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after xenotransplantation into nude mice.

Comparative ultrastructural examination of the primary tumour and of cells grown in tissue culture and in xenografts demonstrated the preservation of most tumour type speci- fic structural criteria in the ex vivo/in vitro systems. The present data show that not only tumour cells from small cell car- cinoma but also from other histological types are capable of synthesizing a broad spectrum of immunoreactive peptide hormones. This re- sult might be interpreted as indicating a common expression of hormone biosynthesis and secretion by all lung tumours.

Neurotensin is Produced by and Secreted from Classic Small Cell Lung Cancer Cells. Moody, T.W., Carney, D.N., Korman, L.Y., et al. Department of Biochemistry, The George Washington University School of Medicine and Health Sciences, Washington, DC 20037, U.S.A. Life Sci. 36: 1727-1732, 1985.

The presence of neurotensin in various human tumor cell lines was investigated by radioimmunoassay. High concentrations (0.06 - 5.1 pmol/mg protein) were detected in 50% of the classic but not variant small cell lung cancer or other human tumor cell lines examined. Biochemical studies indicated that the main peak of immunoreactivity coeluted with synthetic neurotensin using gel filtra- tion and high pressure liquid chromatography techniques. Also, the rate of neurotensin secretion increased approximately 2-fold when theophylline was added which elevated intra- cellular levels of cAMP 4-fold. Becaus~ neurotensin is present in and secreted from many classic small cell lung cancer cells, it may function as a regulatory peptide in this disease.

Irmnuno-Oncological Monitoring of Patients with Lung Cancer. IV. Aspects of the Ir~nu- nocompetent System. Mancuso, M., Leonardo, E., Sanfilippo, B. et al. Universita di Torino, Cattedra di Chirurgia Toraco-Polmonare, Torino, Italy. Minerva Med. 76: 619-626, 1985.

Some aspects of the immunocompetent system were tested in 84 lung cancer patients at the time of diagnosis and during the natu- ral course of the disease. Results show no significant variations for many immunologi- cal tests during the course of the neoplasia. Significant alterations are observed in T- lymphocyte and macrophage evaluation. More- over, some immunological data are related to lung cancer post-surgical survival.

Amplification and Enhanced Expression of Cellular Oncogene c-Ki-ras-2 in a H~unan Epidermoid Carcinoma of the LLmg. Mi~aki, M., Sato, C., Matsui, T., et al. Tokyo Metropolitan Institute of Medical

Science, Bunkyo-ku, Tokyo 113, Japan.

Jpn. J. Cancer Res., Gann 76: 260~265, 1985.

The level of c-Ki-ras-2-specific mRNA was found to be markedly enhanced (i0- to 20-fold) in a human epidermoid lung carcinoma transplan- ted into nude mice, compared with that in other lung carcinomas. Analysis of DNA revealed that c-Ki-ras-2 gene was amplified approximately 10-fold in this carcinoma, while c-Ha-ras, c- myc and c-sis were not amplified. Chromosome abnormalities were also observed in this car- cinoma.

Amplification of the c-myc 0ncogene in a Sub- population of H~an Small Cell Lung Cancer. Saksela, K., Bergh, J., Lehto, V.P., et al. Department of Virology, Recombinant DNA Labo- ratory, University of Helsinki, 00290 Helsinki 29, Finland. Cancer Res. 45: 1823-1827, 1985.

We have examined a panel of human lung can- cer cell lines for amplification and expressi- on of the c-myc, N-myc, and c-myb oncogenes. The cell lines analyzed represent various histo- pathological types of lung cancer: small cell carcinoma with neuroendocrine properties; squa- mous cell carcinoma with epithelial markers; and large cell carcinoma with a mixed neuroen- docrine-epithelial phenotype. Two of six cell lines, both of which were small cell carcinomas, showed about a 20-fold amplification of the c-myc oncogene. In both cell lines, the ampli- fication is accompanied by an enhanced expres- sion of c-myc. The N-myc or c-myb genes were not amplified in any of the cell lines, nor were they expressed in detectable amounts. The results confirm and extend earlier find- ings on c-myc amplification in small cell lung cancer.

Inmunocytochemical Localization of the Surfac- tant Apoprotein and Clara Cell Antigen in Che- mically Induced and Naturally Occurring Pulmo- nary Neoplasms of Mice. Ward, J.M., Singh, G., Katyal, S.L., et al. Pathogenesis and Perinatal Carcinogenesis Sec- tions, Laboratory of Comparative Carcinogene- sis, National Cancer Institute, Frederick MD, U.S.A. Am. J, Pathol. 118: 493-499, 1985.

The localization of surfactant apoprotein (SAP) and the Clara cell antigen(s) (CCA) was studied in naturally occurring and experimen- tally induced pulmonary hyperplasias and neo- plasms by avidin-biotin peroxidase complex (ABC) immunocytochemistry. Lungs of B6C3FI and A strain mice with naturally occurring lesions, B6C3FI mice given injections of N-nitrosodie- thylamine (DEN), BALB/c nu/nu or nu/+ mice ex- posed transplancentally on Day 16 of gestation to ethylnitrosourea (ENU), or BALV/c nu/+ mice exposed to BNU at 8-12 weeks of age were pre- served in formalin or Bouin's fixative. After ABC immunocytochemistry, SAP was found in the cytoplasm of normal alveolar Type II cells; in the majority of cells in focal alveolar and solid hyperplasias originating in peribronchi-

olaf or peripheral locations; and in solid,