Hypermethylation of p73 Gene and Expression of p73 mRNA in ...

[Abstract]

More than half of all human cancers possess alterations of the of the p53 gene. Wild-type p53 is considered to be the guardian of the genome because the protein markedly increases with DNA injury, resulting in G/G and G/M cell-cycle arrest. If DAN injury is too severe, p53 helps to mediate apoptosis. In contrast, mutant p53 cannot limit cells to a daughter cells. Recently, a new member of the p53 gene family has been isolated, known as p73 are similar to those of p53. Over expression of p73 can induce the cyclin-dependent kinaso inhibitor known as p21 and cause apoptosis in the p53-negative osteosarcoma cell, SAOS-2.p73 can also activate p53 can bind to p73 and inhibit the ability of 73 to both activate p53-responsive promoters, and mutant, but not wild-type ,p53 can bind to p73 and induce apoptosis. Taken together, investigators have suggested that p73 may be a new tumor suppressor.Key tumor suppressor genes altered in cancers include p53, p15, p16 andRb. These genes can be inactivated by mutation, deletion, and hypermethylation. Each of these tumor suppressors has been reported to be altered in lymphoid malignancies. Furtermore, alterations of the p53,p16, and Rb genes have been reported to be associated with an unfavorable prognosis of acute lymphoid leukemias (ALLs) and B non-Hodgkin?s lymphomas(B-NHLs) .TO investigate whether p73 is altered in lymphoid malignancies, we examined 26 patients of lymphoid leukemias ,38.5% patient had not p73 expression. Some <WP=37>articles has been reported that a sizable number of lymphomas and leukemias had negligible or only limited expression of the p73 gene.We hypothesized that an absence or low level of p73 expression might be caused by hypemethylation of the CpG island located in exon1. Hypermethylation and sileneing of several tumour suppressor genes. incuding p16, has previously been noted. The methylation status of the CG-rich region in exon 1 of p73 (Fig5A) was examined. The genomic DAN was digested in parallel with a methycytosine-sensitive and resistant isoschizomeric enzyme, HpaII and MspI .The digests were amplified by PCR using the primer sets that could amplify exon1. The p73-negative cell lines were methylated in this region Also, the cell lings with relatively low expression of p73 were methylated. The p73-expressing cell lines and normal cells were not methylated in this region, consistent with our hypothesis that methylation of this region was important for the expression of p73. To strengthen hypothesis, some people determined if 5-AC could enhance p73 expression in selected cell lines. The p73 non-or low-expressing cell lines were cultured with 5-AC for 3 days. After 3 days of treatment of the p73-negative cell line, ALL-Sil expressed p73 low expressors increased their p73 expression when culyured in the presence of 5-AC.Of 26 patients, there are 10 patients without p73 mRNA expression, lymphoid leukemias had hypermethylation as detected by digestion with the methylcytosine sensitive enzyme, these date indicate a correlation between hypomethylation and p73 gene expression. The aim of testing methylation of gene is to direct demethylated therapy. <WP=38>Mutation, translocations, and deletions can alter or cause loss of expression of gene products. The p73 is a homologe of p53 and is licated at ip36.33,a region and other cancers. Forced expression of p73 in p53-negative cells resulted in their apoptosis. Because of these observations, p73 is regarded as a potential tumor suppressor. We performed PCR-SSCP analysis with DNA to identify possible point the 3 mutational hotspots of the p53 gene , which are frequently altered in various cancer.Nomutationsin26patients from hematopoietic.Taken together, these date suggest that hypermethylation of the CpG island of p73 might silence expression of the gene in lymphoblastic leukermia patient samples. Absence or low expression of p73 may contribute to the development or progression of lymphoblastic leukemia.

Title: Hypermethylation of p73 Gene and Expression of p73 mRNA in Lymphoid Leukemia

Category: Cervix Cancer

Filename: Hypermethylation of p73 Gene and Expression of p73 mRNA in Lymphoid Leukemia.pdf

Pages: 117

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