Smoking and XPC Gene Polymorphism Interact to Modulate the Risk of Oral Cancer

Purpose Oral cancer is the most common cancer among the Indian men and the second most common cancer among the Indian women. Such high incidence of oral cancer in India is due to consumption of tobacco in different form including smoking of cigarette. Smoke of tobacco contains different carcinogens...
Ausführliche Beschreibung

Gespeichert in:

Autor*in:	Nigam, Kumud [verfasserIn] Samadi, Fahad M. [verfasserIn] Srivastava, Saurabh [verfasserIn] Mohammad, Shadab [verfasserIn] Sanyal, Somali [verfasserIn]

Format:	E-Artikel
Sprache:	Englisch

Erschienen:	2020

Schlagwörter:	Smoking Oral cancer XPC Polymorphism

Anmerkung:	© The Association of Oral and Maxillofacial Surgeons of India 2020

Übergeordnetes Werk:	Enthalten in: Journal of maxillofacial and oral surgery - Neu Delhi : Springer India, 2009, 20(2020), 4 vom: 27. Feb., Seite 607-611
Übergeordnetes Werk:	volume:20 ; year:2020 ; number:4 ; day:27 ; month:02 ; pages:607-611

Links:	Volltext

DOI / URN:	10.1007/s12663-020-01340-z

Katalog-ID:	SPR045415420

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520			\|a Purpose Oral cancer is the most common cancer among the Indian men and the second most common cancer among the Indian women. Such high incidence of oral cancer in India is due to consumption of tobacco in different form including smoking of cigarette. Smoke of tobacco contains different carcinogens which causes DNA damage. Such DNA damage if remain unrepaired due to faulty DNA repair system can cause mutation and eventual development of cancer. Methodology In the present study, we aimed to check the role of smoking as well as interaction of smoking and XPC polymorphism in risk modulation of oral cancer. Total of 372 subjects including 300 healthy controls and 72 patients of oral cancers been genotyped for the XPC PAT D/I, A/C and C/T polymorphisms with PCR based or PCR–RFLP based method. Genotype frequency was analyzed by chi-square test and strength of associations by odds ratio with 95% confidence intervals. Results The present study showed that compared to nonsmokers, smokers are at five times higher risk to develop oral cancer (p value= 0.001, OR= 5.03, 95% CI 2.91–8.69) and three times higher risk to develop node-positive (p value= 0.01, OR= 3.66, 95% CI 1.34–9.95) oral cancer. It has also been observed that individuals who were smokers and carrier of variant allele genotypes (AC and CC) for XPC A/C polymorphism were at threefold higher risk (p value= 0.01, OR=2.97, 95% CI 1.29–6.86) to develop oral cancer compared to individual who were smokers but do not carry the C allele (AA genotype). This observation indicates that C allele of XPC A/C polymorphism interacts with smoking and significantly increases the risk of oral cancer. Conclusion This study demonstrates a possible role of smoking and gene–smoking interaction in risk enhancement of oral cancer.
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912			\|a GBV_ILN_151
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912			\|a GBV_ILN_187
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912			\|a GBV_ILN_213
912			\|a GBV_ILN_224
912			\|a GBV_ILN_230
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912			\|a GBV_ILN_602
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Indexfelder

author_variant	k n kn f m s fm fms s s ss s m sm s s ss
matchkey_str	article:0974942X:2020----::mknadpgnplmrhsitrctmdltt
hierarchy_sort_str	2020
bklnumber	44.96
publishDate	2020
allfields	10.1007/s12663-020-01340-z doi (DE-627)SPR045415420 (SPR)s12663-020-01340-z-e DE-627 ger DE-627 rakwb eng 610 ASE 44.96 bkl Nigam, Kumud verfasserin aut Smoking and XPC Gene Polymorphism Interact to Modulate the Risk of Oral Cancer 2020 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier © The Association of Oral and Maxillofacial Surgeons of India 2020 Purpose Oral cancer is the most common cancer among the Indian men and the second most common cancer among the Indian women. Such high incidence of oral cancer in India is due to consumption of tobacco in different form including smoking of cigarette. Smoke of tobacco contains different carcinogens which causes DNA damage. Such DNA damage if remain unrepaired due to faulty DNA repair system can cause mutation and eventual development of cancer. Methodology In the present study, we aimed to check the role of smoking as well as interaction of smoking and XPC polymorphism in risk