@article{oai:repo.qst.go.jp:00045633, author = {Ishii, Hideshi and Saito, Toshiyuki and 齋藤 俊行}, journal = {Progress in DNA Damage Research (Nova Biomedical)}, month = {Jul}, note = {Oxidative stress, a biochemical condition that is characterized by an imbalance between the presence of relatively high levels of toxic reactive species and antioxidative defense mechanisms, has been linked to various cellular philology and disorders characterized by cell death, such as stem cells of neural and hematopoietic systems. Recent studies indicate that common chromosome fragile sites, non-random targets of double stranded breaks under replication perturbation that are characteristic of tumors, paradoxically encode the tumor suppressor FHIT gene, which modulates response to oxidative stress and DNA damage. Since it is inactivated in precancer or early stages of carcinogenesis, we propose that the FHIT gene plays a role in the creation of cancer initiating cells. Mechanistic roles of FHIT in modulating oxidative stress and DNA damage checkpoints of cancer initiating cells are also discussed.}, pages = {243--251}, title = {How does tumor suppressor FHIT modulate oxidative stress and DNA damage checkpoints in early cancer?}, year = {2008} }