Reactivity of the monoclonal antibody 791T/36 with secondary malignant deposits has been investigated in frozen sections of 74 human liver biopsy specimens. There was no reactivity with hepatocytes but in some instances binding to fibrous tissues and in one case to portal tract lymphocytes was observed. Sections from 9 biopsy specimens contained malignant deposits. In seven of these 791T/36 bound either to malignant cells or to pseudoacinar contents (3 colorectal adenocarcinomas; 1 probable pancreatic adenocarcinoma; 1 medullary cell carcinoma of thyroid; 1 oat cell carcinoma of bronchus and 1 deposit of nodular sclerosing Hodgkins Disease). Two undifferentiated tumours (1 gastric adenocarcinoma and 1 oat cell bronchial carcinoma) showed no antibody binding. The histological pattern of reactivity previously reported with primary tumours appears to be similar in secondary deposits. A wider range of tumours than recognised hitherto binds 791T/36. Whether the binding to fibrous tissue seen in some instances is sufficient to cause diagnostic uncertainty when 791T/36 is used for scanning requires further investigation. Images Figure 1 Figure 2 Figure 3 Figure 4 Figure 5

A new method with a low pH step to dissociate serum complexes has been developed to measure serum levels of antigens associated with ovarian cancer. The antigens are detected by monoclonal antibodies HMFG1 and HMFG2 and have been compared to an existing ovarian cancer associated antigen detected by the antibody CA125. Elevated HMFG1 was found in 56%, and elevated HMFG2 in 65% of 924 sera from 85 patients with ovarian cancer. CA125 was elevated in 85% of these sera. When the three markers were used in conjunction, 95% of sera from patients with ovarian cancer were positive--compared with 7% in sera from healthy control subjects. Therefore, the combination of HMFG1, HMFG2 and CA125 increases the diagnostic accuracy. If all three markers are normal in a patient previously treated for ovarian cancer then no further positive information regarding disease status can be obtained by ultrasound and CT scanning.

Antibodies directed against tumour associated antigens provide a means for delivering preferentially cytotoxic radionuclides to the cells of primary and secondary tumours. The factors that influence the effectiveness of the radiation in the tumour compared with its effect on the radiosensitive normal tissues include the specificity of the antibody, the distribution of targeted energy within the tumour and the host's response to the injected foreign antibody. Recently some encouraging results from clinical trials of radioimmunotherapy have been reported in the literature. There is a continual search for more avid and specific antibodies, and the techniques of genetic engineering are being applied to the problem of reducing the antigenicity and mass of the carrier antibody. The improved efficiency of the labelled antibody needs to be supplemented by an identification of those tumours most likely to respond to this form of therapy.

The radioprotector 2-[(aminopropyl)amino] ethanethiol (WR1065) was investigated with respect to its ability to affect radiation-induced DNA damage and repair in V79 cells. Studies were performed to evaluate the protector under conditions in which it is known to be effective in reducing the cytotoxic and mutagenic effects of gamma-irradiation. At a concentration of 4 mM, WR1065 protected against the formation of single strand breaks (SSB), as determined by the method of alkaline elution, when it was present during irradiation. The protector appeared, however, to inhibit the subsequent postirradiation repair or rejoining of SSB. While repair was complete within 24 h, the protector reduced the rate of repair by a factor of 3. This inhibitory effect on the rate of repair did not correlate with either measured differences in cell survival or mutagenesis. The radioprotector was also investigated with respect to its ability to affect cell cycle progression. WR1065 present in the growth medium inhibited the progression of cells through S-phase, and cell-doubling time following a 3 h exposure to the protector was increased from 11 to 18 h. These data are consistent with the well characterized property of thiols to inhibit DNA polymerase activity. It was concluded that, while the presence of WR1065 during irradiation reduced SSB-DNA damage, its effect on the subsequent rejoining of these breaks could not be correlated with its observed effect on protecting against radiation-induced mutagenesis. It may be that the inhibition of cell-cycle progression by the protector allowed more time to enhance the fidelity of repair as measured by the protector's ability to protect against radiation-induced mutagenesis.

Ten previously untreated postmenopausal women with metastatic breast cancer, none of whom had received prior systemic therapy, were treated with the luteinising hormone releasing hormone (LHRH) analogue D-Ser(But)6, Azgly10-LHRH (ICI 118630). Two obtained an objective partial remission, one in bone metastases and one in lung metastases. One patient proved unassessable. Amongst the seven failures, incomplete pituitary gonadotrophin suppression over the relatively short treatment period with the daily injections was noted. The seven patients failing ICI 118630 received tamoxifen and two with high tumour oestrogen receptor values responded. LHRH analogues may provide a novel endocrine therapy for postmenopausal breast cancer although more data are needed. In this study, the monthly depot injection proved superior to daily injections with regard to gonadotrophin suppression, although it is not clear that this provides the mechanism of action. Images Figure 1 Figure 2 Figure 3

A clinico-pathological study of 35 bronchial carcinoid tumours was undertaken. Age, T stage, N stage, lymph node involvement, number of lymph nodes involved and number of cigarettes smoked per day were the clinical variables affecting survival. The histological variables related to survival were; mitotic count, necrosis, nuclear pleomorphism, vascular and lymphatic permeation and an undifferentiated growth pattern. All these features could be detected with routine histological stains, whereas immunocytochemical methods for demonstrating neuron specific enolase were of no help in assessing the prognosis. However there was a tendency for a well differentiated neuroendocrine carcinoma to stain strongly in some areas with carcinoembryonic antigen. Images Figure 1 Figure 2 Figure 3 Figure 4 Figure 5

We report data on the transplantation of primary tumour cells and of lymph nodes containing metastatic cells disseminated by a mammary carcinoma (LMC1) implanted s.c. in the Johns' Strain Wistar rat. A new method is described for deriving the TD50 of metastatic cells and for comparing their lymphnodal clonogenicity in the transplanted and the original, i.e. 'primary' tumour host. The TD50 for transplanted primary LMC1 cells was approximately 12 (fiducial limits 8-20 cells), and the latency of the 8-10mm tumours formed (T8-10) after inocula of 10(2) to 10(5) cells decreased linearly with the logarithmic increase in the number of cells injected. From the T8-10 and tumour incidence data for transplanted inguinal, axillary and para-aortic nodes, the TD50 for metastatic cells was calculated to be 1120 cells (fiducial limits 790-1603 cells) indicating that the clonogenicity of naturally disseminated metastatic cells was about a 100 fold lower than that determined for transplanted primary tumour cells. The incidence and T8-10 data for axillary, inguinal and para-aortic lymph node metastases in primary-tumour-excised hosts suggests that, although metastatic cells may continue translymphnodal dissemination in situ, their TD50 is still consistent with that determined by node transplantation.

A study of mortality from hepatoma and hepatic cirrhosis was conducted in Taiwan, where their mortality rates are among the highest in the world in 1980 being 26.10 and 8.14 per 100,000 population for males and females, respectively, for hepatoma, and 33.01 and 12.90 for males and females, respectively, for cirrhosis. The secular trends of hepatoma and hepatic cirrhosis death rates have been increasing, especially in males, with consequent increase in the sex ratio. The large difference in mortality rates between males and females and the increasing trends in the sex ratio suggest that other factors besides hepatitis B virus (HBV), are involved in the aetiology of hepatoma and cirrhosis of liver.