P-glycoprotein, HER-2/neu, and Mutant p53 Expression in Human Gynecologic Tumors

摘要: BACKGROUND Overexpression of P-glycoprotein has been associated with a worse prognosis for some groups patients not receiving chemotherapy. Recently, it demonstrated that in vitro both c-Ha-Ras overexpression and mutant p53 do activate the MDR1 gene (also known as PGY1) murine NIH 3T3 cells. This direct connection between oncogenic activation, antioncogenic malfunctioning (presence instead wild-type protein), expression constitutes fundamental conceptual model could provide an explanation obscure prognostic role, absence chemotherapy, gene. PURPOSE Our goal was to test whether relationship (P-glycoprotein) expression, protein is also reproducible vivo two human gynecologic tumors. METHODS Fifty tumor specimens (31 mammary, 11 endometrial, eight cervical) were analyzed. They had obtained from previously untreated patients. Aliquots these frozen stored at -70 degrees C since surgical collection or routinely fixed formalin embedded paraffin. DNA extracted single-strand conformation polymorphism (SSCP) analysis. Immunohistochemical techniques used on material determine: 1) using different monoclonal antibodies (c219 JSB1); 2) HER-2/neu (c-erb-B2; ERBB2) NCL-CB11 antibody; 3) PAb 1801 antibody. Polymerase chain reaction (PCR)-SSCP confirm recognition mutated isoform p53. Endometrial cervical carcinomas studied by PCR-SSCP analysis immunohistochemical Only when there full concordance methods endometrial tumors considered express RESULTS A statistically significant (P = .009; Fisher's exact test) association found more aggressive form inoperable, locally advanced mammary carcinoma. Expression similar studied--mammary carcinoma low basal compared significantly .0002; chi-square higher levels expression. CONCLUSIONS The highly coexpression took place only subgroup aggressive, advanced, inoperable carcinomas, whereas no be operable No activation