modulation of oral cancer. Total of 372 subjects including 300 healthy controls and 72 patients of oral cancers been genotyped for the XPC PAT D/I, A/C and C/T polymorphisms with PCR based or PCR–RFLP based method. Genotype frequency was analyzed by chi-square test and strength of associations by odds ratio with 95% confidence intervals. Results The present study showed that compared to nonsmokers, smokers are at five times higher risk to develop oral cancer (p value= 0.001, OR= 5.03, 95% CI 2.91–8.69) and three times higher risk to develop node-positive (p value= 0.01, OR= 3.66, 95% CI 1.34–9.95) oral cancer. It has also been observed that individuals who were smokers and carrier of variant allele genotypes (AC and CC) for XPC A/C polymorphism were at threefold higher risk (p value= 0.01, OR=2.97, 95% CI 1.29–6.86) to develop oral cancer compared to individual who were smokers but do not carry the C allele (AA genotype). This observation indicates that C allele of XPC A/C polymorphism interacts with smoking and significantly increases the risk of oral cancer. Conclusion This study demonstrates a possible role of smoking and gene–smoking interaction in risk enhancement of oral cancer. Smoking (dpeaa)DE-He213 Oral cancer (dpeaa)DE-He213 XPC (dpeaa)DE-He213 Polymorphism (dpeaa)DE-He213 Samadi, Fahad M. verfasserin aut Srivastava, Saurabh verfasserin aut Mohammad, Shadab verfasserin aut Sanyal, Somali verfasserin aut Enthalten in Journal of maxillofacial and oral surgery Neu Delhi : Springer India, 2009 20(2020), 4 vom: 27. Feb., Seite 607-611 (DE-627)604074921 (DE-600)2502352-4 0974-942X nnns volume:20 year:2020 number:4 day:27 month:02 pages:607-611 https://dx.doi.org/10.1007/s12663-020-01340-z lizenzpflichtig Volltext GBV_USEFLAG_A SYSFLAG_A GBV_SPRINGER SSG-OLC-PHA GBV_ILN_11 GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_31 GBV_ILN_32 GBV_ILN_39 GBV_ILN_40 GBV_ILN_60 GBV_ILN_62 GBV_ILN_63 GBV_ILN_65 GBV_ILN_69 GBV_ILN_70 GBV_ILN_73 GBV_ILN_74 GBV_ILN_90 GBV_ILN_95 GBV_ILN_100 GBV_ILN_101 GBV_ILN_105 GBV_ILN_110 GBV_ILN_120 GBV_ILN_138 GBV_ILN_150 GBV_ILN_151 GBV_ILN_152 GBV_ILN_161 GBV_ILN_170 GBV_ILN_171 GBV_ILN_187 GBV_ILN_206 GBV_ILN_213 GBV_ILN_224 GBV_ILN_230 GBV_ILN_250 GBV_ILN_281 GBV_ILN_285 GBV_ILN_293 GBV_ILN_370 GBV_ILN_602 GBV_ILN_636 GBV_ILN_702 GBV_ILN_2001 GBV_ILN_2003 GBV_ILN_2004 GBV_ILN_2005 GBV_ILN_2006 GBV_ILN_2007 GBV_ILN_2008 GBV_ILN_2009 GBV_ILN_2010 GBV_ILN_2011 GBV_ILN_2014 GBV_ILN_2015 GBV_ILN_2020 GBV_ILN_2021 GBV_ILN_2025 GBV_ILN_2026 GBV_ILN_2027 GBV_ILN_2031 GBV_ILN_2034 GBV_ILN_2037 GBV_ILN_2038 GBV_ILN_2039 GBV_ILN_2044 GBV_ILN_2048 GBV_ILN_2049 GBV_ILN_2050 GBV_ILN_2055 GBV_ILN_2056 GBV_ILN_2057 GBV_ILN_2059 GBV_ILN_2061 GBV_ILN_2064 GBV_ILN_2065 GBV_ILN_2068 GBV_ILN_2088 GBV_ILN_2093 GBV_ILN_2106 GBV_ILN_2107 GBV_ILN_2108 GBV_ILN_2110 GBV_ILN_2111 GBV_ILN_2112 GBV_ILN_2113 GBV_ILN_2118 GBV_ILN_2122 GBV_ILN_2129 GBV_ILN_2143 GBV_ILN_2144 GBV_ILN_2147 GBV_ILN_2148 GBV_ILN_2152 GBV_ILN_2153 GBV_ILN_2188 GBV_ILN_2190 GBV_ILN_2232 GBV_ILN_2336 GBV_ILN_2446 GBV_ILN_2470 GBV_ILN_2472 GBV_ILN_2507 GBV_ILN_2522 GBV_ILN_2548 GBV_ILN_4012 GBV_ILN_4035 GBV_ILN_4037 GBV_ILN_4046 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4242 GBV_ILN_4246 GBV_ILN_4249 GBV_ILN_4251 GBV_ILN_4305 GBV_ILN_4306 GBV_ILN_4307 GBV_ILN_4313 GBV_ILN_4322 GBV_ILN_4323 GBV_ILN_4324 GBV_ILN_4325 GBV_ILN_4326 GBV_ILN_4328 GBV_ILN_4333 GBV_ILN_4334 GBV_ILN_4335 GBV_ILN_4336 GBV_ILN_4338 GBV_ILN_4367 GBV_ILN_4393 GBV_ILN_4700 44.96 ASE AR 20 2020 4 27 02 607-611
spelling	10.1007/s12663-020-01340-z doi (DE-627)SPR045415420 (SPR)s12663-020-01340-z-e DE-627 ger DE-627 rakwb eng 610 ASE 44.96 bkl Nigam, Kumud verfasserin aut Smoking and XPC Gene Polymorphism Interact to Modulate the Risk of Oral Cancer 2020 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier © The Association of Oral and Maxillofacial Surgeons of India 2020 Purpose Oral cancer is the most common cancer among the Indian men and the second most common cancer among the Indian women. Such high incidence of oral cancer in India is due to consumption of tobacco in different form including smoking of cigarette. Smoke of tobacco contains different carcinogens which causes DNA damage. Such DNA damage if remain unrepaired due to faulty DNA repair system can cause mutation and eventual development of cancer. Methodology In the present study, we aimed to check the role of smoking as well as interaction of smoking and XPC polymorphism in risk modulation of