Hartwig M
Arch Geschwulstforsch. 1982;52(7):531-4.
A molecular mechanism is proposed by which physical, chemical and viral cancerogens together with DNA topoisomerases of type I effect an increase in the topological winding deficiency of nuclear DNA inside living cells. The resulting conformational changes of DNA, as monitored by an abnormally high negative superhelical density, could be of general relevance in the expression of the malignant cell phenotype.
本文提出了一种分子机制,即物理、化学和病毒致癌物与I型DNA拓扑异构酶共同作用,导致活细胞内核DNA拓扑缠绕缺陷增加。由异常高的负超螺旋密度所监测到的DNA构象变化,可能与恶性细胞表型的表达普遍相关。