British Journal of Cancer

Newell, DR

doi: 10.1038/bjc.1990.35pmid: 2178663

Neades, GT; Hughes, LE

doi: 10.1038/bjc.1990.36pmid: 2178664

Law, MR

doi: 10.1038/bjc.1990.37pmid: 2178665

D'Onofrio, C; Alvino, E; Garaci, E; Bonmassar, E; Santoro, MG

doi: 10.1038/bjc.1990.38pmid: 2310673

Type A prostaglandins (PGA1 and 16,16-dimethyl-PGA2-methyl ester) were found to block the proliferation of HTLV-I infected cord blood lymphocytes (CBL) in vitro, thus preventing the clonal immortalisation that is considered as a predisposing condition to HTLV-I positive leukaemia. PGA1 and di-M-PGA2 did not affect the long-term survival of normal non-infected CBL, whereas they suppressed the proliferation of an established cord-blood derived HTLV-I positive cell line, MT-2. As shown by the number of HTLV-I infected p19+ cells, the block of the selection of immortalised, infected clones by PGAs did not appear to be due to an inhibition of early stages of HTLV-I infection. The possibility that the effect of PGAs could be mediated by an action on the immune response was also examined. PGAs regulated the cell-mediated cytotoxic function of CBL to a different extent when normal non-infected or HTLV-I exposed CBL were compared. In fact, PGAs down-regulated the natural killing and macrophage/lymphocyte cytotoxic response of normal CBL, whereas they did not modify the already depressed immune response of CBL challenged with HTLV-I. These results suggest that the protective effect of PGAs against HTLV-I infection in vitro is mostly related to the direct suppression of the clonal expansion of virus-infected cells, rather than to the anti-viral activity or modulation of the cell-mediated immunity.

Kadagidze, ZG; Tupitsyn, NN; Baryshnikov, AJ; Kadyrov, KhP; Blinov, VM; Bernard, A; Amiot, M; Boumsell, L

doi: 10.1038/bjc.1990.39pmid: 1968760

Solid tumour cells were shown to express VLA-beta and Thy-1 antigens. For identification of these molecules two monoclonal antibodies, K-20 and ICO-10, characterised in detail previously, were used. Four groups of solid tumours have been identified according to their immunophenotype: VLA-beta+ and Thy-1-; VLA-beta+ and Thy-1+; VLA-beta- and Thy-1+; VLA-beta- and Thy-1-. To a certain extent these groups have been shown to reflect tumour histogenesis: tumours of epithelial origin never expressed an ICO-10+, K20-phenotype while soft tissue sarcomas and neuroblastoma cells never expressed the beta-chain of VLA molecular complexes.

Pedley, RB; Boxer, GM; Boden, JA; Southall, PJ; Begent, RHJ; Bagshawe, KD; Humm, J; Searle, F

doi: 10.1038/bjc.1990.40pmid: 2310674

Autoradiography with 125I-labelled antibodies 17-1-A and 11-285-14 (anti-carcinoembryonic antigen) injected singly or together into nude mice carrying two distinct human colorectal cancer xenografts delineates marked changes in distribution and retention of isotope over 72 h, which are relevant to microdosimetry. The antibodies localise independently at low concentrations. Slow accumulation and retention predominantly in membranes of glands and necrotic areas suggest that therapy will succeed best with isotopes whose range, half-life and/or mode of delivery can exploit optimally the greater selectivity of the late retention.

Dobrucki, JW; Demsar, F; Walczak, T; Woods, RK; Bacic, G; Swartz, HM

doi: 10.1038/bjc.1990.41pmid: 2155641

Hurkadli, KS; Sheth, AR; Garde, SV; Doctor, VM; Sheth, NA

doi: 10.1038/bjc.1990.42pmid: 2106911

Immunocytochemical localisation of follicle stimulating hormone (FSH) was carried out in normal, benign and malignant human prostates by indirect immunoperoxidase technique. Positive staining was observed in the epithelial cells of all the three categories, while the stromal cells showed a weakly positive reaction in a few specimens. The brown reaction product was dispersed in the cytoplasm of the epithelial cells. These observations demonstrate the presence of immunoreactive FSH-like peptide in human prostate. The significance of FSH in the aetiopathology of prostatic disorders is discussed.

Bourguet, P; Dazord, L; Desrues, B; Collet, B; Ramee, MP; Delaval, P; Martin, A; Logeais, Y; Pelletier, A; Toujas, L; Bourel, D; Kernec, J; Saccavini, JC; Kremer, M; Herry, JY

Izbicki, JR; Hamilton, SR; Wambach, G; Harnisch, E; Wilker, DK; Dornschneider, G; Eibl-Eibesfeldt, B; Schweiberer, L

doi: 10.1038/bjc.1990.44pmid: 2138029

Epidemiological and experimental studies suggest that androgens influence colonic carcinogenesis. We investigated the effects of hormonal manipulations (surgical and chemical castration, hormone substitution) on colonic tumour development, tumour and mucosal histopathology, and epithelial proliferation in macroscopically normal colonic mucosa in male rats, after induction of chemical colon carcinogenesis by subcutaneous injections of azoxymethane (AOM). Chemical castration with cyproterone acetate, but not surgical castration, resulted in increased colonic tumorigenesis, which was accompanied by decreased crypt length, decreased number of cells per crypt, and increased crypt epithelial mitotic index in the right colon. Chemically castrated rats also had crypt hyperplasia and increased numbers of dysplastic foci in the left colon which were not seen with surgical castration. By contrast, rats given testosterone after surgical castration showed decreased colonic tumorigenesis with an increased proportion of tumours in the left colon and lower percentage of tumours with invasion. The grossly normal mucosa of the testosterone-substituted castrated rats showed decreased crypt length in the right colon similar to the other groups of castrated rats, but no significant increase in mitotic index. Our results suggest that the anti-androgenic progestin cyproterone is a potent enhancer of colonic tumorigenesis and epithelial proliferative abnormalities after AOM administration. Exogenous testosterone after castration alters tumour distribution and characteristics and suppresses epithelial proliferative abnormalities. Finally, androgen effects on the colonic mucosa are more prominent in the right than in the left colon, suggesting different influences of hormones on the epithelium of these anatomical sites.