oral cancer. Total of 372 subjects including 300 healthy controls and 72 patients of oral cancers been genotyped for the XPC PAT D/I, A/C and C/T polymorphisms with PCR based or PCR–RFLP based method. Genotype frequency was analyzed by chi-square test and strength of associations by odds ratio with 95% confidence intervals. Results The present study showed that compared to nonsmokers, smokers are at five times higher risk to develop oral cancer (p value= 0.001, OR= 5.03, 95% CI 2.91–8.69) and three times higher risk to develop node-positive (p value= 0.01, OR= 3.66, 95% CI 1.34–9.95) oral cancer. It has also been observed that individuals who were smokers and carrier of variant allele genotypes (AC and CC) for XPC A/C polymorphism were at threefold higher risk (p value= 0.01, OR=2.97, 95% CI 1.29–6.86) to develop oral cancer compared to individual who were smokers but do not carry the C allele (AA genotype). This observation indicates that C allele of XPC A/C polymorphism interacts with smoking and significantly increases the risk of oral cancer. Conclusion This study demonstrates a possible role of smoking and gene–smoking interaction in risk enhancement of oral cancer. Smoking (dpeaa)DE-He213 Oral cancer (dpeaa)DE-He213 XPC (dpeaa)DE-He213 Polymorphism (dpeaa)DE-He213 Samadi, Fahad M. verfasserin aut Srivastava, Saurabh verfasserin aut Mohammad, Shadab verfasserin aut Sanyal, Somali verfasserin aut Enthalten in Journal of maxillofacial and oral surgery Neu Delhi : Springer India, 2009 20(2020), 4 vom: 27. Feb., Seite 607-611 (DE-627)604074921 (DE-600)2502352-4 0974-942X nnns volume:20 year:2020 number:4 day:27 month:02 pages:607-611 https://dx.doi.org/10.1007/s12663-020-01340-z lizenzpflichtig Volltext GBV_USEFLAG_A SYSFLAG_A GBV_SPRINGER SSG-OLC-PHA GBV_ILN_11 GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_31 GBV_ILN_32 GBV_ILN_39 GBV_ILN_40 GBV_ILN_60 GBV_ILN_62 GBV_ILN_63 GBV_ILN_65 GBV_ILN_69 GBV_ILN_70 GBV_ILN_73 GBV_ILN_74 GBV_ILN_90 GBV_ILN_95 GBV_ILN_100 GBV_ILN_101 GBV_ILN_105 GBV_ILN_110 GBV_ILN_120 GBV_ILN_138 GBV_ILN_150 GBV_ILN_151 GBV_ILN_152 GBV_ILN_161 GBV_ILN_170 GBV_ILN_171 GBV_ILN_187 GBV_ILN_206 GBV_ILN_213 GBV_ILN_224 GBV_ILN_230 GBV_ILN_250 GBV_ILN_281 GBV_ILN_285 GBV_ILN_293 GBV_ILN_370 GBV_ILN_602 GBV_ILN_636 GBV_ILN_702 GBV_ILN_2001 GBV_ILN_2003 GBV_ILN_2004 GBV_ILN_2005 GBV_ILN_2006 GBV_ILN_2007 GBV_ILN_2008 GBV_ILN_2009 GBV_ILN_2010 GBV_ILN_2011 GBV_ILN_2014 GBV_ILN_2015 GBV_ILN_2020 GBV_ILN_2021 GBV_ILN_2025 GBV_ILN_2026 GBV_ILN_2027 GBV_ILN_2031 GBV_ILN_2034 GBV_ILN_2037 GBV_ILN_2038 GBV_ILN_2039 GBV_ILN_2044 GBV_ILN_2048 GBV_ILN_2049 GBV_ILN_2050 GBV_ILN_2055 GBV_ILN_2056 GBV_ILN_2057 GBV_ILN_2059 GBV_ILN_2061 GBV_ILN_2064 GBV_ILN_2065 GBV_ILN_2068 GBV_ILN_2088 GBV_ILN_2093 GBV_ILN_2106 GBV_ILN_2107 GBV_ILN_2108 GBV_ILN_2110 GBV_ILN_2111 GBV_ILN_2112 GBV_ILN_2113 GBV_ILN_2118 GBV_ILN_2122 GBV_ILN_2129 GBV_ILN_2143 GBV_ILN_2144 GBV_ILN_2147 GBV_ILN_2148 GBV_ILN_2152 GBV_ILN_2153 GBV_ILN_2188 GBV_ILN_2190 GBV_ILN_2232 GBV_ILN_2336 GBV_ILN_2446 GBV_ILN_2470 GBV_ILN_2472 GBV_ILN_2507 GBV_ILN_2522 GBV_ILN_2548 GBV_ILN_4012 GBV_ILN_4035 GBV_ILN_4037 GBV_ILN_4046 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4242 GBV_ILN_4246 GBV_ILN_4249 GBV_ILN_4251 GBV_ILN_4305 GBV_ILN_4306 GBV_ILN_4307 GBV_ILN_4313 GBV_ILN_4322 GBV_ILN_4323 GBV_ILN_4324 GBV_ILN_4325 GBV_ILN_4326 GBV_ILN_4328 GBV_ILN_4333 GBV_ILN_4334 GBV_ILN_4335 GBV_ILN_4336 GBV_ILN_4338 GBV_ILN_4367 GBV_ILN_4393 GBV_ILN_4700 44.96 ASE AR 20 2020 4 27 02 607-611
allfields_unstemmed	10.1007/s12663-020-01340-z doi (DE-627)SPR045415420 (SPR)s12663-020-01340-z-e DE-627 ger DE-627 rakwb eng 610 ASE 44.96 bkl Nigam, Kumud verfasserin aut Smoking and XPC Gene Polymorphism Interact to Modulate the Risk of Oral Cancer 2020 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier © The Association of Oral and Maxillofacial Surgeons of India 2020 Purpose Oral cancer is the most common cancer among the Indian men and the second most common cancer among the Indian women. Such high incidence of oral cancer in India is due to consumption of tobacco in different form including smoking of cigarette. Smoke of tobacco contains different carcinogens which causes DNA damage. Such DNA damage if remain unrepaired due to faulty DNA repair system can cause mutation and eventual development of cancer. Methodology In the present study, we aimed to check the role of smoking as well as interaction of smoking and XPC polymorphism in risk modulation