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Last Updated: 02 July 2021

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Laryngeal Cancer is the most frequent form of head and neck cancers in Germany and the second most common form of respiratory tract cancers in the US. 1 2 average age of onset of disease is 64 years and it is more common in males than in females. Cigarette smoking and alcohol consumption are well acknowledged risk factors for laryngeal Cancer. 3-7 Cancer risk is directly related with duration and number of cigarettes smoke, and considerably increase in individuals consuming more than 50 g of alcohol per day. Tobacco smoke contains many carcinogens, including a group of N nitrosamines that produce carcinogenic methyl and pyridyloxobutyl DNA adducts. 8 further constituent of tobacco smoke is highly toxic Acetaldehyde 9 10 which produces genotoxic 1, N 2 propano2deoxyguanosine DNA adducts. 9 11 Acetaldehyde is also an intermediate product of ethanol metabolism and its concentration increases in multiplicative manner in individuals who are simultaneously smoking and drinking alcohol. 12 this observation might explain the synergistic and multiplicative effect found for alcohol and smoking on laryngeal cancer risk. 3 7 DNA repair is of fundamental importance in maintaining genomic stability after exogenous exposures such as smoking and protects against Cancer. 13 14 There are more than 150 human DNA repair genes know. 15 These can be subgrouped into genes associated with DNA damage signaling and regulation of repair system and genes working with distinct repair pathways such as mismatch repair, base excision repair, nucleotide excision repair, direct damage reversal and DNA doublestrand break repair. NER is the main pathway for removing bulky DNA adducts caused by chemical mutagens present in tobacco smoke and alcohol. There are about 30 proteins involved in NER. 16 NER consists of two subpathways, namely global genome repair that repairs anywhere in the genome and transcription couple repair involved in damage repair at actively transcribing sites. Complex interaction of NER proteins in pathways is not completely known yet, but damage recognition is specific for each of these subpathways. In GGR, 2 heterodimers XPCRAD23B and UVDDB recognize DNA distortion and bind to the damage site. 17 18 in TCR, RNA polymerase II get blocked at the damage site. This blockade is recognized and removed by proteins ERCC6 and ERCC8. 18 in the next step, basal transcription factor IIH complex unwinds the DNA duplex. TFIIH comprises up to 10 subunits 19 including ATP dependent helicases ERCC2 and ERCC3 which unwind duplex DNA in 3-5 and 5-3 direction, respectively. This generates open DNA structure around lesion, making room for the RPAXPA complex which stabilizes open DNA structure and assembles the preincision complex. 20 ERCC5 and ERCC1ERCC4 heterodimer are structure specific endonucleases that incise DNA at 3 and 5 junctions between singlestranded and doublestranded DNA, thus releasing 24 to 32 bases long DNA piece. The resulting gap is filled by DNA polymerases and, and ligase I.

* Please keep in mind that all text is machine-generated, we do not bear any responsibility, and you should always get advice from professionals before taking any actions.

* Please keep in mind that all text is machine-generated, we do not bear any responsibility, and you should always get advice from professionals before taking any actions

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