Smoking, variation in N-acetyltransferase 1 (NAT1) and 2 (NAT2), and risk of non-Hodgkin lymphoma: A pooled analysis within the InterLymph consortium

Todd M. Gibson; Karin E. Smedby; Christine F. Skibola; David W. Hein; Susan L. Slager; Silvia De Sanjosé; Claire M. Vajdic; Yawei Zhang; Brian C.H. Chiu; Sophia S. Wang; Henrik Hjalgrim; Alexandra Nieters; Paige M. Bracci; Anne Kricker; Tongzhang Zheng; Carol Kolar; James R. Cerhan; Hatef Darabi; Nikolaus Becker; Lucia Conde; Theodore R. Holford; Dennis D. Weisenburger; Anneclaire J. De Roos; Katja Butterbach; Jacques Riby; Wendy Cozen; Yolanda Benavente; Casey Palmers; Elizabeth A. Holly; Joshua N. Sampson; Nathaniel Rothman; Bruce K. Armstrong; Lindsay M. Morton

doi:10.1007/s10552-012-0098-4

Smoking, variation in N-acetyltransferase 1 (NAT1) and 2 (NAT2), and risk of non-Hodgkin lymphoma: A pooled analysis within the InterLymph consortium

Todd M. Gibson, Karin E. Smedby, Christine F. Skibola, David W. Hein, Susan L. Slager, Silvia De Sanjosé, Claire M. Vajdic, Yawei Zhang, Brian C.H. Chiu, Sophia S. Wang, Henrik Hjalgrim, Alexandra Nieters, Paige M. Bracci, Anne Kricker, Tongzhang Zheng, Carol Kolar, James R. Cerhan, Hatef Darabi, Nikolaus Becker, Lucia CondeTheodore R. Holford, Dennis D. Weisenburger, Anneclaire J. De Roos, Katja Butterbach, Jacques Riby, Wendy Cozen, Yolanda Benavente, Casey Palmers, Elizabeth A. Holly, Joshua N. Sampson, Nathaniel Rothman, Bruce K. Armstrong, Lindsay M. Morton

Quantitative Health Sciences

Research output: Contribution to journal › Article › peer-review

18 Scopus citations

Abstract

Purpose: Studies of smoking and risk of non-Hodgkin lymphoma (NHL) have yielded inconsistent results, possibly due to subtype heterogeneity and/or genetic variation impacting the metabolism of tobacco-derived carcinogens, including substrates of the N-acetyltransferase enzymes NAT1 and NAT2. Methods: We conducted a pooled analysis of 5,026 NHL cases and 4,630 controls from seven case-control studies in the international lymphoma epidemiology consortium to examine associations between smoking, variation in the N-acetyltransferase genes NAT1 and NAT2, and risk of NHL subtypes. Smoking data were harmonized across studies, and genetic variants in NAT1 and NAT2 were used to infer acetylation phenotype of the NAT1 and NAT2 enzymes, respectively. Pooled odds ratios (ORs) and 95 % confidence intervals (95 % CIs) for risk of NHL and subtypes were calculated using joint fixed effects unconditional logistic regression models. Results: Current smoking was associated with a significant 30 % increased risk of follicular lymphoma (n = 1,176) but not NHL overall or other NHL subtypes. The association was similar among NAT2 slow (OR 1.36; 95 % CI 1.07-1.75) and intermediate/rapid (OR 1.27; 95 % CI 0.95-1.69) acetylators (p _interaction = 0.82) and also did not differ by NAT1*10 allelotype. Neither NAT2 phenotype nor NAT1*10 allelotype was associated with risk of NHL overall or NHL subtypes. Conclusion: The current findings provide further evidence for a modest association between current smoking and follicular lymphoma risk and suggest that this association may not be influenced by variation in the N-acetyltransferase enzymes.

Original language	English (US)
Pages (from-to)	125-134
Number of pages	10
Journal	Cancer Causes and Control
Volume	24
Issue number	1
DOIs	https://doi.org/10.1007/s10552-012-0098-4
State	Published - Jan 2013

Keywords

Cigarette smoking
Follicular lymphoma
Gene environment interaction
N-acetyltransferase
Non-Hodgkin lymphoma

ASJC Scopus subject areas

Oncology
Cancer Research

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10.1007/s10552-012-0098-4

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Gibson, T. M., Smedby, K. E., Skibola, C. F., Hein, D. W., Slager, S. L., De Sanjosé, S., Vajdic, C. M., Zhang, Y., Chiu, B. C. H., Wang, S. S., Hjalgrim, H., Nieters, A., Bracci, P. M., Kricker, A., Zheng, T., Kolar, C., Cerhan, J. R., Darabi, H., Becker, N., ... Morton, L. M. (2013). Smoking, variation in N-acetyltransferase 1 (NAT1) and 2 (NAT2), and risk of non-Hodgkin lymphoma: A pooled analysis within the InterLymph consortium. Cancer Causes and Control, 24(1), 125-134. https://doi.org/10.1007/s10552-012-0098-4

