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German Cancer Research Center, D-69120 Heidelberg, Germany [M-C. v. B., M. C. H.]; Laboratory of Human Carcinogenesis, National Cancer Institute, Bethesda, Maryland 20892 [H. M. C., V. M. G. D., W. P. B., L. L., G. E. T.]; China Medical University, Shenyang, Liaoling, People's Republic of China [A-G. H.]; Sun Yat Sen University of Medical Sciences, Guangzhou, People's Republic of China [S. M. Z.]; and Institut Gustave Roussy, Villejuif, Paris, France [T. T., N. J.]
Serum antibodies reacting with the tumor suppressor protein p53 have been detected previously in cancer patients with a variety of neoplasms. Two initial (although insufficient) prerequisites for a B-cell response to occur have been proposed: p53 protein accumulation in the tumor or a mutant p53 gene, or both.
We have examined 65 esophageal cancer cases (42 from Guangzhou and Shenyang, People's Republic of China, and 23 from Paris, France) to obtain a prevalence estimate of anti-p53 antibodies for this type of cancer and to define the relationship of p53 tumor status to B-cell immune response. Sera were analyzed in a triplicate assay (enzyme-linked immunoassay, immunoprecipitation, and immunoblot) for anti-p53 antibodies. Tumor DNA was screened for mutations in exons 5–8, and tumor tissue was examined by immunohistochemistry for abnormal p53 protein accumulation. p53 mutations were found in 36 (58%) of 62 cases analyzed.
Sixteen patients (25%) had circulating antibodies to the tumor suppressor protein. All but two (88%) of the tumors from seropositive cases had a mutation in the DNA binding region of the p53 gene, and with one exception, these tumors also showed nuclear accumulation of the p53 protein. In contrast, tumor mutations were found in just 22 (46%) of the 48 individuals in whom we did not detect anti-p53 antibodies. Among the 22 seronegative cases for which we found no tumor mutations, 11 revealed p53 protein accumulation by immunohistochemical analysis.
Thus, circulating anti-p53 antibodies may be present in one-fourth of esophageal cancer patients, most of whom also would be expected to have a p53 gene mutation in their tumors. Patients without such mutations appear considerably less likely to mount a B-cell response to the p53 tumor suppressor protein than those that do (P < 0.01).
1 Present address: Istituto Nazionale Tumori, Divisione di Oncologia Sperimentale, via G. Venezian 1, 20133 Milano, Italy.
2 Present address: Department of Biology, Johns Hopkins University, Baltimore, MD 21205.
3 To whom requests for reprints should be addressed, at Laboratory of Human Carcinogenesis, National Cancer Institute, Building 37, Room 2C05, National Institutes of Health, Bethesda, MD 20892. Phone: (301) 496-2048; Fax: (301) 496-4097; E-mail: triversg @intra.nci.nih.gov.
Received 5/ 6/96. Accepted 8/29/96.
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