Figure 6.1

Flow chart showing development of malignant cells from initial α-particle damage to cells. DNA strand breaks are repaired by homologous or nonhomologous (illegitimate) double strand break rejoining, and damaged bases by base excision repair. Activation of p53 protein, initiates pathways leading to cell cycle delays and apoptosis, and surviving cells may contain gene deletions, rearrangements, amplifications, and persistant genomic instability. Mutations in oncogenes, loss of function in tumor suppressors, and loss of heterozygosity produces a heterogeneous population of cells which escapes from normal cell and tissue homeostasis to become malignant.



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