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• W2321762226 abstract "The central biochemical events in tumor induction are not completely understood. In a novel cell biochemical approach somequestions are answered here. A proliferative mutation allows replication shortcuts to the S-phase in the cell cycle. The repair systemis involved in tumor formation, and many tumor cells cannot be brought to apoptosis induction. This study illuminates the biochemicalpathways of these features. Mutational translocations within the gene ALL-1 might cause human acute leukemia. In those leukemiccell lines, replication starts immediately after mitosis. Mutations thus, allow replication without control, defining ALL-1 as theproliferative gene. Cells metabolize their DNA continuously. The repair system is constantly active. Cells are blind to DNA damage bymethylating 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." @default.
• W2321762226 created "2016-06-24" @default.
• W2321762226 creator A5009307675 @default.
• W2321762226 date "2012-01-01" @default.
• W2321762226 modified "2023-09-24" @default.
• W2321762226 title "Inhibition of Apoptosis in ALL-1 Leukemic Cell Lines: Allowance of Replication, Constant Repair Replication, Defect DNA Damage Control" @default.
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• W2321762226 doi "https://doi.org/10.4172/2157-7013.1000133" @default.
• W2321762226 hasPublicationYear "2012" @default.
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