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Query: UNIPROT:P04637 (p53)
 77,613 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Primary cutaneous diffuse large B-cell lymphoma (DLBCL) is an uncommon lymphoma. Some authors have suggested that large B-cell lymphoma can be segregated based on anatomic site, with tumors of the lower extremity being unique. We report 15 cases of primary cutaneous DLBCL. Each case was analyzed immunohistochemically using antibodies specific for CD3, CD5, CD10, CD20, bcl-2, bcl-6, and p53. Polymerase chain reaction analysis for t(14;18)(q32;q21) also was performed. There were 13 men and 2 women (median age, 64 years). Thirteen tumors were composed predominantly of centroblasts, and 2 were immunoblastic. There was a median follow-up of 72 months. Of the 4 patients with primary cutaneous DLBCL of the lower extremity (thigh, knee, leg), 2 (50%) experienced a recurrence and 1 patient died of disease. In the non-lower extremity cases, 18% (2/11) recurred and no patients died of disease. We conclude that primary cutaneous DLBCL usually occurs in elderly patients with a male predominance. Recurrences are common, but death of disease is rare.
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PMID:Primary cutaneous diffuse large B-cell lymphoma: a clinicopathologic study of 15 cases. 1193 32

To analyse the role of Pasteurella haemolytica Leukotoxin (LKT) in the mechanism of apoptotic cell death of bovine lymphocytes, we evaluated DNA fragmentation and p53 and c-myc expression. P. haemolytica strain ATCC 14003 was cultivated for LKT production. DNA fragmentation was analysed by electrophoresis on Agarose gel. DNA strand breaks in individual apoptotic cells were also detected by an in situ Terminal deoxy nucleotidyl Transferase (TdT). The Polymerase Chain Reaction (PCR) procedure was used for verified p53 and c-myc activation by P. haemolytica LKT. LKT was able to induce DNA fragmentation in a dose and time-dependent fashion. The greatest apoptotic effect was obtained using LKT at a concentration of 0.25 U. The results show that p53 and c-myc activation by LKT is correlated with apoptosis of bovine lymphocytes and monocytes. Our data suggest that LKT may have an important role in the bacterial virulence of Pasteurella haemolytica.
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PMID:p53 and c-myc activation by Pasteurella haemolytica leukotoxin is correlated with bovine mononuclear cells apoptosis. 1201 26

Molecular-based diagnosis ofthyroid carcinomas can be more easily establishedby utilizing specific mRNAs that are expressed in a restricted manner in cancer tissues. Accordingly, several cancer-specific mRNAs in thyroid carcinomas have been identified by means of sequence specific-differential display (SS-DD), serial analysis of gene expression (SAGE) and other new techniques. By using these cancer-specific mRNAs, some new methods of preoperative diagnosis of thyroid carcinomas have been developed. In one such method, Aspiration Biopsy-Reverse Transcription-Polymerase Chain Reaction (ABRP), RNA is extracted from leftover cells within the needle used for fine needle aspiration biopsies (FNABs), thereby allowing cytological and molecular-based diagnoses to be performed simultaneously. ABRP provides both RNA information and a cytological diagnosis without further invasion to the patient. By ABRP detection of cancer-specific mRNAs, papillary, anaplastic and medullary carcinomas and a part of malignant lymphomas can be accurately diagnosed preoperatively. It remains to be clarified why cancer-specific mRNAs, especially those that are overexpressed in fetal tissues, can clearly distinguish benign tissues from carcinomas, while genomic alternations, such as mutations in the RAS or P53 gene cannot. Further, the widely accepted hypothesis of multi-step carcinogenesis cannot explain some of the clinical and experimental findings of thyroid carcinomas. Considering these facts, we propose a novel hypothesis of thyroid carcinogenesis, the "germ-cell carcinogenesis" hypothesis, in which cancer cells derive from the remnants of fetal thyroid germ cells (thyroblasts) instead of normal thyroid follicular cells.
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PMID:Cancer-specific mRNAs in thyroid carcinomas: detection, use, and their implication in thyroid carcinogenesis. 1208 Dec 46

