obstruction alone. All patients with obstruction alone died of their disease, while all patients with bleeding alone are alive or have died of an unrelated cause; four out of eight patients with both obstruction and bleeding are alive. There was no significant relationship between treatment modality and outcome. Histologic subtypes included epithelioid (n = 10), spindle-cell (n = 4), small-cell (n = 3) and pleomorphic (n = 1). Eight out of 11 cases from whom samples of paraffin-embedded tissue were available showed more prominent staining for HMB-45 than for S-100. In two cases, only rare (< 0.1%) cells stained for S-100. Cell type, mitotic rate and P53 expression were unrelated to disease outcome. Six out of seven patients with < or = 10% of cells showing intense staining for PCNA were alive or had died of an unrelated cause, while three out of four with > 10% staining died of their disease.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Sinonasal malignant melanoma--a clinicopathologic analysis of 18 cases. 749 62

A 69-year-old woman was admitted to Hokuso Shiroi Hospital because of recurrent pain in the lower right side of the abdomen. Small-intestinal cancer was strongly suspected after fluoroscopy of the small intestine. Laparotomy showed advanced cancer of the ileum, of complete annular constrictive type, 9.5 x 5cm in size. Histologically it was moderately differentiated tubular adenocarcinoma. Neither visceral nor nodal metastases were found, and the patient has been well for the 20 months since surgery. The strong resemblance between the epidemiological characteristics of small-intestinal cancers and colorectal cancers prompted us to investigate the carcinogenetic mechanisms at the molecular level. A point mutation at codon 12 of the K-ras gene was found, while no alterations were noted in the p53 gene, whose mutations are frequent in colon cancers. The carcinogenetic mechanisms of the small-intestinal cancer we experienced may thus differ from those of colon cancers.
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PMID:Primary cancer of the small intestine and mutational analysis of the K-ras and p53 genes. 965 20

Pancreatic cancer is a major cause of death from cancer in both men and women in the USA and Europe. The disease causes pain and has a significant impact on the performance status of the patient. In a randomized trial vs 5-fluorouracil, the novel nucleoside analogue gemcitabine (GEMZAR) has been shown to provide clinical benefit for patients (decreased pain and improved performance status) as well as to improve the time to tumour progression and survival for patients with the disease. There are also other new agents that are presented in this discussion, such as the multi-targeted antifolate MTA, capecitabine and the ONYX-015 adenovirus, which replicates in, and kills, only p53-abnormal cells, which have the potential to have an impact on this terrible disease.
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PMID:Advances in the treatment of patients with pancreatic cancer: improvement in symptoms and survival time. The San Antonio Drug Development Team. 971 85

This recent symposium featured speakers from several clinical and research disciplines. Among the findings: peptic ulcer disease is a significant predisposing risk factor (odds ratio = 3.9) for pancreatic cancer; as many as 50% of all intraductal papillary mucinous neoplasms are associated with invasive adenocarcinomas; alteration of gene expression via methylation of a gene promotor region constitutes a potentially reversible method of tumor suppressor gene inactivation; > 400 transcriptional alterations of gene expression have been identified for pancreatic cancer; some common molecular markers such as p53 and HER-2/neu may be related to morphologic alterations of in situ neoplasia and to transcriptional alterations of gene expression rather than mutational events; epidermal growth factor (EGF), transforming growth factor beta (TGF-beta), and related molecules may modulate gene transcription via "autocrine" or "paracrine" mechanisms; several cytokines, amylin (islet amyloid polypeptide), and other cachexia factors are responsible for paraneoplastic peripheral insulin resistance, ineffective utilization of glucose, and profound cachexia. In the clinical diagnostic arena: the World Health Organization established a standard nomenclature for intraductal papillary mucinous neoplasms, mucinous cystic tumors, intraductal mucinous hyperplasias, and solid pseudopapillary tumors; focal glandular differentiation may be commonly identified within pancreatic endocrine neoplasms (islet cell tumors) while not necessarily implying an unfavorable prognosis typical of ductal adenocarcinomas; positron emission tomography scanning may be used for evaluation of early tumor response to novel chemotherapeutic regimens; helical computed tomography (CT) is the state of the art in preoperative imaging for pancreatic cancer; neoadjuvant 5-fluorouracil (5-FU)-based chemoradiation in 39 "resectable" patients provided a median survival of 19 months, actuarial 4-year survival of 19%, and improved local tumor control; gemcitabine has shown promise in alleviating tumor-related symptoms with a significantly better "clinical benefit response" than single agent 5-FU (23.8 vs. 4.8%, p = 0.0022) based on change in pain intensity, daily analgesic consumption, performance status, and weight; a significant survival advantage was demonstrated in patients treated with conventional therapies whose tumors expressed p21WAF-1, an important inhibitor of cell cycle progression and downstream molecule of p53 and TGF-beta; a p21-adenovirus (rAD-p21) gene therapy resulted in significant growth inhibition of pancreatic cancer cell lines in tissue culture, and development of a successful SCID mouse-human pancreatic adenocarcinoma xenograft model provided an animal model for preclinical trials of rAD-p21.
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PMID:Current concepts in pancreatic cancer: symposium summary. 982 Nov 73

