Lutz W, Krajewska B
Zakładu Diagnostyki Laboratoryjnej Instytutu Medycyny Pracy, Lodzi.
Med Pr. 1996;47(5):511-8.
Over a whole life-span a genetic machinery of human cells is exposed to carcinogenic effect of various chemical, physical and biological factors leading to cellular changes in the genome like point mutation and translocation or amplification of genes. Together with growing an ageing of the human organism, the number and heterogeneity of mutated cells increase. Thus, the presence or absence of the neoplastic process may depend on the length of life, efficiency of the immunological system, cumulation of adverse affects of environmental factors or inherited susceptibility to a disease. There is no doubt that neoplasms which develop due to inheritance of different genetic defects or due to direct environmental effect progress in line with similar mutations, resulting finally in the genome destabilisation and disturbances in the balance between proliferation and differentiation processes. The knowledge as to how far environmental carcinogens affect cellular genome is still limited. Nevertheless, data collected to date help to understand the mechanisms by which environmental carcinogens may initiate the process of transforming normal cells into neoplastic ones. It is most likely that activation of some oncoproteins and deactivation of some suppressive genes and related qualitative and quantitative changes in oncoproteins and anti-oncoproteins participating in the growth control and cellular division, are the essential mechanisms which are involved in this process. The discovery that activation of oncoproteins and related emergence of oncoprotein in cells, increased in the number of changed, can be monitored in easily available biological fluids, such as blood or urine, has become of great importance for occupational medicine and environmental health. That has provided new diagnostic measures for evaluating carcinogenic effects of the working and living environments. The fact, that the emergence of oncoproteins in biological fluids may precede by many months or even years clinical manifestations of neoplastic disease should greatly contribute to undertaking more effective preventive measures.
在人的整个生命周期中，人体细胞的遗传机制会受到各种化学、物理和生物因素的致癌作用影响，从而导致基因组发生细胞变化，如点突变、基因易位或扩增。随着人类机体的生长和衰老，突变细胞的数量和异质性会增加。因此，肿瘤形成过程的发生与否可能取决于寿命长短、免疫系统的效率、环境因素不良影响的累积或对疾病的遗传易感性。毫无疑问，由于不同遗传缺陷的遗传或直接环境影响而发生的肿瘤，会按照相似的突变进程发展，最终导致基因组不稳定以及增殖和分化过程之间的平衡失调。关于环境致癌物对细胞基因组影响程度的认识仍然有限。然而，迄今为止收集的数据有助于理解环境致癌物引发正常细胞向肿瘤细胞转化过程的机制。很可能是某些癌蛋白的激活、某些抑癌基因的失活以及参与生长控制和细胞分裂的癌蛋白和抗癌蛋白相关的定性和定量变化，是这一过程中涉及的关键机制。在血液或尿液等易于获取的生物体液中，可以监测到细胞中癌蛋白的激活以及相关癌蛋白数量的增加，这一发现对职业医学和环境卫生具有重要意义。这为评估工作和生活环境的致癌作用提供了新的诊断措施。生物体液中癌蛋白的出现可能比肿瘤疾病的临床表现提前数月甚至数年，这一事实应能极大地促进采取更有效的预防措施。
