The effects of malachite green (MG) and phenobarbitone (PB) were compared on the development of pre-neoplastic lesions during N-nitrosodiethylamine(DEN)-induced hepatocarcinogenesis in male Wistar rats. Rats were administered 200 p.p.m. DEN in drinking water for a period of 1 month. After an interval of 2 weeks the animals were given either MG (25 p.p.m.) or PB (500 p.p.m.) in drinking water for 2.5 months. The effects were monitored on the basis of the morphological appearance of the liver, histological pattern, gamma-glutamyltranspeptidase (GGT)-positive foci, total GGT activity and the induction of glycogen-deficient islands. Both MG and PB were found to enhance liver carcinogenesis to a significant extent when compared with either their corresponding controls or animals given DEN alone. The enhancing effect of MG at 25 p.p.m. is comparable with PB at 500 p.p.m. An enhancing effect of MG on DEN-induced hepatocarcinogenesis in the rats was demonstrated.

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23 SummaryThe occurrence of megaoesophagus in (CRC/ HiCri mice afforded opportunities to study the genetics and histology of this condition. The anomaly was found to be inherited as a recessive character. Histology indicated abnormality in the myenteric plexus. Keywords: Megaoesophagus; MiceJCRC/HiCri is a large-sized albino strain of mice which has been maintained at the Cancer Research Institute since 1957. It was originally obtained from the Haffkine Institute, Bombay, as a random-bred colony which on inbreeding developed mammary tumours and leukaemia. Megaoesophagus was observed from the fifteenth generation onwards. Later, owing to inbreeding, the anomaly was observed in all animals irrespective of whether mammary tumours or leukaemia occurred in them. Another subline without mammary tumours (ICRC/HiCrif) was developed by fostering (Shirke & Pai, 1978). Even in this strain all mice revealed a grossly dilated oesophagus on postmortem examination. The disease was not observed in 12 other strains of mice which were bred under the same conditions and fed the same diet. All these strains, which are maintained in an air-conditioned animal house, are healthy and free from infection. The occurrence of this abnormality in both males and females suggested that the condition was inherited. This study was therefore undertaken to investigate the mode of inheritance and histopathology of this condition. Materials and methodsThe strains of mice used were ICRC/HiCri with megaoesophagus and DBN2fNCri which did not have an oesophageal abnormality. The average adult body weights of the 20 male and 20 female JCRC mice investigated were 30·6 ± 0·7 g and 26·9 ± 0·6 g respectively. The average life span of ICRC mice is 12·8 ± 0·5 months (mean ± SE; n = 30). Breeding experiments between JCRC and DBA mice were carried out for genetic studies. The histology of the oesophagus was studied in animals of both sexes ranging from newborn to 1 year old. A total of 75 mice were investigated.Longitudinal and transverse sections (6 !-lm thick) of formalin-fixed paraffin-embedded tissues were stained with haematoxylin and eosin (H&E). A few sections were also stained with phosphotungstic acid-haematoxylin. Results GeneticsAs seen from the breeding experiments summarized in Table 1, the appearance of a normal oesophagus in all the FI hybrids between ICRC and DBA mice indicated that megaoesophagus is a recessive condition. The proportions from the intercross and backcross matings gave ratios which did not differ significantly from the expected values of 3: 1 and I: 1 respectively.In addition, all offspring from incrosses of ICRC mice developed megaoesophagus.These data indicate that megaoesophagus occurred in mice that were homozygous for an autosomal recessive gene. This recessive allele showed a wide range of expression from a slightly enlarged to a dilated oesophagus.

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Both growth factors and steroid hormones are known to be associated with breast cancer. We have studied the epidermal growth factor receptor (EGFR) in canine mammary tumors and have shown the presence of a single class of 125I-EGF binding receptor sites in 9 out of 13 (70%) tumors, using Scatchard plot. The dissociation constant (KD) was 10(-9)M. An inverse correlation between EGFR and estrogen receptor (ER) was observed in 54% of the tumors. Our data suggest that EGFR might be used as a biochemical marker in canine mammary tumors.