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Detection of circulating adenocarcinoma-associated antigen in the sera of cancer patients with a monoclonal antibody
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ministration of Dimethyl Hydrogen Phosphite. Dunnick, J,K., Boorman, G.A., Haseman, J,K. et al. National Institute of Environmental Health Science, National Toxicology Program, Research Triangle Park, NC 27709, U.S.A. Cancer Res. 46: 264-270, 1986. Dimethyl hydrogen phosphite (DMHP), an intermediate in the production of insecticides or herbicides, was a~ministered by p.o. gavage for 2 yr to male Fischer 344/N rats and male and female B6C3F. mice at doses of 0, i00, or 200 mg/kg andlto female Fischer 344/N rats at doses of 0, 50 or i00 mg/kg. Dose related toxicity was seen in the lungs of treated male and female rats. The lung lesions were most prevalent in the high dose male rat group which received a dose twice that given to the high dose female rats. Lung lesions included alveolar epithelial hyperplasia, chemically related pneumonia, alveolar-bronchiolar adenoma, alveolar-bronchiolar carcinoma, and squamous cell carcinoma. DMHP also caused neoplastic and nonneoplastic lesions of the forestomach in male rats; a similar but less pronounced effect was observed in female rats. Nonneoplastic lesions associated with administration of DMHP included mineralization of the cerebellum in male rat and focal calcification of the testis in male mice. Under the conditions of this study, there was clear evidence for carcinogenicity for male rats, equivocal evidence for carcinogenicity in female rats, and no evidence for carcinogenicity in either male or female mice. DMHP caused the highest incidence of lung tumors in the male rat of all chemicals studied to date in the National Cancer Institute-National Toxicology Program Carcinogenesis Testing Program.
3,
BASICBIOLOGY Cloning 0f Human Lun~ Cancer Cells.
Walls, G.A., Twentyman, P.R. MRC Clinical Oncology and Radiotherapeutics Unit, Cambridge, U.K. Br. J. Cancer 52: 505-513, 1985. We have carried out a comparison of two different methods for cloning human lung cancer cells. The method of Courtenay & Mills (1979) generally gave higher platlng efficiencies (PE) than the method of Carney et al. (1980). The number o ~ coloni ~ es increased with incubation time in both methods and t h e w e e k l y medium replenishLent in the Courtenay method was advantagenous for longer incUbation times of several weeks. In the Courtenay method, the use of August rat red blood cells (RBC) and low oxygen tension ware both found to be necessary factors for maximum platin C efficiency. The usefulness of heavily i~radiated feeder cells in improving PE is less certain; each cell type may have its own
~equirement. Diagnostic Application of a M 0 n o c l o n a l A n t i body Against Small Cell Lung Cancer. Postmus, P.E., Hirschler-Schulte, T.J.W., De-Leij, L. et al. Department of Pulmonary Diseases, University Hospital Groningen, 9713 EZ Groningen, Netherlands. Cancer 57: 60-63, 1986. A monoc~onal antibody (MOC-I) directed against an antigen present in small cell lung cancer (SCLC) was used for diagnostic purposes. After screening of biopsy specimens of lung tumors, MOC-I was found to react with SCLC (n=10) and adenocarcinoma of the lung (4 of 9 cases). Except for a few cells in a poorly differentiated tumor, the reaction with squamous cell cancer was negative ,(n=6). Staining with MOC-1 by an immunoperoxidase technique on imprints of biopsy specimens procured by rigid bronchoscopy was found to be a reliable and rapid method for diagnosing SCLC (16 of 17 positive). All cytologically proven bone marrow and pleural metastases of SCLC were found by staining on a cytospin preparation with MOC-I. Moreover, in three cytologically negative cases, MOC-I positive cells were detected.
Detection o f C i r c u l a t i n g Adenocarcinoma-Ass o c i a t e d Antigen in the Sera o f Cancer Pat i e n t s with a Monoclonal Antibody. Hinoda, Y., Imai, K., Endo, T. et al. Department of Internal Medicine, Sapporo Medical College, Chuo-ku, Sapporo 060, Japan. Jpn. J. Cancer Res., Gann 76: 1203-1211, 1985. The antigen (YH206 antigen) corresponding to the monoclonal antibody (MoAb) YH206 (IgM), which was produced against a lung adenocarcinoma cell line A549, was found to be an extremely high-molecularweight protein of over 330,000 daltons by means of SDS-PAGE and Western blot analysis. The ~,~,unohistological distribution of the antigenic determinant recognized by MoAb YH206 was found to be limited to adenocarcinoma tissues. It was shown by reversed passive hemagglutinin assay (RPHA) that the antigen could be detected not only in the spent medium from human lung cancer cell line A549 but also in the sera from cancer patients. Only 3 out of 30 (10%) healthy donors and 4 of 31 (12.9%) patients with benign diseases had serum antigen levels of more than 1/64 dilution. In contrast, 42 of 87 (48.3%) patients with lung cancer and 29 of 50 (58.0%) patients with cancers of the digestive organs had elevated levels of the antigen. As regards the relation between antigen levels and clinical stages of lung cancer, values of more than 1/128 dilution were detected only in patients with stage III or IV disease.
