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. 1979;95(3):273-80.
doi: 10.1007/BF00410648.

Incorporation studies of nucleic acid precursors in gastric cancer: an attempt in individualized chemotherapy

P Schlag, J Veser, G Geier, D Breitig, P Merkle

Incorporation studies of nucleic acid precursors in gastric cancer: an attempt in individualized chemotherapy

P Schlag et al. J Cancer Res Clin Oncol. 1979.

Abstract
in English, German

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.

Durch Messung der Einbaurate radioaktiv markierter Nucleinsäurepräkursoren in die DNA bzw. RNA bei Magenkarzinom-Zellsuspension ergaben sich Hinweise auf eine unterschiedliche Proliferationsaktivität der Tumoren. Der Markierungsindex korrelierte im allgemeinen mit demzytologischen Differenzierungsgrad des Karzionoms. Mit Entdifferenzierung der Tumoren stieg die Proliferationsrate an. Hieraus ergibt sich bei bekannter proliferationsabhängiger Wirkung der meisten Zytostatika eine weitgehende Zytostatika-Resistenz der hochdifferenzierten Magenkarzinome. Die Nucleinsäuresynthese proliferationsaktive Tumoren konnte nur teilweise durch die getesteten Zytostatika (5-Fluoro-Uracil, Adriamycin) gehemmt werden. Karzinome mit Stoffwechselkompensationsmöglichkeiten gegenüber dem Wirkungsmechanismus der Zytostatika erwiesen sich biochemisch resistent. Eine Aussage über zytostatikasensible Tumoren ist neben den sich hierbei ergebenden methodischen Problemen auch aufgrund nicht erfaßter Patient-bedingter Resistenzursachen anhand von Incorporationsstudien problematisch.

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