Scientific researches demonstrate that a number of proven and suspected carcinogens (cancer-causing agents) in tobacco cigarette smoke cause damage of the human genetic material (DNA). The damage can, under certain circumstances, be repaired by cellular DNA repair mechanisms. However, if not repaired, cells will attempt to duplicate their DNA during normal cell division, but are impeded by the damage and will carry out an error-prone duplication process leading to gene mutations (changes in the gene). Such gene mutations are then found many years later in the DNA of lung tumors. The carcinogens in tobacco smoking result in the combined DNA damage or gene mutations, which are particularly harmful if they occur in multiple genes that control cell division rates or genetic stability. Gene mutations have been found tumor suppressor genes, such as p53 and P16, and oncogenes, such ras and myc, at a high frequency in human lung cancer related to tobacco smoking.