We report a case of lipodystrophia centrifugalis abdominalis infantilis (LCAI) showing apoptosis during the lipoatrophic process by immunohistochemical staining. A 3-year-old boy was seen with a 3-month history of a centrifugally spreading depressed eruption without pain and pruritus on his abdomen. He had fever, diarrhea and vomiting for a week at the beginning of his eruption. Physical examination revealed a palm-sized well-demarcated atrophic plaque on his lower abdomen and left inguinal fold. His plaque showed fine erythema peripherally. A skin biopsy specimen showed remarkably decreased subcutaneous fatty tissue. Inflammatory cell infiltration including lymphocytes and histiocytes was noted in the degenerating fatty tissue. In the degenerating subcutaneous fatty tissue, positive staining for HLA-DR, Fas, bcl-2, p53 and transferase-mediated uridine nick end labeling in mononuclear cells were observed. He was diagnosed as having LCAI. The present case showed the possible involvement of apoptosis in the fatty tissue degeneration in LCAI.
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PMID:Lipodystrophia centrifugalis abdominalis infantilis-- immunohistochemical demonstration of an apoptotic process in the degenerating fatty tissue. 1114 55

Five cases of malignant melanomata of the nasal cavities have been diagnosed and studied at ENT--and Anatomopathological Departments, between 1990 and 1997, the group ranging from 65 to 90 years, middle age 74.2. Paramount symptoms were epistaxis and lack of pain in all patients. Radical surgery was performed only in one case, followed by radiotherapy; the remainder were submitted to palliative treatment. We have reviewed the literature and also an immunohistochemical analysis about p53, p16INK4 and Rb oncogenes with the aim to establish its importance in these tumor's type. The whole group have showed high levels of p53 and MIB-1 and 60 percent a loss of oncogen p16 expression.
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PMID:[Malignant melanoma of the nasal cavity. Retrospective study. The analysis of p53 and p16INK4 expression]. 1145 87

Hepatocellular carcinoma (HCC) is one of the most common cancers worldwide. The prognosis of HCC is poor and current therapies are largely ineffective. Genetic abnormalities are commonly seen in HCC tumors particularly with inactivation of the p53 tumor suppressor. Gene therapy with E1B-deleted (dl1520) adenovirus could be of therapeutic value as it offers the potential of tumor growth control in patients with p53 mutation. Ten patients with posthepatitis cirrhosis and histologically proven HCC were enrolled into an open label, randomized prospective study. Randomization was to receive either percutaneous ethanol injection (control group) or dl1520. Toxicity and complications in the ethanol group were pain and fever, whereas in the gene therapy group complications were minimal. Grade I-II toxicity fever, stable performance status, and no significant rise in liver enzymes were observed in patients treated with dl1520. Analysis of patients' response to treatment in the gene therapy group showed one patient with a partial response and four patients with progressive disease. In the ethanol-treated group two patients had stable disease and three patients showed disease progression. In conclusion, this study showed that the adenovirus was well tolerated, but did not seem to offer significant tumor control. Although only a small number of patients were treated here it appears that more effective vectors are needed to achieve a useful clinical impact.
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PMID:Clinical trial of E1B-deleted adenovirus (dl1520) gene therapy for hepatocellular carcinoma. 1189 41

