title: Monitoring of p53 autoantibodies in lung cancer during therapy: relationship to response to treatment.
abstract: Alteration of the p53 gene is the most frequent genetic alteration in human cancer, and it leads to the accumulation of mutant p53 in the nucleus of tumor cells. In addition, it has been shown that patients with various types of neoplasias have p53 antibodies in their sera. ELISA was used to detect anti-p53 antibodies in their sera of 167 patients with lung cancer. Among these, 32 individuals (16 positive for p53 antibodies and 16 negative) were monitored over a period of 30 months for p53 antibodies. Twelve of 16 antibody positive patients had reduced titers during chemotherapy that led to partial or complete remissions of disease. The specificity of these antibodies was confirmed by two different ELISA procedures and by immunoprecipitation. The very rapid, specific decrease in these antibodies during therapy suggests that a constant level of tumoral cells with nuclear accumulating p53 protein is necessary for a detectable humoral anti-p53 response. The good correlation found between the specific evolution of the p53 antibody titer and the response to therapy suggests that p53 antibodies could represent a useful tool for checking the response to therapy and for monitoring some relapses before they are clinically detectable.
authors.affiliation: Service de Pneumologie, Hôpital Saint-Louis, Paris, France.
authors.forename: G
authors.initials: G
authors.lastname: Zalcman
authors.forename: B
authors.initials: B
authors.lastname: Schlichtholz
authors.forename: J
authors.initials: J
authors.lastname: Trédaniel
authors.forename: T
authors.initials: T
authors.lastname: Urban
authors.forename: R
authors.initials: R
authors.lastname: Lubin
authors.forename: I
authors.initials: I
authors.lastname: Dubois
authors.forename: B
authors.initials: B
authors.lastname: Milleron
authors.forename: A
authors.initials: A
authors.lastname: Hirsch
authors.forename: T
authors.initials: T
authors.lastname: Soussi
mesh_terms: D000917:Antibody Formation; D000918:Antibody Specificity; D000971:Antineoplastic Combined Chemotherapy Protocols / Q000627:therapeutic use*; D001323:Autoantibodies / Q000097:blood*; D002289:Carcinoma, Non-Small-Cell Lung / Q000097:blood / Q000276:immunology* / Q000473:pathology / Q000628:therapy; D018288:Carcinoma, Small Cell / Q000097:blood / Q000276:immunology* / Q000401:mortality / Q000628:therapy; D002945:Cisplatin / Q000008:administration & dosage; D003131:Combined Modality Therapy; D004797:Enzyme-Linked Immunosorbent Assay; D005047:Etoposide / Q000008:administration & dosage; D016158:Genes, p53; D006801:Humans; D008175:Lung Neoplasms / Q000097:blood / Q000276:immunology* / Q000473:pathology / Q000628:therapy*; D015166:Monitoring, Immunologic; D009367:Neoplasm Staging; D011379:Prognosis; D011878:Radiotherapy / Q000379:methods*; D015996:Survival Rate; D016159:Tumor Suppressor Protein p53 / Q000235:genetics / Q000276:immunology*
chemical_list: D001323:Autoantibodies; D016159:Tumor Suppressor Protein p53; D005047:Etoposide; D002945:Cisplatin