細胞科学と治療のジャーナル
オープンアクセス

概要

Inhibition of Apoptosis in ALL-1 Leukemic Cell Lines: Allowance of Replication, Constant Repair Replication, Defect DNA Damage Control

Isolde Riede

The central biochemical events in tumor induction are not completely understood. In a novel cell biochemical approach some
questions are answered here. A proliferative mutation allows replication shortcuts to the S-phase in the cell cycle. The repair system
is involved in tumor formation, and many tumor cells cannot be brought to apoptosis induction. This study illuminates the biochemical
pathways of these features. Mutational translocations within the gene ALL-1 might cause human acute leukemia. In those leukemic
cell lines, replication starts immediately after mitosis. Mutations thus, allow replication without control, defining ALL-1 as the
proliferative gene. Cells metabolize their DNA continuously. The repair system is constantly active. Cells are blind to DNA damage by
methylating agents and then replicate and repair their DNA. Induction of apoptosis fails. Thus, chemotherapy resistance is intrinsic.
Tumor induction occurs by a mutation that allows replication and turns on the repair system.