| The p53 gene is the most important tumor suppressor gene in humancancers. Mutations in the p53 gene are found in more than 50 types of humantumors. Now the p53 gene has been the leading edge and hot spot in tumormolecular biology. The p73 gene has been isolated from the p53 family lately,which infuses new vigour in the field of p53 research.Lympho-plasmacytic disease is a kind of hematopathy, which includeslymphocyte leukemia, lymphoma and multiple myeloma. Experiments andresearches have proved that the p53 and p73 genes play an important role inthe development, progression and prognosis of lympho-plasmacytic disease.Wild-type p53 is considered to be the guardian of the genome because theprotein markedly increases when DNA injury, resulting in G0/G1and G2/Mcell-cycle arrest. p53 mediates apoptosis when DNA injury is too severe. Incontrast, injured DNA is passed to daughter cells when p53 mutates. Recently,a new member of the p53 gene family has been isolated, known as p73, it issimilar to p53 in DNA binding domain, translation-activated domain. Overexpression of p73 induces the develop of cyclin-dependent kinaso inhibitorknown as p21 and leads apoptosis in the p53-negative cell lines such asosteosarcoma cell and SAOS-2. p73 also activates p53-responsive promoters,while mutant p53 can bind to p73 and inhibit the ability of p73 to both activatep53-responsive promoters and induce apoptosis.The tumor suppressor gene p53 is frequently mutated in human cancers butit isn't a universal phenomenon in malignant hematopathy. The mechanism ofp53 mutation in malignant hematopathy is not very clear, also the relationshipbetween p53 mutation and the prognosis of this disease is not distinct. Theresearch of p73 genes in hemotologic tumor has just begun oversas. There are afew of reports about low expression of p73 gene in lymphocyte leukemia andlymphoma. There are only 2 reports about p73 gene low expression in childhoodlymphocyte leukemia in our country. No advice is reported in adult lymphatictumor.In this research PCR-SSCP, RT-PCR, PEP and immunohistochemistrymethods were used to detect the abnormalities of p53 and p73 in 26 lymphocyteleukemias, 12 multiple myelomas and 12 lymphomas at gene levels and itssignificance was implicated. Concretely, we used SSCP to detect the mutationsof p53 and p73 at exons of 5,6,7;RT-PCR to analyses the expression ofp73mRNA; REP to detect the methylation of CpG in exon 1 of p73;immuneohistochemistry to study the expression of p53 protein in lymphatictumors. Results:1) 3 p53 mutations (all are T –ALL ) of 26 in lymphocyteleukemias,2 p53 mutations (stage III) of 12 multiple myelomas were detected.No p73 mutations were found. 2) The negative expression rate of p73mRNA is24%(12/50) in lymphatic system tumors. While the expression rate of P73mRNAin control group is 100%. 3) Hypermethylation methylations in CpG island ofexon 1 were found in 10 acute lymphocyte leukemias and 3 non-Hodgkinlymphomas. No methylation was found in the control group and 12 multiplemyelomas. 4) p53 protein was all negative in samples of control group.P53protein in 20 of 26 was detected in acute lymphocyte leukemia.(79.6%). 3 low-malignant samples were p53 negative, while 7 high-malignant samples were p53positive(85.7%) among the 10 non-Hodgkin lymphomas,.Conclusions :1)Thep53 mutation rate was low in lymphatic system tumors(8.3-16.7%).2)Themutation p53 protein expression rate in the initial-diagnostic lymphatic systemtumor patients was higher than that in the control group. There was no signifcantdifference between B-ALL and T-ALL.The p53 protein expression in malignant...
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