Summary Fallopian tube carcinoma (FTC) is a rare but lethal gynaecological malignancy. Four out of seven FTCs were identified with three point missense mutations, one single base deletion and one silent point mutation in the p53 gene. Genital-type HPV sequences were not detected. The S-phase fraction of tumours with mutant and wild-type p53 was 25.74% (median) and 12.55% (median) respectively.Keywords: fallopian tube cancer; p53 mutation; cell cycle; human papilloma virus (HPV) Primary fallopian tube carcinoma (FTC) is an aggressive, malignant tumour of the female genital tract with an unfavourable prognosis and an approximately 10% 5 year survival in the later stages (Eddy et al., 1984;Rose et al., 1990;Rosen et al., 1993). FTCs are rare, constituting about 1% of all female genital tract cancers. The vast majority represent adenocarcinomas and show histopathological similarities to epithelial ovarian cancer. In non-familial ovarian cancer, alteration of the p53 tumour-suppressor gene by somatic mutation is the most common single-gene alteration identified so far (Marks et al., 1991;Okamoto et al., 1991;Tsao et al., 1991;Kupryjanczyk et al., 1993;Milner et al., 1993; Runnebaum et al., 1994a; Runnebaum et al., 1995a). Wild-type p53 is a potent suppressor of tumorigenesis in different tumour types (Eliyahu et al., 1989;Baker et al., 1990;Cheng et al., 1992;Runnebaum et al., 1994c; Runnebaum and Kreienberg 1995). p53 acts as a transcription factor (Kern et al., 1991;Unger et al., 1992) regulating cellular functions such as DNA damage response (Kastan et al., 1991(Kastan et al., , 1992, induction of apoptosis by transactivating Bax and transrepressing Bcl-2 (Miyashita et al., 1994;Miyashita and Reed, 1995) or inducing G1 cell cycle arrest by transactivating p2iWAFI/CIPI (Lowe and Ruley 1993;Yonish-Rouach et al., 1993; Runnebaum et al., 1995b). A p53 mutation in FTC has first been identified in the cell line FT-MZ-1 established in our laboratory (Runnebaum et al., 1994b extracted from the paraffin-embedded formalin-fixed sections as described previously (Runnebaum et al., 1991(Runnebaum et al., , 1994b (Table II). Two mutations were identified in tumour no. 777, one silent point mutation in exon 8 not leading to an amino acid change and one single base deletion in exon 6 shifting the reading frame (Figure 1). The presence of mutant (mt) and wild-type (wt) sequence in nos. 339 and 777 indicated heterozygosity at the p53 locus.Immunohistochemistry showed accumulation of p53 protein with a marked stain in three tumours. In tumours 906, with a homozygous point missense mutation in codon 285, and 6097, with the Hisl75 mutant, the strong stain of more than 80% of the tumour cells resulted in an IRS of 12 (Figure 2) (Eddy et al., 1984;Rosen et al., 1993; Lacy et al., 1995). The tumours in this study were papillary adenocarcinomas representative for FTC. The tumours were metastatic at the time of diagnosis with FIGO stages IIA and IIIC (Nordin, 1994). In four out of seven FTCs, mutations in the p53 tumour-suppresso...