ministration of Dimethyl Hydrogen Phosphite. Dunnick, J,K., Boorman, G.A., Haseman, J,K. et al. National Institute of Environmental Health Science, National Toxicology Program, Research Triangle Park, NC 27709, U.S.A. Cancer Res. 46: 264-270, 1986. Dimethyl hydrogen phosphite (DMHP), an intermediate in the production of insecticides or herbicides, was a~ministered by p.o. gavage for 2 yr to male Fischer 344/N rats and male and female B6C3F. mice at doses of 0, i00, or 200 mg/kg andlto female Fischer 344/N rats at doses of 0, 50 or i00 mg/kg. Dose related toxicity was seen in the lungs of treated male and female rats. The lung lesions were most prevalent in the high dose male rat group which received a dose twice that given to the high dose female rats. Lung lesions included alveolar epithelial hyperplasia, chemically related pneumonia, alveolar-bronchiolar adenoma, alveolar-bronchiolar carcinoma, and squamous cell carcinoma. DMHP also caused neoplastic and nonneoplastic lesions of the forestomach in male rats; a similar but less pronounced effect was observed in female rats. Nonneoplastic lesions associated with administration of DMHP included mineralization of the cerebellum in male rat and focal calcification of the testis in male mice. Under the conditions of this study, there was clear evidence for carcinogenicity for male rats, equivocal evidence for carcinogenicity in female rats, and no evidence for carcinogenicity in either male or female mice. DMHP caused the highest incidence of lung tumors in the male rat of all chemicals studied to date in the National Cancer Institute-National Toxicology Program Carcinogenesis Testing Program.
3,
BASICBIOLOGY Cloning 0f Human Lun~ Cancer Cells.
Walls, G.A., Twentyman, P.R. MRC Clinical Oncology and Radiotherapeutics Unit, Cambridge, U.K. Br. J. Cancer 52: 505-513, 1985. We have carried out a comparison of two different methods for cloning human lung cancer cells. The method of Courtenay & Mills (1979) generally gave higher platlng efficiencies (PE) than the method of Carney et al. (1980). The number o ~ coloni ~ es increased with incubation time in both methods and t h e w e e k l y medium replenishLent in the Courtenay method was advantagenous for longer incUbation times of several weeks. In the Courtenay method, the use of August rat red blood cells (RBC) and low oxygen tension ware both found to be necessary factors for maximum platin C efficiency. The usefulness of heavily i~radiated feeder cells in improving PE is less certain; each cell type may have its own
~equirement. Diagnostic Application of a M 0 n o c l o n a l A n t i body Against Small Cell Lung Cancer. Postmus, P.E., Hirschler-Schulte, T.J.W., De-Leij, L. et al. Department of Pulmonary Diseases, University Hospital Groningen, 9713 EZ Groningen, Netherlands. Cancer 57: 60-63, 1986. A monoc~onal antibody (MOC-I) directed against an antigen present in small cell lung cancer (SCLC) was used for diagnostic purposes. After screening of biopsy specimens of lung tumors, MOC-I was found to react with SCLC (n=10) and adenocarcinoma of the lung (4 of 9 cases). Except for a few cells in a poorly differentiated tumor, the reaction with squamous cell cancer was negative ,(n=6). Staining with MOC-1 by an immunoperoxidase technique on imprints of biopsy specimens procured by rigid bronchoscopy was found to be a reliable and rapid method for diagnosing SCLC (16 of 17 positive). All cytologically proven bone marrow and pleural metastases of SCLC were found by staining on a cytospin preparation with MOC-I. Moreover, in three cytologically negative cases, MOC-I positive cells were detected.
Detection o f C i r c u l a t i n g Adenocarcinoma-Ass o c i a t e d Antigen in the Sera o f Cancer Pat i e n t s with a Monoclonal Antibody. Hinoda, Y., Imai, K., Endo, T. et al. Department of Internal Medicine, Sapporo Medical College, Chuo-ku, Sapporo 060, Japan. Jpn. J. Cancer Res., Gann 76: 1203-1211, 1985. The antigen (YH206 antigen) corresponding to the monoclonal antibody (MoAb) YH206 (IgM), which was produced against a lung adenocarcinoma cell line A549, was found to be an extremely high-molecularweight protein of over 330,000 daltons by means of SDS-PAGE and Western blot analysis. The ~,~,unohistological distribution of the antigenic determinant recognized by MoAb YH206 was found to be limited to adenocarcinoma tissues. It was shown by reversed passive hemagglutinin assay (RPHA) that the antigen could be detected not only in the spent medium from human lung cancer cell line A549 but also in the sera from cancer patients. Only 3 out of 30 (10%) healthy donors and 4 of 31 (12.9%) patients with benign diseases had serum antigen levels of more than 1/64 dilution. In contrast, 42 of 87 (48.3%) patients with lung cancer and 29 of 50 (58.0%) patients with cancers of the digestive organs had elevated levels of the antigen. As regards the relation between antigen levels and clinical stages of lung cancer, values of more than 1/128 dilution were detected only in patients with stage III or IV disease.