| ObjectiveBreast cancer is the second common carcinoma in women, is the second main cause of the death in the women with cancer. Chemotherapy is the most common therapy to carcinoma. In most carcinoma, the main causes of the failure to chemotherapy are primary and secondary multidrug resistance. Breast cancer is the solid carcinoma, which is sensitive to chemotherapy, many patients of breast cancer have alleviation with the first chemotherapy of different drug with different structure, but the rate of alleviation is high and the time of alleviation is short, and most of them have MDR. As a result, the main researches from how to discover the cell of breast carcinoma to search the pathogenesis responsible for the formation of breast cancer. The conventional concept is that the pathogenesis of breast cancer correlates to the activation of oncogene and inactivation of tumor suppressor gene. Recent years, the studies discovered that many correlated products of oncogene and tumor suppressor gene are factors of signal regulatory pathways regulating cell growth, proliferation, differentiation and so on. For example, Akt (PKB) in the PI -3K pathway is the product of oncogene. Therefore, the abnormity of signal regulatory pathway induce the abnormity of cell growth, proliferation, differentiation and malignant transformation. The study of cell signal regulatory pathway will help us search more pathogenesis of malignant transformation, for new way of anticancer therapies, and for the early detection of breast cancer, provide us a reference index.Many mechanisms take part in the tumor multidrug resistance, the main manifests are: (1) the over - expression of multidrug resistance gene MDR and its coding of P - glycoprotein; (2) the alteration of activation of glutathione S transferase; (3) the alteration of content or activation of DNA topoisomerase; And so on.The occuning and developing of carcinomas are the processes of multiple factors, multiple phases, and multiple genes, include the inactivation of tumor suppressor gene. At present, the mechanisms of tumor suppressor gene PTEN are accomplish by several pathways; (1) the dephosphorylation of PIP3; (2) the modulation of cell cycle protein; (3) the dephosphorylation of FAK; (4) the signal regulatory pathway of MAPK; (5) the cell apoptosis pathway induced by FAS.At the present time, wide p53 , PTEN gene are tumor - suppressor gene, now the study discovered that the loss of the function of the wide p53 maybe cause the high expression of the multidrug resistance gene( MDR1) and its coding of P - glycoprotein, and make breast cancer cell acquire type of multidrug resistance. Gene PTEN and p53 are the same important tumor suppressor gene. It was more and more important since 1997; the loss and mutation of gene PTEN are more similar to p53. So gene PTEN is similar to p53, is also a gene correlate to multidrug resistance? Our study will discover the mechanism of multidrug resistance from another way, when tumor suppressor gene p53 and PTEN inactivation cell carcinogenesis, and at the same time; they will modulate the generation of multidrug resistance.At present, the study shows that tumor - suppressor genes PTEN control proliferation through disturb the signal regulatory pathway of PIP3/AKT, expression of PTEN is loss. At the same time AKT is phosphorylated and activated, activated AKT is a factor of make cell alive, help the cell escape apoptosis, and it is the key tache of the tumor generation. Therefore, Akt is not only the key factor for cell existent, but also have more important meanings to formation, diagnosis , and therapy of tumor.MethodsThe studies collect breast hyperplasia 10 case, primary breast carcinoma with operation. We select 260 cases with integrity record and TNM grade, and select 10 cases as normal antitheses from apart from the tumor 5 - 7cm. Adopt Streptavidin - Peroxidase immunohistochemical method examine the expression of P - glycoprotein ( P-gp) ,glutathione s transferase - ( GST-),DNA Topoi-somerase II (Topo II) ,mutation P5...
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