RESUMO
The receptor for Müllerian Inhibiting Substance (MIS), a gonadal glycoprotein hormone, has not been previously identified. Plasma membranes from MIS-sensitive human tumor cell lines (HTB-111, endometrial carcinoma; and A-431, vulvar squamous carcinoma) were detergent extracted and incubated with 125I-labeled MIS anti-idiotypic antibody, or radioiodinated human recombinant MIS (125I rhMIS), with and without unlabeled competitors. 125I anti-idiotypic MIS antibody bound to HTB-111 membrane extracts was displaceable by unlabeled anti-idiotypic antibody, but not by anti-isotypic antibody prior to cross-linking. Specific binding of the anti-idiotypic MIS antibody to endometrial carcinoma cells was verified using fluorescence activated cell analysis and fluoresceinated antibody. Furthermore, unlabeled anti-idiotypic MIS antibody competed for 125I rhMIS binding to A-431 vulvar carcinoma membranes. The labeled anti-idiotypic MIS antibody binding complex could be separated from 32P labeled EGF receptor in the A-431 membranes, indicating that EGF, a natural inhibitor of MIS activity, and MIS itself bind to different receptors. These studies demonstrate a specific, displaceable binder for MIS in the plasmalemmae of two human tumor lines. Purification of this cell surface receptor protein will be greatly aided by using the MIS anti-idiotypic antibody.
Assuntos
Carcinoma de Células Escamosas/metabolismo , Neoplasias do Endométrio/metabolismo , Glicoproteínas , Inibidores do Crescimento/metabolismo , Hormônios Testiculares/metabolismo , Neoplasias Vulvares/metabolismo , Hormônio Antimülleriano , Anticorpos/imunologia , Anticorpos/metabolismo , Especificidade de Anticorpos , Sítios de Ligação de Anticorpos , Ligação Competitiva , Membrana Celular/metabolismo , Feminino , Citometria de Fluxo , Inibidores do Crescimento/imunologia , Humanos , Idiótipos de Imunoglobulinas/imunologia , Radioisótopos do Iodo , Proteínas Recombinantes/metabolismo , Hormônios Testiculares/imunologia , Células Tumorais CultivadasRESUMO
Among our 56 patients who have undergone urinary tract reconstruction with intact bladders 45 have required some compensation for lost ureteral length. Of these patients 33 had only distal ureteral loss and underwent reconstruction with a combination of a psoas hitch, transureteroureterostomy and primary reimplantation. Four patients with more extensive ureteral loss underwent a Boari flap procedure, and of the 8 patients with major ureteral loss 6 had small bowel interposition and 2 have had renal autotransplantation to compensate for lost ureteral length. All patients are well with stable renal function at 1 to 7-year followup.