of oral cancer. Total of 372 subjects including 300 healthy controls and 72 patients of oral cancers been genotyped for the XPC PAT D/I, A/C and C/T polymorphisms with PCR based or PCR–RFLP based method. Genotype frequency was analyzed by chi-square test and strength of associations by odds ratio with 95% confidence intervals. Results The present study showed that compared to nonsmokers, smokers are at five times higher risk to develop oral cancer (p value= 0.001, OR= 5.03, 95% CI 2.91–8.69) and three times higher risk to develop node-positive (p value= 0.01, OR= 3.66, 95% CI 1.34–9.95) oral cancer. It has also been observed that individuals who were smokers and carrier of variant allele genotypes (AC and CC) for XPC A/C polymorphism were at threefold higher risk (p value= 0.01, OR=2.97, 95% CI 1.29–6.86) to develop oral cancer compared to individual who were smokers but do not carry the C allele (AA genotype). This observation indicates that C allele of XPC A/C polymorphism interacts with smoking and significantly increases the risk of oral cancer. Conclusion This study demonstrates a possible role of smoking and gene–smoking interaction in risk enhancement of oral cancer. Smoking (dpeaa)DE-He213 Oral cancer (dpeaa)DE-He213 XPC (dpeaa)DE-He213 Polymorphism (dpeaa)DE-He213 Samadi, Fahad M. verfasserin aut Srivastava, Saurabh verfasserin aut Mohammad, Shadab verfasserin aut Sanyal, Somali verfasserin aut Enthalten in Journal of maxillofacial and oral surgery Neu Delhi : Springer India, 2009 20(2020), 4 vom: 27. Feb., Seite 607-611 (DE-627)604074921 (DE-600)2502352-4 0974-942X nnns volume:20 year:2020 number:4 day:27 month:02 pages:607-611 https://dx.doi.org/10.1007/s12663-020-01340-z lizenzpflichtig Volltext GBV_USEFLAG_A SYSFLAG_A GBV_SPRINGER SSG-OLC-PHA GBV_ILN_11 GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_31 GBV_ILN_32 GBV_ILN_39 GBV_ILN_40 GBV_ILN_60 GBV_ILN_62 GBV_ILN_63 GBV_ILN_65 GBV_ILN_69 GBV_ILN_70 GBV_ILN_73 GBV_ILN_74 GBV_ILN_90 GBV_ILN_95 GBV_ILN_100 GBV_ILN_101 GBV_ILN_105 GBV_ILN_110 GBV_ILN_120 GBV_ILN_138 GBV_ILN_150 GBV_ILN_151 GBV_ILN_152 GBV_ILN_161 GBV_ILN_170 GBV_ILN_171 GBV_ILN_187 GBV_ILN_206 GBV_ILN_213 GBV_ILN_224 GBV_ILN_230 GBV_ILN_250 GBV_ILN_281 GBV_ILN_285 GBV_ILN_293 GBV_ILN_370 GBV_ILN_602 GBV_ILN_636 GBV_ILN_702 GBV_ILN_2001 GBV_ILN_2003 GBV_ILN_2004 GBV_ILN_2005 GBV_ILN_2006 GBV_ILN_2007 GBV_ILN_2008 GBV_ILN_2009 GBV_ILN_2010 GBV_ILN_2011 GBV_ILN_2014 GBV_ILN_2015 GBV_ILN_2020 GBV_ILN_2021 GBV_ILN_2025 GBV_ILN_2026 GBV_ILN_2027 GBV_ILN_2031 GBV_ILN_2034 GBV_ILN_2037 GBV_ILN_2038 GBV_ILN_2039 GBV_ILN_2044 GBV_ILN_2048 GBV_ILN_2049 GBV_ILN_2050 GBV_ILN_2055 GBV_ILN_2056 GBV_ILN_2057 GBV_ILN_2059 GBV_ILN_2061 GBV_ILN_2064 GBV_ILN_2065 GBV_ILN_2068 GBV_ILN_2088 GBV_ILN_2093 GBV_ILN_2106 GBV_ILN_2107 GBV_ILN_2108 GBV_ILN_2110 GBV_ILN_2111 GBV_ILN_2112 GBV_ILN_2113 GBV_ILN_2118 GBV_ILN_2122 GBV_ILN_2129 GBV_ILN_2143 GBV_ILN_2144 GBV_ILN_2147 GBV_ILN_2148 GBV_ILN_2152 GBV_ILN_2153 GBV_ILN_2188 GBV_ILN_2190 GBV_ILN_2232 GBV_ILN_2336 GBV_ILN_2446 GBV_ILN_2470 GBV_ILN_2472 GBV_ILN_2507 GBV_ILN_2522 GBV_ILN_2548 GBV_ILN_4012 GBV_ILN_4035 GBV_ILN_4037 GBV_ILN_4046 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4242 GBV_ILN_4246 GBV_ILN_4249 GBV_ILN_4251 GBV_ILN_4305 GBV_ILN_4306 GBV_ILN_4307 GBV_ILN_4313 GBV_ILN_4322 GBV_ILN_4323 GBV_ILN_4324 GBV_ILN_4325 GBV_ILN_4326 GBV_ILN_4328 GBV_ILN_4333 GBV_ILN_4334 GBV_ILN_4335 GBV_ILN_4336 GBV_ILN_4338 GBV_ILN_4367 GBV_ILN_4393 GBV_ILN_4700 44.96 ASE AR 20 2020 4 27 02 607-611
allfieldsGer	10.1007/s12663-020-01340-z doi (DE-627)SPR045415420 (SPR)s12663-020-01340-z-e DE-627 ger DE-627 rakwb eng 610 ASE 44.96 bkl Nigam, Kumud verfasserin aut Smoking and XPC Gene Polymorphism Interact to Modulate the Risk of Oral Cancer 2020 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier © The Association of Oral and Maxillofacial Surgeons of India 2020 Purpose Oral cancer is the most common cancer among the Indian men and the second most common cancer among the Indian women. Such high incidence of oral cancer in India is due to consumption of tobacco in different form including smoking of cigarette. Smoke of tobacco contains different carcinogens which causes DNA damage. Such DNA damage if remain unrepaired due to faulty DNA repair system can cause mutation and eventual development of cancer. Methodology In the present study, we aimed to check the role of smoking as well as interaction of smoking and XPC polymorphism in risk modulation of oral