Schlag P, Veser J, Geier G, Breitig D, Merkle P
J Cancer Res Clin Oncol. 1979;95(3):273-80. doi: 10.1007/BF00410648.
Measurements of the rate of incorporation of radioactively labeled nucleic acid precursors into the DNA and RNA of gastric carcinoma cell suspensions indicated variable rates of proliferation for the tumors. The rate of incorporation generally correlates to the cytological level of differentiation of the carcinoma. Reduced differentiation of the tumors showed a corresponding increase in the rate of proliferation. Knowing the proliferation-dependent effect of most cytostatica, this results in a resistance to cytostatica of highly differentiated gastric cancers. The nucleic acid synthesis of proliferatively active tumors could only be partially inhibited by the cytostatica tested (5-fluorouracil, adriamycin). Carcinomas with metabolic possibility for compensation of the active mechanism of the cytostatica were biochemically resistant. Due to the resulting methodical problems and unaccountable patient-dependent causes of resistance, a conclusive statement about cytostatica-sensitive tumors is difficult to make in incorporation studies.
对放射性标记的核酸前体掺入胃癌细胞悬液的DNA和RNA的速率进行测量，结果表明肿瘤的增殖速率各不相同。掺入速率通常与癌的细胞学分化水平相关。肿瘤分化程度降低表明增殖速率相应增加。鉴于大多数细胞抑制剂具有依赖增殖的作用，这导致高分化胃癌对细胞抑制剂产生抗性。所测试的细胞抑制剂（5-氟尿嘧啶、阿霉素）只能部分抑制增殖活跃肿瘤的核酸合成。具有补偿细胞抑制剂活性机制代谢可能性的癌在生化上具有抗性。由于由此产生的方法学问题以及患者个体差异导致的无法解释的抗性原因，在掺入研究中很难对细胞抑制剂敏感肿瘤做出确凿的结论。
