Abstract

Dimensional resolution of malignant transformation events in cells is a putative reflection of susceptibility hot spots in DNA biology of response to genomic damage. It is further to such understanding that repair processes are potentially a vast array of complementary pathways that significantly promote the resistance to therapeutic attempts at cancerous lesion ablation. Sufficient promotional repair of single-strand and double-strand breaks may subsequently compromise susceptibility to therapy once cell replication is initiated. The toxic nature of abasic sites is a prime example for a need for selective phase susceptibility during the cell cycling of tumor cells to engineered or natural chemotherapeutic agents or to ionizing radiation.

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