cancer. Total of 372 subjects including 300 healthy controls and 72 patients of oral cancers been genotyped for the XPC PAT D/I, A/C and C/T polymorphisms with PCR based or PCR–RFLP based method. Genotype frequency was analyzed by chi-square test and strength of associations by odds ratio with 95% confidence intervals. Results The present study showed that compared to nonsmokers, smokers are at five times higher risk to develop oral cancer (p value= 0.001, OR= 5.03, 95% CI 2.91–8.69) and three times higher risk to develop node-positive (p value= 0.01, OR= 3.66, 95% CI 1.34–9.95) oral cancer. It has also been observed that individuals who were smokers and carrier of variant allele genotypes (AC and CC) for XPC A/C polymorphism were at threefold higher risk (p value= 0.01, OR=2.97, 95% CI 1.29–6.86) to develop oral cancer compared to individual who were smokers but do not carry the C allele (AA genotype). This observation indicates that C allele of XPC A/C polymorphism interacts with smoking and significantly increases the risk of oral cancer. Conclusion This study demonstrates a possible role of smoking and gene–smoking interaction in risk enhancement of oral cancer. Smoking (dpeaa)DE-He213 Oral cancer (dpeaa)DE-He213 XPC (dpeaa)DE-He213 Polymorphism (dpeaa)DE-He213 Samadi, Fahad M. verfasserin aut Srivastava, Saurabh verfasserin aut Mohammad, Shadab verfasserin aut Sanyal, Somali verfasserin aut Enthalten in Journal of maxillofacial and oral surgery Neu Delhi : Springer India, 2009 20(2020), 4 vom: 27. Feb., Seite 607-611 (DE-627)604074921 (DE-600)2502352-4 0974-942X nnns volume:20 year:2020 number:4 day:27 month:02 pages:607-611 https://dx.doi.org/10.1007/s12663-020-01340-z lizenzpflichtig Volltext GBV_USEFLAG_A SYSFLAG_A GBV_SPRINGER SSG-OLC-PHA GBV_ILN_11 GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_31 GBV_ILN_32 GBV_ILN_39 GBV_ILN_40 GBV_ILN_60 GBV_ILN_62 GBV_ILN_63 GBV_ILN_65 GBV_ILN_69 GBV_ILN_70 GBV_ILN_73 GBV_ILN_74 GBV_ILN_90 GBV_ILN_95 GBV_ILN_100 GBV_ILN_101 GBV_ILN_105 GBV_ILN_110 GBV_ILN_120 GBV_ILN_138 GBV_ILN_150 GBV_ILN_151 GBV_ILN_152 GBV_ILN_161 GBV_ILN_170 GBV_ILN_171 GBV_ILN_187 GBV_ILN_206 GBV_ILN_213 GBV_ILN_224 GBV_ILN_230 GBV_ILN_250 GBV_ILN_281 GBV_ILN_285 GBV_ILN_293 GBV_ILN_370 GBV_ILN_602 GBV_ILN_636 GBV_ILN_702 GBV_ILN_2001 GBV_ILN_2003 GBV_ILN_2004 GBV_ILN_2005 GBV_ILN_2006 GBV_ILN_2007 GBV_ILN_2008 GBV_ILN_2009 GBV_ILN_2010 GBV_ILN_2011 GBV_ILN_2014 GBV_ILN_2015 GBV_ILN_2020 GBV_ILN_2021 GBV_ILN_2025 GBV_ILN_2026 GBV_ILN_2027 GBV_ILN_2031 GBV_ILN_2034 GBV_ILN_2037 GBV_ILN_2038 GBV_ILN_2039 GBV_ILN_2044 GBV_ILN_2048 GBV_ILN_2049 GBV_ILN_2050 GBV_ILN_2055 GBV_ILN_2056 GBV_ILN_2057 GBV_ILN_2059 GBV_ILN_2061 GBV_ILN_2064 GBV_ILN_2065 GBV_ILN_2068 GBV_ILN_2088 GBV_ILN_2093 GBV_ILN_2106 GBV_ILN_2107 GBV_ILN_2108 GBV_ILN_2110 GBV_ILN_2111 GBV_ILN_2112 GBV_ILN_2113 GBV_ILN_2118 GBV_ILN_2122 GBV_ILN_2129 GBV_ILN_2143 GBV_ILN_2144 GBV_ILN_2147 GBV_ILN_2148 GBV_ILN_2152 GBV_ILN_2153 GBV_ILN_2188 GBV_ILN_2190 GBV_ILN_2232 GBV_ILN_2336 GBV_ILN_2446 GBV_ILN_2470 GBV_ILN_2472 GBV_ILN_2507 GBV_ILN_2522 GBV_ILN_2548 GBV_ILN_4012 GBV_ILN_4035 GBV_ILN_4037 GBV_ILN_4046 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4242 GBV_ILN_4246 GBV_ILN_4249 GBV_ILN_4251 GBV_ILN_4305 GBV_ILN_4306 GBV_ILN_4307 GBV_ILN_4313 GBV_ILN_4322 GBV_ILN_4323 GBV_ILN_4324 GBV_ILN_4325 GBV_ILN_4326 GBV_ILN_4328 GBV_ILN_4333 GBV_ILN_4334 GBV_ILN_4335 GBV_ILN_4336 GBV_ILN_4338 GBV_ILN_4367 GBV_ILN_4393 GBV_ILN_4700 44.96 ASE AR 20 2020 4 27 02 607-611
allfieldsSound	10.1007/s12663-020-01340-z doi (DE-627)SPR045415420 (SPR)s12663-020-01340-z-e DE-627 ger DE-627 rakwb eng 610 ASE 44.96 bkl Nigam, Kumud verfasserin aut Smoking and XPC Gene Polymorphism Interact to Modulate the Risk of Oral Cancer 2020 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier © The Association of Oral and Maxillofacial Surgeons of India 2020 Purpose Oral cancer is the most common cancer among the Indian men and the second most common cancer among the Indian women. Such high incidence of oral cancer in India is due to consumption of tobacco in different form including smoking of cigarette. Smoke of tobacco contains different carcinogens which causes DNA damage. Such DNA damage if remain unrepaired due to faulty DNA repair system can cause mutation and eventual development of cancer. Methodology In the present study, we aimed to check the role of smoking as well as interaction of smoking and XPC polymorphism in risk modulation of oral