___

• 1- Futreal PA. Kasprzyk A. Birney E. Mullikin JC. Wooster R. Stratton M. (2001). Cancer and genomics. Nature 6822: 850-2
• 2-Fearnhead HO. (2004). Getting back on track, or what to do when apoptosis is de-railed: recoupling oncogenes to the apoptotic machinery. Cancer Biol Ther. 3(1):21-8.
• 3-Williams GM. (2001). Mechanisms of chemical carcinogenesis and application to human cancer risk assessment. Toxicology; 14:166 (1- 2):3-10.
• 4-Williams GM. (1979). Review of in vitro test systems using DNA damage and repair for screening of chemical carcinogens. J. Assoc. Official Anal. Chemists 62: 857–63.
• 5-Williams GM. (1985). Genotoxic and epigenetic carcinogens. In: Homburger F, ed. Safety Evaluation and Regulation of Chemicals 2. Impact of Regulations-Improvement of Methods. Basel: Karger. 251–6.
• 6-Williams GM. (1987). DNA reactive and epigenetic carcinogens. In: Barrett JC, ed. Mechanisms of Environmental Carcinogenesis, Vol 1: Role of Genetic and Epigenetic Changes. Boca Raton, FL: CRC Press, Inc. 113–27.
• 7-Williams GM. (1987). Definition of a human cancer hazard. In: Nongenotoxic Mechanisms in Carcinogenesis. New York: Banbury Report 25, Cold Spring Harbor Laboratory. 367–80.
• 8-Williams GM. (1992). DNA reactive and epigenetic carcinogens. Experimental and Toxicologic Pathology. 44: 457– 64.
• 9-Yokuş B. Çakır DÜ. (202) İnvivo Oksidatif DNA Hasarı Biyomarkerı; 8- Hydroxy-2’-deoxyguanosine. Türkiye Klinikleri Tıp Bilimleri Dergisi.5: 535- 43.
• 10- Sahu SC. (1990). Onkogenes, onkogenesis and oxygen radicals. Biomed Environ Sci 2: 183-201.
• 11- Heynick L.N. Johnston S.A. Mason P.A. (2003). Radio Frequency Electromagnetic Fields: Cancer, Mutagenesis, and Genotoxicity. Bioelectromagnetics S6: 74-100.
• 12- Yokuş B. Mete N. (2003). Oksidatif DNA hasarı. Klinik Laboratuar Araştırma Dergisi. 7(2); 51-64
• 13- Jajte J. Zmyslony M. Palus J. Dziubaltowska E. Rajkowska E. (2001). Protective effect of melatonin against in vitro iron ions and 7 mT 50 Hz magnetic field-induced DNA damage in rat lymphocytes. Mutat Res. 483(1-2):57-64.
• 14- Ivancsits S. Diem E. Jahn O. Rudiger HW. (2003).Intermittent extremely low frequency electromagnetic fields cause DNA damage in a dose-dependent way. Int Arch Occup Environ Health. 76(6):431-6.
• 15- Yokuş B. Çakır D.Ü, Akdağ.Z, Mete.N, Sert C. (2005). Oxidative DNA Damage in Rats Exposed to Extremely Low Frequency Electro Magnetic Fields. Free Radical Research. 39(3): 317-323.
• 16- Yokus B, Akdag M.Z. Dasdag S. Cakir D.U, Kizil M.(2008). Extremely Low Frequency Electromagnetıc Fıelds Cause Oxıdatıve DNA Damage in Rats. International Journal of Radiation Biology, 8 (10), 789-795.
• 17- Halliwell B, Aruoma OI. (1991). DNA damage by oxygen-derived species; İts mechanism and measurement in mammalian systems. FEBS letters 281: 9-19.
• 18- Deshpande SS, Irani K. (2002). Oxidant signalling in carcinogenesis: a commentary. Hum Exp Toxicol 2: 63- 4.
• 19- Williams GM, Jeffrey A. (2000). Oxidative DNA damage: endogenous and chemically induced. Reg. Pharmacol. Toxicol 32: 283–92.
• 20- Devereux TR, Risinger JI, Barrett JC. (1999) Mutations and altered expression of the human cancer genes: What they tell us about causes. IARC Scientific Publications 146: 19-42.
• 21- Berenblum I: Frontiers of Biology. (1974) In: Carcinogenesis as a Biological Problem. Amsterdam: North-Holland Pub. Co. New York: 212-24
• 22- Elenbaas L, Spirio F, Koerner MD, Fleming DB, Zimonjic JL, Donaher NC, Popescu WC. (2001). Human breast cancer cells generated by onkogenic transformation of primary mammary epithelial cells. Genes Dev 15: 50–65.
• 23- Sherr J. (1996). Cancer cell cycle. Science 274: 1672–7.
• 24- Weinstein M. Begemann P. Zhou EK. Han A. Sgambato Y. Doki N. Arber M. Ciaparrone H. Yamatoto H. (1997). Disorders in cell circuitry associated with multistage carcinogenesis: exploitable targets for cancer prevention and therapy. Clin. Cancer Res; 3: 2696–702.