p53 codon 72, which produces variant proteins with an arginine (Arg) or proline (Pro), has been reported to be associated with cancers of the lung, esophagus and cervix. However, there have been no reports on the p53 codon 72 polymorphism in gastric cancer susceptibility in patients with Helicobacter pylori-associated chronic gastritis (H. pylori-CG). We, therefore, examined the polymorphism in 117 gastric cancer patients (72 intestinal type and 45 diffuse type) with H. pylori-CG and 116 H. pylori-CG patients without gastric cancer as controls. Polymerase chain reaction-restriction fragment length polymorphism (PCR-RFLP) analysis was performed to analyze the p53 codon 72 polymorphism. The crude genotypic frequencies in the gastric cancer patients were similar to those of the controls. However, when gastric cancers were classified by histologic subtype, the Pro/Pro was more frequent in the patients with diffuse type gastric cancer than in the controls (22.2% of cases vs. 12.1% of controls). The Pro/Pro genotype was associated with a 2.98-fold higher risk of diffuse-type cancer compared to the Arg/Arg genotype (95% confidence interval [CI] 1.07-8.32, p = 0.038). These results suggest that the Pro/Pro genotype at p53 codon 72 contributes to susceptibility for diffuse-type gastric cancer in patients with H. pylori-CG. The p53 codon 72 polymorphism may serve as the genetic marker for the risk assessment of the diffuse-type gastric cancer development in patients with H. pylori-CG.
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PMID:p53 Codon 72 polymorphism in gastric cancer susceptibility in patients with Helicobacter pylori-associated chronic gastritis. 1211 45

Xanthogranulomatous Cholecystitis is a chronic inflammatory disease of the gallbladder, a variant of the chronic cholecystitis. As xanthogranulomatous cholecystitis is occasionally seen with carcinoma of the gallbladder, the association with cancer is a controversial issue. A focal type of xanthogranulomatous cholecystitis is found simultaneously with gastric cancer diagnosed preoperatively. The resected specimen was genetically studied. Polymerase chain reaction amplification, single-strand conformational polymorphism analysis for mutation of p53 showed no abnormality indicating that less association with cancer in which the mutation of p53 is often seen. Etiopathologic factors of xanthogranulomatous cholecystitis might have relation with cancer, but xanthogranulomatous cholecystitis itself may not be the direct cause for cancer.
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PMID:Genetic analysis of xanthogranulomatous cholecystitis: precancerous lesion of gallbladder cancer? 1214 46

A case of intraductal oncocytic papillary neoplasm of the pancreas, with the rare progression to invasive carcinoma, is described. The intraductal oncocytic papillary neoplasm component had the features typical of this entity, with stratified layers of oncocytic cuboidal tumor cells growing in papillary and pseudopapillary arrangements within dilated pancreatic ducts. The invasive carcinoma formed a discrete fleshy tumor with well-circumscribed borders. The invasive carcinoma grew in solid lobules, subdivided by fine fibrovascular septae into predominantly organoid and trabecular growth patterns. Molecular analysis showed no loss of heterozygosity for microsatellite markers at the tumor suppressor loci of TP53, CDKN2A (p16/INK4A), and MADH4 (Smad4/DPC4) in the invasive carcinoma, although loss of heterozygosity was detected at one CDKN2A marker in the intraductal component. DNA sequencing of polymerase chain reaction amplification products of exons 1 and 2 of the CDKN2A gene showed no mutation in either tumor component. TP53 immunohistochemistry showed no increased levels of staining, consistent with the presence of wild-type gene product. Polymerase chain reaction and DNA sequencing showed no mutation of codons 12 and 13 of the KRAS proto-oncogene. These results suggest that intraductal oncocytic papillary neoplasm is a neoplasm with genetic changes that are distinct from typical pancreatic adenocarcinoma. The lack of mutation in these genes may be an explanation for the typically indolent clinical behavior of intraductal oncocytic papillary neoplasms.
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PMID:Genetic analysis of invasive carcinoma arising in intraductal oncocytic papillary neoplasm of the pancreas. 1217 96