cancer. Total of 372 subjects including 300 healthy controls and 72 patients of oral cancers been genotyped for the XPC PAT D/I, A/C and C/T polymorphisms with PCR based or PCR–RFLP based method. Genotype frequency was analyzed by chi-square test and strength of associations by odds ratio with 95% confidence intervals. Results The present study showed that compared to nonsmokers, smokers are at five times higher risk to develop oral cancer (p value= 0.001, OR= 5.03, 95% CI 2.91–8.69) and three times higher risk to develop node-positive (p value= 0.01, OR= 3.66, 95% CI 1.34–9.95) oral cancer. It has also been observed that individuals who were smokers and carrier of variant allele genotypes (AC and CC) for XPC A/C polymorphism were at threefold higher risk (p value= 0.01, OR=2.97, 95% CI 1.29–6.86) to develop oral cancer compared to individual who were smokers but do not carry the C allele (AA genotype). This observation indicates that C allele of XPC A/C polymorphism interacts with smoking and significantly increases the risk of oral cancer. Conclusion This study demonstrates a possible role of smoking and gene–smoking interaction in risk enhancement of oral cancer. Smoking (dpeaa)DE-He213 Oral cancer (dpeaa)DE-He213 XPC (dpeaa)DE-He213 Polymorphism (dpeaa)DE-He213 Samadi, Fahad M. verfasserin aut Srivastava, Saurabh verfasserin aut Mohammad, Shadab verfasserin aut Sanyal, Somali verfasserin aut Enthalten in Journal of maxillofacial and oral surgery Neu Delhi : Springer India, 2009 20(2020), 4 vom: 27. Feb., Seite 607-611 (DE-627)604074921 (DE-600)2502352-4 0974-942X nnns volume:20 year:2020 number:4 day:27 month:02 pages:607-611 https://dx.doi.org/10.1007/s12663-020-01340-z lizenzpflichtig Volltext GBV_USEFLAG_A SYSFLAG_A GBV_SPRINGER SSG-OLC-PHA GBV_ILN_11 GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_31 GBV_ILN_32 GBV_ILN_39 GBV_ILN_40 GBV_ILN_60 GBV_ILN_62 GBV_ILN_63 GBV_ILN_65 GBV_ILN_69 GBV_ILN_70 GBV_ILN_73 GBV_ILN_74 GBV_ILN_90 GBV_ILN_95 GBV_ILN_100 GBV_ILN_101 GBV_ILN_105 GBV_ILN_110 GBV_ILN_120 GBV_ILN_138 GBV_ILN_150 GBV_ILN_151 GBV_ILN_152 GBV_ILN_161 GBV_ILN_170 GBV_ILN_171 GBV_ILN_187 GBV_ILN_206 GBV_ILN_213 GBV_ILN_224 GBV_ILN_230 GBV_ILN_250 GBV_ILN_281 GBV_ILN_285 GBV_ILN_293 GBV_ILN_370 GBV_ILN_602 GBV_ILN_636 GBV_ILN_702 GBV_ILN_2001 GBV_ILN_2003 GBV_ILN_2004 GBV_ILN_2005 GBV_ILN_2006 GBV_ILN_2007 GBV_ILN_2008 GBV_ILN_2009 GBV_ILN_2010 GBV_ILN_2011 GBV_ILN_2014 GBV_ILN_2015 GBV_ILN_2020 GBV_ILN_2021 GBV_ILN_2025 GBV_ILN_2026 GBV_ILN_2027 GBV_ILN_2031 GBV_ILN_2034 GBV_ILN_2037 GBV_ILN_2038 GBV_ILN_2039 GBV_ILN_2044 GBV_ILN_2048 GBV_ILN_2049 GBV_ILN_2050 GBV_ILN_2055 GBV_ILN_2056 GBV_ILN_2057 GBV_ILN_2059 GBV_ILN_2061 GBV_ILN_2064 GBV_ILN_2065 GBV_ILN_2068 GBV_ILN_2088 GBV_ILN_2093 GBV_ILN_2106 GBV_ILN_2107 GBV_ILN_2108 GBV_ILN_2110 GBV_ILN_2111 GBV_ILN_2112 GBV_ILN_2113 GBV_ILN_2118 GBV_ILN_2122 GBV_ILN_2129 GBV_ILN_2143 GBV_ILN_2144 GBV_ILN_2147 GBV_ILN_2148 GBV_ILN_2152 GBV_ILN_2153 GBV_ILN_2188 GBV_ILN_2190 GBV_ILN_2232 GBV_ILN_2336 GBV_ILN_2446 GBV_ILN_2470 GBV_ILN_2472 GBV_ILN_2507 GBV_ILN_2522 GBV_ILN_2548 GBV_ILN_4012 GBV_ILN_4035 GBV_ILN_4037 GBV_ILN_4046 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4242 GBV_ILN_4246 GBV_ILN_4249 GBV_ILN_4251 GBV_ILN_4305 GBV_ILN_4306 GBV_ILN_4307 GBV_ILN_4313 GBV_ILN_4322 GBV_ILN_4323 GBV_ILN_4324 GBV_ILN_4325 GBV_ILN_4326 GBV_ILN_4328 GBV_ILN_4333 GBV_ILN_4334 GBV_ILN_4335 GBV_ILN_4336 GBV_ILN_4338 GBV_ILN_4367 GBV_ILN_4393 GBV_ILN_4700 44.96 ASE AR 20 2020 4 27 02 607-611
language	English
source	Enthalten in Journal of maxillofacial and oral surgery 20(2020), 4 vom: 27. Feb., Seite 607-611 volume:20 year:2020 number:4 day:27 month:02 pages:607-611
sourceStr	Enthalten in Journal of maxillofacial and oral surgery 20(2020), 4 vom: 27. Feb., Seite 607-611 volume:20 year:2020 number:4 day:27 month:02 pages:607-611
format_phy_str_mv	Article
institution	findex.gbv.de
topic_facet	Smoking Oral cancer XPC Polymorphism
dewey-raw	610
isfreeaccess_bool	false
container_title	Journal of maxillofacial and oral surgery
authorswithroles_txt_mv	Nigam, Kumud @@aut@@ Samadi, Fahad M. @@aut@@ Srivastava, Saurabh @@aut@@ Mohammad, Shadab @@aut@@ Sanyal, Somali @@aut@@
publishDateDaySort_date	2020-02-27T00:00:00Z
hierarchy_top_id	604074921
dewey-sort	3610
id	SPR045415420
language_de	englisch
