Four classes of<unk> s are (1) spontaneous<unk> s (molecular decay), (2)<unk> s due to error-prone replication bypass of naturally occurring DNA damage (also called error-prone translesion synthesis), (3) errors introduced during DNA repair, and (4) induced<unk> s caused by mutagens. Scientists may also deliberately introduce mutant sequences through DNA manipulation for the sake of scientific experimentation. One 2017 study claimed that 66% of cancer-causing<unk> s are random, 29% are due to the environment (the studied population spanned 69 countries), and 5% are inherited. Humans on average pass 60 new<unk> s to their children but fathers pass more<unk> s depending on their age with every year adding two new<unk> s to a child. Spontaneous<unk>  Spontaneous<unk> s occur with non-zero probability even given a healthy, uncontaminated cell. Naturally occurring oxidative DNA damage is estimated to occur 10,000 times per cell per day in humans and 100,000 times per cell per day in rats. Spontaneous<unk> s can be characterized by the specific change: * Tautomerism – A base is changed by the repositioning of a hydrogen atom, altering the hydrogen bonding pattern of that base, resulting in incorrect base pairing during replication. * Depurination – Loss of a purine base (A or G) to form an apurinic site (AP site). * Deamination – Hydrolysis changes a normal base to an atypical base containing a keto group in place of the original amine group. Examples include C → U and A → HX (hypoxanthine), which can be corrected by DNA repair mechanisms; and 5MeC (5-methylcytosine) → T, which is less likely to be detected as a<unk>  because thymine is a normal DNA base. * Slipped strand mispairing – Denaturation of the new strand from the template during replication, followed by renaturation in a different spot ("slipping"). This can lead to insertions or deletions. * Replication slippage Error-prone replication bypass There is increasing evidence that the majority of spontaneously arising<unk> s are due to error-prone replication (translesion synthesis) past DNA damage in the template strand. In mice, the majority of<unk> s are caused by translesion synthesis. Likewise, in yeast, Kunz et al. found that more than 60% of the spontaneous single base pair substitutions and deletions were caused by translesion synthesis. Errors introduced during DNA repair Although naturally occurring double-strand breaks occur at a relatively low frequency in DNA, their repair often causes<unk> . Non-homologous end joining (NHEJ) is a major pathway for repairing double-strand breaks. NHEJ involves removal of a few nucleotides to allow somewhat inaccurate alignment of the two ends for rejoining followed by addition of nucleotides to fill in gaps. As a consequence, NHEJ often introduces<unk> s. benzoapyrene, the major mutagen in tobacco smoke, and DNA Induced<unk>  Induced<unk> s are alterations in the gene after it has come in contact with mutagens and environmental causes. Induced<unk> s on the molecular level can be caused by: * Chemicals * Hydroxylamine * Base analogs (e.g., Bromodeoxyuridine (BrdU)) * Alkylating agents (e.g., N-ethyl-N-nitrosourea (ENU). These agents can mutate both replicating and non-replicating DNA. In contrast, a base analog can mutate the DNA only when the analog is incorporated in replicating the DNA. Each of these classes of chemical mutagens has certain effects that then lead to transitions, transversions, or deletions. * Agents that form DNA adducts (e.g., ochratoxin A) * DNA intercalating agents (e.g., ethidium bromide) * DNA crosslinkers * Oxidative damage * Nitrous acid converts amine groups on A and C to diazo groups, altering their hydrogen bonding patterns, which leads to incorrect base pairing during replication. * Radiation * Ultraviolet light (UV) (including non-ionizing radiation). Two nucleotide bases in DNA—cytosine and thymine—are most vulnerable to radiation that can change their properties. UV light can induce adjacent pyrimidine bases in a DNA strand to become covalently joined as a pyrimidine dimer. UV radiation, in particular longer-wave UVA, can also cause oxidative damage to DNA. * Ionizing radiation. Exposure to ionizing radiation, such as gamma radiation, can result in<unk> , possibly resulting in cancer or death. Whereas in former times<unk> s were assumed to occur by chance, or induced by mutagens, molecular mechanisms of<unk>  have been discovered in bacteria and across the tree of life. As S. Rosenberg states, "These mechanisms reveal a picture of highly regulated mutagenesis, up-regulated temporally by stress responses and activated when cells/organisms are maladapted to their environments—when stressed—potentially accelerating adaptation." Since they are self-induced mutagenic mechanisms that increase the adaptation rate of organisms, they have some times been named as adaptive mutagenesis mechanisms, and include the SOS response in bacteria, ectopic intrachromosomal recombination and other chromosomal events such as duplications.
Mutation
Deletion 
Resistance 
Deficiency 
Variegation 
Aplasia
Trisomy
Parasitism