Gibson, TM, Smedby, KE, Skibola, CF, Hein, DW, Slager, SL, De Sanjosé, S, Vajdic, CM, Zhang, Y, Chiu, BCH, Wang, SS, Hjalgrim, H, Nieters, A, Bracci, PM, Kricker, A, Zheng, T, Kolar, C, Cerhan, JR, Darabi, H, Becker, N, Conde, L, Holford, TR, Weisenburger, DD, De Roos, AJ, Butterbach, K, Riby, J, Cozen, W, Benavente, Y, Palmers, C, Holly, EA, Sampson, JN, Rothman, N, Armstrong, BK & Morton, LM 2013, 'Smoking, variation in N-acetyltransferase 1 (NAT1) and 2 (NAT2), and risk of non-Hodgkin lymphoma: A pooled analysis within the InterLymph consortium', Cancer Causes and Control, vol. 24, no. 1, pp. 125-134. https://doi.org/10.1007/s10552-012-0098-4

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title = "Smoking, variation in N-acetyltransferase 1 (NAT1) and 2 (NAT2), and risk of non-Hodgkin lymphoma: A pooled analysis within the InterLymph consortium",

abstract = "Purpose: Studies of smoking and risk of non-Hodgkin lymphoma (NHL) have yielded inconsistent results, possibly due to subtype heterogeneity and/or genetic variation impacting the metabolism of tobacco-derived carcinogens, including substrates of the N-acetyltransferase enzymes NAT1 and NAT2. Methods: We conducted a pooled analysis of 5,026 NHL cases and 4,630 controls from seven case-control studies in the international lymphoma epidemiology consortium to examine associations between smoking, variation in the N-acetyltransferase genes NAT1 and NAT2, and risk of NHL subtypes. Smoking data were harmonized across studies, and genetic variants in NAT1 and NAT2 were used to infer acetylation phenotype of the NAT1 and NAT2 enzymes, respectively. Pooled odds ratios (ORs) and 95 % confidence intervals (95 % CIs) for risk of NHL and subtypes were calculated using joint fixed effects unconditional logistic regression models. Results: Current smoking was associated with a significant 30 % increased risk of follicular lymphoma (n = 1,176) but not NHL overall or other NHL subtypes. The association was similar among NAT2 slow (OR 1.36; 95 % CI 1.07-1.75) and intermediate/rapid (OR 1.27; 95 % CI 0.95-1.69) acetylators (p interaction = 0.82) and also did not differ by NAT1*10 allelotype. Neither NAT2 phenotype nor NAT1*10 allelotype was associated with risk of NHL overall or NHL subtypes. Conclusion: The current findings provide further evidence for a modest association between current smoking and follicular lymphoma risk and suggest that this association may not be influenced by variation in the N-acetyltransferase enzymes.",

keywords = "Cigarette smoking, Follicular lymphoma, Gene environment interaction, N-acetyltransferase, Non-Hodgkin lymphoma",

author = "Gibson, {Todd M.} and Smedby, {Karin E.} and Skibola, {Christine F.} and Hein, {David W.} and Slager, {Susan L.} and {De Sanjos{\'e}}, Silvia and Vajdic, {Claire M.} and Yawei Zhang and Chiu, {Brian C.H.} and Wang, {Sophia S.} and Henrik Hjalgrim and Alexandra Nieters and Bracci, {Paige M.} and Anne Kricker and Tongzhang Zheng and Carol Kolar and Cerhan, {James R.} and Hatef Darabi and Nikolaus Becker and Lucia Conde and Holford, {Theodore R.} and Weisenburger, {Dennis D.} and {De Roos}, {Anneclaire J.} and Katja Butterbach and Jacques Riby and Wendy Cozen and Yolanda Benavente and Casey Palmers and Holly, {Elizabeth A.} and Sampson, {Joshua N.} and Nathaniel Rothman and Armstrong, {Bruce K.} and Morton, {Lindsay M.}",

note = "Funding Information: Acknowledgments Intramural Research Program of the National Cancer Institute; Spanish Ministry of Health FISS grant PI11/01810, AGAUR_SGR01465, and CIBERESP 06/06/0073 (EpiLymph-Spain); Swedish Cancer Society (090659); Danish Medical Research Council (FSS 09-63424); National Cancer Institute (CA069269-01 and CA92153-01); National Health and Medical Research Council, Australia, grant 990920.",

year = "2013",

month = jan,

doi = "10.1007/s10552-012-0098-4",

language = "English (US)",

volume = "24",

pages = "125--134",

journal = "Cancer Causes and Control",

issn = "0957-5243",

publisher = "Springer Netherlands",

number = "1",

}

TY - JOUR

T1 - Smoking, variation in N-acetyltransferase 1 (NAT1) and 2 (NAT2), and risk of non-Hodgkin lymphoma

T2 - A pooled analysis within the InterLymph consortium

AU - Gibson, Todd M.

AU - Smedby, Karin E.

AU - Skibola, Christine F.

AU - Hein, David W.

AU - Slager, Susan L.

AU - De Sanjosé, Silvia

AU - Vajdic, Claire M.