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Such high incidence of oral cancer in India is due to consumption of tobacco in different form including smoking of cigarette. Smoke of tobacco contains different carcinogens which causes DNA damage. Such DNA damage if remain unrepaired due to faulty DNA repair system can cause mutation and eventual development of cancer. Methodology In the present study, we aimed to check the role of smoking as well as interaction of smoking and XPC polymorphism in risk modulation of oral cancer. Total of 372 subjects including 300 healthy controls and 72 patients of oral cancers been genotyped for the XPC PAT D/I, A/C and C/T polymorphisms with PCR based or PCR–RFLP based method. Genotype frequency was analyzed by chi-square test and strength of associations by odds ratio with 95% confidence intervals. Results The present study showed that compared to nonsmokers, smokers are at five times higher risk to develop oral cancer (p value= 0.001, OR= 5.03, 95% CI 2.91–8.69) and three times higher risk to develop node-positive (p value= 0.01, OR= 3.66, 95% CI 1.34–9.95) oral cancer. It has also been observed that individuals who were smokers and carrier of variant allele genotypes (AC and CC) for XPC A/C polymorphism were at threefold higher risk (p value= 0.01, OR=2.97, 95% CI 1.29–6.86) to develop oral cancer compared to individual who were smokers but do not carry the C allele (AA genotype). This observation indicates that C allele of XPC A/C polymorphism interacts with smoking and significantly increases the risk of oral cancer. 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author	Nigam, Kumud
spellingShingle	Nigam, Kumud ddc 610 bkl 44.96 misc Smoking misc Oral cancer misc XPC misc Polymorphism Smoking and XPC Gene Polymorphism Interact to Modulate the Risk of Oral Cancer
authorStr	Nigam, Kumud
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topic_title	610 ASE 44.96 bkl Smoking and XPC Gene Polymorphism Interact to Modulate the Risk of Oral Cancer Smoking (dpeaa)DE-He213 Oral cancer (dpeaa)DE-He213 XPC (dpeaa)DE-He213 Polymorphism (dpeaa)DE-He213
topic	ddc 610 bkl 44.96 misc Smoking misc Oral cancer misc XPC misc Polymorphism
topic_unstemmed	ddc 610 bkl 44.96 misc Smoking misc Oral cancer misc XPC misc Polymorphism
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title	Smoking and XPC Gene Polymorphism Interact to Modulate the Risk of Oral Cancer
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title_full	Smoking and XPC Gene Polymorphism Interact to Modulate the Risk of Oral Cancer
author_sort	Nigam, Kumud
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author_browse	Nigam, Kumud Samadi, Fahad M. Srivastava, Saurabh Mohammad, Shadab Sanyal, Somali
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title_sort	smoking and xpc gene polymorphism interact to modulate the risk of oral cancer
title_auth	Smoking and XPC Gene Polymorphism Interact to Modulate the Risk of Oral Cancer
abstract	Purpose Oral cancer is the most common cancer among the Indian men and the second most common cancer among the Indian women. Such high incidence of oral cancer in India is due to consumption of tobacco in different form including smoking of cigarette. Smoke of tobacco contains different carcinogens which causes DNA damage. Such DNA damage if remain unrepaired due to faulty DNA repair system can cause mutation and eventual development of cancer. Methodology In the present study, we aimed to check the role of smoking as well as interaction of smoking and XPC polymorphism in risk modulation of oral cancer. Total of 372 subjects including 300 healthy controls and 72 patients of oral cancers been genotyped for the XPC PAT D/I, A/C and C/T polymorphisms with PCR based or PCR–RFLP based method. Genotype frequency was analyzed by chi-square test and strength of associations by odds ratio with 95% confidence intervals. Results The present study showed that compared to nonsmokers, smokers are at five times higher risk to develop oral cancer (p value= 0.001, OR= 5.03, 95% CI 2.91–8.69) and three times higher risk to develop node-positive (p value= 0.01, OR= 3.66, 95% CI 1.34–9.95) oral cancer. It has also been observed that individuals who were smokers and carrier of variant allele genotypes (AC and CC) for XPC A/C polymorphism were at threefold higher risk (p value= 0.01, OR=2.97, 95% CI 1.29–6.86) to develop oral cancer compared to individual who were smokers but do not carry the C allele (AA genotype). This observation indicates that C allele of XPC A/C polymorphism interacts with smoking and significantly increases the risk of oral cancer. Conclusion This study demonstrates a possible role of smoking and gene–smoking interaction in risk enhancement of oral cancer. © The Association of Oral and Maxillofacial Surgeons of India 2020