A male patient initially diagnosed with acute lymphoblastic leukemia at age 9 years received chemotherapy (total body irradiation, 12 Gy) followed by allogeneic bone marrow transplantation. Since then, he had been in complete remission. Three years after the bone marrow transplantation, he complained of increasing pain in the right knee. Radiological and histological examinations led to a diagnosis of conventional osteosarcoma. We performed intensive chemotherapy and wide local excision of the osteosarcoma. Intensive chemotherapy was accomplished as planned, although recovery from myelosuppression was delayed during some cycles. Polymerase chain reaction-single-strand conformation polymorphism analysis revealed a p53 gene mutation in exon 7 in the tumor cells, but not in skin or blood cells. This is an extremely rare case of osteosarcoma after bone marrow transplantation.
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PMID:Osteosarcoma after bone marrow transplantation for acute lymphoblastic leukemia. 1240 67

A 41-year-old female presented in April 1996 with a tumor of the hard palate revealed by increasing left palate pain. Adenoid cystic carcinoma was suspected on clinical and imaging data. Two limited surgical procedures showed a tumor histologically made of small lobules of granular cells, PAS positive and expressing S100 protein, infiltrating some medullary spaces of the palatine bone, consistent with a granular-cell tumour. Pain recurred in the territory of the maxillary branch of the left trigeminal nerve (V2). Imaging showed a tumor of the origin of V2-extending through the foramen rotondum. Two radical interventions in September and in October 2000 showed an infiltrating tumor of the V2 and palatine mucosa, with the same histology. There was no immuno-staining for p53, and less than 5% of nuclei expressed Ki67. Malignant Abrikossof tumors are exceptional, morphologically difficult to differentiate from benign ones, only metastasis proving malignancy. Tumor size above 5 cm, recurrence and infiltrative character are considered pejorative. The value of p53 and Ki67 expression remains controversial. We discuss our observation according to these criteria.
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PMID:[A palate tumor revealed by pain]. 1241 Jan 57

Opioid effects on tumor growth have been a controversial topic of discussion. In the present study, morphine inhibited tumor cell proliferation at concentrations of >or=10 micro M. This was primarily caused by inhibition of cell cycle progression from G(1) to S phase. At higher concentrations (>or=500 micro M for 24 h), morphine also caused cell death. In nude mice, morphine significantly reduced the growth of MCF-7 and MDA-MB231 tumors but had no effect on HT-29 tumor growth. In these experiments, morphine plasma concentrations were similar to those found in cancer patients receiving chronic morphine treatment for pain relief (0.9-3.4 micro M). In MCF-7 and MDA-MB231 cells, morphine caused a naloxone (Nx)- and pertussis toxin-sensitive, concentration-dependent increase of GTPase activity, indicating that morphine signals could be transduced by opioid receptors via a G protein. However, the antiproliferative effects of morphine were not antagonized by Nx, pertussis toxin, forskolin, and 8-bromo-cAMP, suggesting that the typical opioid receptor-coupled signaling cascade involving the G(i), adenylyl cyclase, and protein kinase A was not involved. Instead, morphine caused an NH(2)-terminal phosphorylation of p53 at Ser(9) and/or Ser(15) and a stabilization of p53 in MCF-7 cells that express wild-type p53. p53 phosphorylation was not antagonized by Nx and resulted in an increase of p53-dependent proteins including p21, Bax, and the death receptor Fas. Blockade of Fas by Fas-fusion protein or inhibition of caspase 8 resulted in a partial inhibition of morphine-induced apoptosis. In addition, Fas ligand only induced apoptosis when administered together with morphine. However, the sensitivity of the tumor cells toward Fas ligand remained low. HT-29 cells, which express dominant negative p53 and show no increase of GTPase activity when treated with morphine, were less sensitive in vitro and were not affected in vivo. Our results suggest that morphine, alone or in combination with Nx, may reduce the growth of certain tumors, apparently in part through activation of p53.
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PMID:G protein-independent G1 cell cycle block and apoptosis with morphine in adenocarcinoma cells: involvement of p53 phosphorylation. 1270 72


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