{"title":"Biological markers of early health effects in the assessment of the risk of cancer in people exposed to environmental carcinogens.","authors":"J A Indulski, W Lutz, B Krajewska","doi":"","DOIUrl":null,"url":null,"abstract":"<p><p>Biomarkers of early health effects represent the intermediate stages of the carcinogenesis process, between the initiation and conversion stage and the clinically overt neoplastic disease. The cellular processes indicated by those markers correspond, therefore, to the promotion process. Detection of those cellular processes is extremely important, as the promotion process lasts for many years and bears some signs of being reversible. The promotion process, consisting of a range of consecutive cellular changes involves, among others, activation of proto-oncogens and their transformation into oncogens, and inactivation of the suppressor genes. Therefore, the possibility of observing the trends of those changes by monitoring protein products of the oncogens and suppressor genes in the easily available material (blood, urine) is very useful. Inhibition of intercellular communication seems to play an extremely important role in the complex mechanism of transformation of a normal cell into a neoplastic one. During the carcinogenic process promotion stage, the inhibition is associated with the proteins which form the intercellular junctions and participate in cellular adhesion. That group of proteins includes carcinoembryonal antigen (CEA) and tissue polypeptide antigen (TPA), the tumour antigens which have been known for years. The possible relationship between increased TPA and CEA concentrations is supported not only by the data from the oncology but also by the data from the studies on populations exposed to agents known to increase the risk of neoplastic disease.</p>","PeriodicalId":20359,"journal":{"name":"Polish journal of occupational medicine and environmental health","volume":"6 2","pages":"149-56"},"PeriodicalIF":0.0000,"publicationDate":"1993-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":"0","resultStr":null,"platform":"Semanticscholar","paperid":null,"PeriodicalName":"Polish journal of occupational medicine and environmental health","FirstCategoryId":"1085","ListUrlMain":"","RegionNum":0,"RegionCategory":null,"ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"","PubModel":"","JCR":"","JCRName":"","Score":null,"Total":0}
引用次数: 0
Abstract
Biomarkers of early health effects represent the intermediate stages of the carcinogenesis process, between the initiation and conversion stage and the clinically overt neoplastic disease. The cellular processes indicated by those markers correspond, therefore, to the promotion process. Detection of those cellular processes is extremely important, as the promotion process lasts for many years and bears some signs of being reversible. The promotion process, consisting of a range of consecutive cellular changes involves, among others, activation of proto-oncogens and their transformation into oncogens, and inactivation of the suppressor genes. Therefore, the possibility of observing the trends of those changes by monitoring protein products of the oncogens and suppressor genes in the easily available material (blood, urine) is very useful. Inhibition of intercellular communication seems to play an extremely important role in the complex mechanism of transformation of a normal cell into a neoplastic one. During the carcinogenic process promotion stage, the inhibition is associated with the proteins which form the intercellular junctions and participate in cellular adhesion. That group of proteins includes carcinoembryonal antigen (CEA) and tissue polypeptide antigen (TPA), the tumour antigens which have been known for years. The possible relationship between increased TPA and CEA concentrations is supported not only by the data from the oncology but also by the data from the studies on populations exposed to agents known to increase the risk of neoplastic disease.