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A set of monoclonal antibodies was constructed by immunising mice with peptide fragments of the c-myc oncogene product. One such antibody, Myc 1-6E10 was shown to bind to a 62,000 dalton protein identifiable with the c-myc product (p62c-mYc). The antigen recognised was not destroyed by paraflin wax embedding. Myc 1-6E10 was used to characterise the distribution of p62C-fYC in archival testicular tumour material. Normal testes expressed only small amounts of p62c-mYc. Seminomas showed increased nuclear and cytoplasmic staining. Undifferentiated teratoma showed little activity, whereas p62c-mYc was abundant in the nuclei of differentiating epithelial structures, yolk sacs and embryoid bodiesl Only small amounts of p62c-"Yc were seen in the tumours of 5 patients who subsequently died from their disease. The demonstration that human cancer cells may show abnormal expression of unique segments of DNA, called oncogenes, provides an exciting new avenue for clinical investigation. Over 25 of these genes have now been identified, molecularly cloned and sequenced (Krontiris, 1983; Hamlyn & Sikora, 1983). Changes in the coding or control regions of these genes have been implicated in the development of cancer (Cooper & Lane, 1984; Bishop, 1984). Several molecular mechanisms resulting in either the increased production of normal oncogene products or the development of aberrant proteins that subvert the normal growth control processes have now been uncovered (Der & Cooper, 1983; Stewart et al., 1984b). These include gene amplification , translocation, mutation and rearrangement. Such changes have been documented in fresh tumour biopsies from patients as well as cultured cell lines (Rothberg et al., 1984; Favera et al., 1982). Using DNA hybridisation techniques, the N-myc gene has found to be amplified up to 100-fold in neuroblastoma (Schwab et al., 1983) and retino-blastoma (Lee et al., 1984). In one patient with chronic myelocytic leukaemia, the c-myc sequence was amplified 16-fold and rearranged within the genome during episodes of transformation (McCarthy et al., 1984). Oncogene RNA transcripts have also been measured in fresh tumour material. K-ras and H-ras mRNA has been found elevated in colonic carcinoma, colonic polyps (Spandidos & Kerr, 1984) and breast cancer (Spandidos & Agnantis, 1984). Most interest has surrounded the ras and myc genes as considerable variation has been found in the quantity of their transcripts in clinical biopsies at the RNA level (Slamon et al., 1984). DNA and RNA hybridisation analysis is difficult to perform with many clinical samples. Low copy number genes and message cannot be detected …