No abstract

(Zaridze & Boyle, 1987). Death from localised prostate cancer is uncommon partly because it tends to affect elderly men and partly because of its slow growth (Blute et al., 1986;George, 1988). There is a need to identify those tumours that are likely to progress sufficiently to become symptomatic.The retinoblastoma susceptibility gene (RB1) was first localised to chromosome 13ql4.1 by cytogenetic studies (Yunis & Ramsay, 1978). The gene was cloned by Friend et al. (1986) and was the first tumour-suppressor gene to be identified (Benedict et al., 1990). Osteosarcomas occur with an increased incidence in surviving adults with hereditary retinoblastoma and show the same mechanism of RB1 loss as in retinoblastoma (Friend et al., 1986 (Yandell et al., 1989; Cairns et al., 1991) and in other various tumours. The protein product of the RB1 gene (pRB) has a pivotal role in the control of the cell cycle, blocking entry into the S-phase when dephosphorylated (Hinds el al., 1992

These findings suggest that losses of the RB1 and APC tumour suppressor genes and suspected tumour suppressor genes on 10p, 10q and 16q may be important events in the genesis of prostatic tumours.

A 19 year old man presented with uni-

Evidence of RB1 allele loss was found in only 6% of pancreatic cancers, and we found no significant sequence abnormalities nor loss of RB protein expression in a panel of tumors and cell lines. Using reverse transcription-polymerase chain reaction and Southern blot analysis, we found no evidence for loss of DCC expression in pancreatic cancer cell lines, and allele loss only rarely in tumor biopsies. These findings suggest that abnormalities of RB1 and DCC are unlikely to play a major role in pancreatic carcinogenesis.