• 25- Bos JL. van Kreijl CF. (1992). In: Vainio H, Magee PN, McGregor DB, McMichael AJ. Eds. Genes and Gene Products that Regulate Proliferation and Differentiation: Critical Targets in Carcinogenesis. Mechanisms of Carcinogenesis in Risk Identification. Lyon: International Agency for Research of Cancer. 57–65.
• 26- Vogelstein A. Kinzler KW. (1993). The multistep nature of cancer. Trends Genet 9: 138–41.
• 27- Hussein SP, Harris CC. (1998). Molecular epidemiology of human cancer. Recent Results Cancer Res 154: 22–36.
• 28- Weinberg RA. (1995). The retinoblastoma protein and cell cycle control. Cell 81: 323–30.
• 29- Nowell P. (1976). The clonal evolution of tümör cell populations. Science 194: 23–28.
• 30- Butterworth BE. Popp JA. Conolly RB. Goldsworthy TL. Chemically induced cell proliferation in carcinogenesis. In: Vainio H, Magee PN, McGregor DB, McMichael AJ, eds. Mechanisms of Carcinogenesis in Risk Identification. Lyon: International Agency for Research of Cancer. 1992: 279–305.
• 31- Foulds L. Neoplastic Development 1. (1969). New York: Academic Pres, 122-34
• 32- Corn PG., El-Deiry WS. (2002). Derangement of growth and differentiation control in onkogenesis. Bioessays 1: 83-90.
• 33- Pucci B, Giordano A. (1999). Cell cycle and cancer. Clin Ter. 2:135-41.
• 34- Ho A. Dowdy SF. (2002) Regulation of G1 cell-cycle progression by onkogenes and tumor suppressor genes. Current Opinion in Genetics & Development 1: 47-52
• 35- Onat T. Emerk K. Sözmen EY. (2002). İnsan Biyokimyası. Ankara: Palme yayıncılık 569-75.
• 36- Pediconi N. Ianari A. Costanzo A. Belloni L. Gallo R. et.al. (2003). Differential regulation of E2F1 apoptotic target genes in response to DNA damage. Nat Cell Biol. 6:552-8.
• 37- Scriver CR. Beaudet AL, Sly WS., Valle D. (2001). The Metabolic & Molecular Bases of Inherited Disease. McGraw-Hill; 613-74.
• 38- Kopnin BP. (2000). Targets of onkogenes and tümör suppressors: key for understanding basic mechanisms of carcinogenesis. Biochemistry (Mosc) 1: 2-27.
• 39- Heuvel van den. Harlow E. (1993). Distinct roles for cyclin-dependent kinases in cell cycle control. Science262: 2050–4.
• 40- Weinberg RA. (1995). The retinoblastoma protein and cell cycle control. Cell 81: 323–30.
• 41- Brown VD. Phillips RA. Gallie BL. (1999). Cumulative effect of phosphorylation of pRB on regulation of E2F activity. Mol Cell Biol 19:3246–56.
• 42- Cotran R. Kumar V. Collins T. (1998). Robins Pathologic Basis of Disease. In: Cellular Pathology I: Cell Injury and Cell Death. Cellular Pathology, II: Adaptations, Intracellular Accumulations, and Cell Aging. Philadelphia: WB Saunders Co. 238- 85.
• 43- Ohtsubo M. Theodoras A. Schumacher J. Roberts J. Pagano M. (1995). Human cyclin E, a nuclear protein essential for the G1-to-S phase transition. Mol Cell Biol 15: 2612–24.
• 44- Abbas AK. Lichtman AH. (2003). Cellular and Molecular Immunology; 5th edition Philadelphia: Saunders Co. 243-74.
• 45- Smith MR. Matthews NT. Jones KA. Kung HF. (1993). Biological actions of onkogenes. Pharmacol Ther. 2: 211-36.
• 46- Labazi M, Phillips AC. (2003). Oncogenes as regulators of apoptosis. Essays Biochem. 39: 89-104.
• 47- Liu D. Wang LH. (1994). Onkogenes, Protein Tyrosine Kinases, and Signal Transduction. J Biomed Sci. 2: 65-82.
• 48- Loeb K.R. Loeb LA. (2000). Signigicance of multiple mutations in cancer. Carcinogenesis 21: 379–85.
• 49- Felsher DW. (2004). Reversibility of oncogene-induced cancer. Curr Opin Genet Dev. 14(1):37-42.
• 50- Seemayer TA, Cavenee WK. (1989). Molecular mechanisms of onkogenesis. Lab Invest. 5: 585-99.
• 51- Almasan A. Yin Y. Kelly R. Lee E. Bradley A., Li W. Bertino J. Wahl G. (1995). Deficiency of retinoblastoma protein leads to inappropriate S-phase entry, activation of E2F-responsive genes, and apoptosis. Proc Natl Acad Sci USA 92: 5436–40.
• 52- Hughes RM. (2004). Strategies for cancer gene therapy. J Surg Oncol. 85(1):28-35.