roduced during the replication process (Shannon, 1998).
             Although both mismatch repair and nucleotide excision repair are both capable of fixing improper DNA sequences, they perform their duties in two rather unique and different ways. While mismatch repair focuses on sequence errors arising during replication, NER deals with DNA sequences which are altered by external factors, such as chemical and physical agents. These agents may damage the DNA, disrupting its function and altering its sequence by a much different process than in replication errors. NER acts to repair this type of damage with two distinct types of repair: global NER and transcription-coupled NER. Global NER repairs damage over the entire genome, while transcription-coupled NER repairs damage in transcribed DNA strands that blocks transcription (De Laat et all, 1998). Global NER and transcription-coupled NER, which may be abbreviated as GG-NER and TC-NER for convenience, are exceedingly important because of the possible connection between these DNA repair mode!
             s and cancer. This is based on the idea that an individual's ability to respond to DNA damage caused by dangerous chemical agents may directly relate to the likelihood of cancer development (Bonn 1998). These two mechanisms of nucleotide excision repair share several unifying characteristics, as well as a number of distinct differences, and may ultimately be thought of as DNA's frontline of defense against sequence-damaging agents and a possible defense mechanism against many forms of cancer.
             Nucleotide excision repair is the method of choice for repairing DNA regions damaged by destructive chemical agents, which commonly distort the shape of the DNA double helix at the site of disruption (De Laat et all, 1998). The repair of these regions is initiated by specific proteins that recognize the deformed shape of the molecule that corresponds to disturbances of the DNA sequence at these locations. T...