abstractGer	Purpose Oral cancer is the most common cancer among the Indian men and the second most common cancer among the Indian women. Such high incidence of oral cancer in India is due to consumption of tobacco in different form including smoking of cigarette. Smoke of tobacco contains different carcinogens which causes DNA damage. Such DNA damage if remain unrepaired due to faulty DNA repair system can cause mutation and eventual development of cancer. Methodology In the present study, we aimed to check the role of smoking as well as interaction of smoking and XPC polymorphism in risk modulation of oral cancer. Total of 372 subjects including 300 healthy controls and 72 patients of oral cancers been genotyped for the XPC PAT D/I, A/C and C/T polymorphisms with PCR based or PCR–RFLP based method. Genotype frequency was analyzed by chi-square test and strength of associations by odds ratio with 95% confidence intervals. Results The present study showed that compared to nonsmokers, smokers are at five times higher risk to develop oral cancer (p value= 0.001, OR= 5.03, 95% CI 2.91–8.69) and three times higher risk to develop node-positive (p value= 0.01, OR= 3.66, 95% CI 1.34–9.95) oral cancer. It has also been observed that individuals who were smokers and carrier of variant allele genotypes (AC and CC) for XPC A/C polymorphism were at threefold higher risk (p value= 0.01, OR=2.97, 95% CI 1.29–6.86) to develop oral cancer compared to individual who were smokers but do not carry the C allele (AA genotype). This observation indicates that C allele of XPC A/C polymorphism interacts with smoking and significantly increases the risk of oral cancer. Conclusion This study demonstrates a possible role of smoking and gene–smoking interaction in risk enhancement of oral cancer. © The Association of Oral and Maxillofacial Surgeons of India 2020
abstract_unstemmed	Purpose Oral cancer is the most common cancer among the Indian men and the second most common cancer among the Indian women. Such high incidence of oral cancer in India is due to consumption of tobacco in different form including smoking of cigarette. Smoke of tobacco contains different carcinogens which causes DNA damage. Such DNA damage if remain unrepaired due to faulty DNA repair system can cause mutation and eventual development of cancer. Methodology In the present study, we aimed to check the role of smoking as well as interaction of smoking and XPC polymorphism in risk modulation of oral cancer. Total of 372 subjects including 300 healthy controls and 72 patients of oral cancers been genotyped for the XPC PAT D/I, A/C and C/T polymorphisms with PCR based or PCR–RFLP based method. Genotype frequency was analyzed by chi-square test and strength of associations by odds ratio with 95% confidence intervals. Results The present study showed that compared to nonsmokers, smokers are at five times higher risk to develop oral cancer (p value= 0.001, OR= 5.03, 95% CI 2.91–8.69) and three times higher risk to develop node-positive (p value= 0.01, OR= 3.66, 95% CI 1.34–9.95) oral cancer. It has also been observed that individuals who were smokers and carrier of variant allele genotypes (AC and CC) for XPC A/C polymorphism were at threefold higher risk (p value= 0.01, OR=2.97, 95% CI 1.29–6.86) to develop oral cancer compared to individual who were smokers but do not carry the C allele (AA genotype). This observation indicates that C allele of XPC A/C polymorphism interacts with smoking and significantly increases the risk of oral cancer. Conclusion This study demonstrates a possible role of smoking and gene–smoking interaction in risk enhancement of oral cancer. © The Association of Oral and Maxillofacial Surgeons of India 2020
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container_issue	4
title_short	Smoking and XPC Gene Polymorphism Interact to Modulate the Risk of Oral Cancer
url	https://dx.doi.org/10.1007/s12663-020-01340-z
remote_bool	true
author2	Samadi, Fahad M. Srivastava, Saurabh Mohammad, Shadab Sanyal, Somali
author2Str	Samadi, Fahad M. Srivastava, Saurabh Mohammad, Shadab Sanyal, Somali
ppnlink	604074921
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doi_str	10.1007/s12663-020-01340-z
up_date	2024-07-03T15:51:23.760Z
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