Abstract
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.
Highlights
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)
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, 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)
Summary
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. 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). A p53 mutation in FTC has first been identified in the cell line FT-MZ-1 established in our laboratory (Runnebaum et al, 1994b). We tested primary FTCs for p53 gene mutation and aberrant protein accumulation, integration of human papillomavirus (HPV) sequences and the association of cell cycle parameters with p53 alterations
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