It may increase reactive oxygen species production, DNA damage, and frequency of misrepair
, contributing to malignant transformation and chemoresistance.
BACKGROUND: It is widely accepted that DNA double-strand breaks (DSBs) and their misrepair in stem cells are critical events in the multistage origination of various leukemias and tumors, including gliomas.
DNA double-strand breaks (DSBs) and their misrepair are critical molecular events resulting in chromosomal aberrations, which have often been associated with origination of various leukemias and tumors, including gliomas (Fischer and Meese 2007).
In addition, misrepair
of double strand breaks can cause structural chromosome instability also contributing to neoplastic transformation and cancer (15-17) (49,61).
In discussing the biologic effects of low doses of ionizing radiation, the authors, while mentioning the potential cancer-inducing implications of DNA double-strand breaks and their misrepair
, do not consider the adaptive response of humans to ionizing radiation.
have much more ominous consequences for the
of radiation-induced DNA double-strand breaks and its relevance for tumorigenesis and cancer treatment (review).
can cause mutation, and mutants may be the start of a tumor.
Among various type of DNA damages, the DSBs in DNA may be the most damaging and genotoxic, which elevate the frequencies of gene translocations, rearrangements, amplifications, and deletions during repair and misrepair
of DSBs (Khanna and Jackson 2001).
the DNA and the misrepair
of those DNA strands is analogous to a
Oxidative damage to DNA and its subsequent misrepair
In the second role, pol [Iota] could also prevent misrepair
of GT mismatches.