AU - Zhang, Yawei

AU - Chiu, Brian C.H.

AU - Wang, Sophia S.

AU - Hjalgrim, Henrik

AU - Nieters, Alexandra

AU - Bracci, Paige M.

AU - Kricker, Anne

AU - Zheng, Tongzhang

AU - Kolar, Carol

AU - Cerhan, James R.

AU - Darabi, Hatef

AU - Becker, Nikolaus

AU - Conde, Lucia

AU - Holford, Theodore R.

AU - Weisenburger, Dennis D.

AU - De Roos, Anneclaire J.

AU - Butterbach, Katja

AU - Riby, Jacques

AU - Cozen, Wendy

AU - Benavente, Yolanda

AU - Palmers, Casey

AU - Holly, Elizabeth A.

AU - Sampson, Joshua N.

AU - Rothman, Nathaniel

AU - Armstrong, Bruce K.

AU - Morton, Lindsay M.

N1 - Funding Information: Acknowledgments Intramural Research Program of the National Cancer Institute; Spanish Ministry of Health FISS grant PI11/01810, AGAUR_SGR01465, and CIBERESP 06/06/0073 (EpiLymph-Spain); Swedish Cancer Society (090659); Danish Medical Research Council (FSS 09-63424); National Cancer Institute (CA069269-01 and CA92153-01); National Health and Medical Research Council, Australia, grant 990920.

PY - 2013/1

Y1 - 2013/1

N2 - Purpose: Studies of smoking and risk of non-Hodgkin lymphoma (NHL) have yielded inconsistent results, possibly due to subtype heterogeneity and/or genetic variation impacting the metabolism of tobacco-derived carcinogens, including substrates of the N-acetyltransferase enzymes NAT1 and NAT2. Methods: We conducted a pooled analysis of 5,026 NHL cases and 4,630 controls from seven case-control studies in the international lymphoma epidemiology consortium to examine associations between smoking, variation in the N-acetyltransferase genes NAT1 and NAT2, and risk of NHL subtypes. Smoking data were harmonized across studies, and genetic variants in NAT1 and NAT2 were used to infer acetylation phenotype of the NAT1 and NAT2 enzymes, respectively. Pooled odds ratios (ORs) and 95 % confidence intervals (95 % CIs) for risk of NHL and subtypes were calculated using joint fixed effects unconditional logistic regression models. Results: Current smoking was associated with a significant 30 % increased risk of follicular lymphoma (n = 1,176) but not NHL overall or other NHL subtypes. The association was similar among NAT2 slow (OR 1.36; 95 % CI 1.07-1.75) and intermediate/rapid (OR 1.27; 95 % CI 0.95-1.69) acetylators (p interaction = 0.82) and also did not differ by NAT1*10 allelotype. Neither NAT2 phenotype nor NAT1*10 allelotype was associated with risk of NHL overall or NHL subtypes. Conclusion: The current findings provide further evidence for a modest association between current smoking and follicular lymphoma risk and suggest that this association may not be influenced by variation in the N-acetyltransferase enzymes.

AB - Purpose: Studies of smoking and risk of non-Hodgkin lymphoma (NHL) have yielded inconsistent results, possibly due to subtype heterogeneity and/or genetic variation impacting the metabolism of tobacco-derived carcinogens, including substrates of the N-acetyltransferase enzymes NAT1 and NAT2. Methods: We conducted a pooled analysis of 5,026 NHL cases and 4,630 controls from seven case-control studies in the international lymphoma epidemiology consortium to examine associations between smoking, variation in the N-acetyltransferase genes NAT1 and NAT2, and risk of NHL subtypes. Smoking data were harmonized across studies, and genetic variants in NAT1 and NAT2 were used to infer acetylation phenotype of the NAT1 and NAT2 enzymes, respectively. Pooled odds ratios (ORs) and 95 % confidence intervals (95 % CIs) for risk of NHL and subtypes were calculated using joint fixed effects unconditional logistic regression models. Results: Current smoking was associated with a significant 30 % increased risk of follicular lymphoma (n = 1,176) but not NHL overall or other NHL subtypes. The association was similar among NAT2 slow (OR 1.36; 95 % CI 1.07-1.75) and intermediate/rapid (OR 1.27; 95 % CI 0.95-1.69) acetylators (p interaction = 0.82) and also did not differ by NAT1*10 allelotype. Neither NAT2 phenotype nor NAT1*10 allelotype was associated with risk of NHL overall or NHL subtypes. Conclusion: The current findings provide further evidence for a modest association between current smoking and follicular lymphoma risk and suggest that this association may not be influenced by variation in the N-acetyltransferase enzymes.

KW - Cigarette smoking

KW - Follicular lymphoma

KW - Gene environment interaction

KW - N-acetyltransferase

KW - Non-Hodgkin lymphoma

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SN - 0957-5243

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JO - Cancer Causes and Control

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Smoking, variation in N-acetyltransferase 1 (NAT1) and 2 (NAT2), and risk of non-Hodgkin lymphoma: A pooled analysis within the InterLymph consortium

Abstract

Keywords

ASJC Scopus subject areas

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