Hepatocellular adenoma (HA) and focal nodular hyperplasia (FNH) are 2 rare, benign liver neoplasms that often are discovered incidentally. To date, few genetic changes have been found in these 2 benign lesions. However, the 2 pathways of p53 and Wnt signaling, which may be the most common molecular targets involved in liver tumorgenesis, were studied in HA and FNH. Ten HAs and 11 FNHs were analyzed for loss of heterozygosity (LOH) and sequencing analysis of mutation hot spots in exons 5 to 8 of the p53 gene. No LOH or mutant sequences were identified, indicating that p53 was not associated with these benign lesions. Genes in the Wnt signaling pathway, including beta-catenin, axin, and adenomatous polyposis coli (APC), also were studied. Polymerase chain reaction (PCR) amplification and direct sequencing of all samples of HA and FNH displayed no mutations in exon 3 of the beta-catenin gene. However, 3 HAs (30%) contained interstitial deletions from exon 3 to exon 4. Truncated forms of beta-catenin detected by Western blot and immunohistochemical analyses showed they had accumulated in the cytoplasm and nuclei. However, for the axin and APC genes, no genetic changes, including allelic loss, interstitial deletions and point mutations, were detected in any of the HAs and FNHs. In conclusion, beta-catenin, which participates in the Wnt signaling pathway, might play a more important role in the formation of HA than in that of FNH, but p53 is not associated with the development of either HA or FNH.
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PMID:P53 gene and Wnt signaling in benign neoplasms: beta-catenin mutations in hepatic adenoma but not in focal nodular hyperplasia. 1254 Aug 6

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

Areas of the limbic system of adult male Wistar rats were screened for kainic-acid-induced gene expression. Polymerase-chain-reaction-based differential display identified a 147-bp cDNA fragment, which represented an mRNA that was upregulated in the entorhinal cortex and hippocampus in the kainic-acid-treated animals. The sequence was 97.8% homologous to rat 14-3-3 zeta isoform mRNA. Detailed Northern analysis revealed increased mRNA levels in the entorhinal cortex 1 h after kainic acid exposure and continued elevation 24 h post-injection in both the entorhinal cortex and hippocampus. Western blot analyses confirmed that the protein product of this gene was also present in increased amounts over the same time period. Immunohistochemistry and terminal transferase-mediated dUTP nick end labelling (TUNEL) detected expression of 14-3-3 zeta protein exclusively in the entorhinal cortex and hippocampus, and only in TUNEL-positive neuronal cells. Expression of the tumor suppressor protein, p53 was also induced by kainate injection, and was co-localized with 14-3-3 zeta protein in selected cells only in the affected brain regions. The increase gene expression of 14-3-3 zeta represents a transcription-mediated response associated with region selective neuronal damage induced by kainic acid.
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PMID:Kainic acid induces 14-3-3 zeta expression in distinct regions of rat brain. 1242 53

We report the clinical, cytogenetic, fluorescence in situ hybridization (FISH) and molecular findings in a 54-yr-old male patient diagnosed with B-cell chronic lymphocytic leukemia (B-CLL), who showed progression to a diffuse large B-cell lymphoma (Richter's syndrome). Genetic studies were performed at diagnosis and during the Richter's transformation (RT). A clonal karyotype with two dicentric chromosomes, psu dic(12,21)(q24;q10) and dic(17,18)(p11.2;p11.2), was found. Both rearrangements were confirmed by FISH. Molecular cytogenetics analysis using p53 probe showed monoallelic loss of this tumor suppressor gene in 43.8% and 77.3% of cells for the first and the second studies, respectively). In both studies, deletions of D13S319 (18% and 12% of cells) and D13S25 loci (13% and 12% of cells) at 13q14 were found. Polymerase chain reaction analysis showed the MBR/JH rearrangement of the bcl-2 gene. FISH studies using LSI bcl-2/IgH probe allowed quantifying the clonal cell population with this rearrangement (4% and 6.6% of cells at diagnosis and RT, respectively). To our knowledge, this is the first case with a psu dic(12,21) described in B-CLL. The low percentage of cells with the 13q14 deletion and bcl-2/IgH rearrangement suggests that they were secondary events that resulted from clonal evolution. Our patient had a short survival (9 months) and a clear lack of response to several therapeutic agents, confirming the association of p53 gene deletion and karyotypic evolution with disease progression.
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PMID:Cytogenetic, FISH, and molecular studies in a case of B-cell chronic lymphocytic leukemia with karyotypic evolution. 1246 Feb 36


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