Sun exposure, vitamin D receptor gene polymorphisms and risk of non-Hodgkin lymphoma

Mark P. Purdue, Patricia Hartge, Scott Davis, James R Cerhan, Joanne S. Colt, Wendy Cozen, Richard K. Severson, Yan Li, Stephen J. Chanock, Nathaniel Rothman, Sophia S. Wang

Research output: Contribution to journalArticle

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Abstract

Objective: Recent findings suggest that ultraviolet (UV) radiation exposure may reduce risk of developing non-Hodgkin lymphoma (NHL), but the biologic basis for this relationship remains unclear. We analyzed data from our US population-based case-control study of NHL to investigate whether our previously reported inverse association with sun exposure was dependent upon variants in the vitamin D receptor gene (IVS10 + 283G > A (BsmI), Ex11 + 32T > C (TaqI)), and genes linked to UV-induced immune modulation (IL4, IL10, IL12A, IL12B, TNF). Methods: UV exposure data was collected from an in-person interview with 551 cases and 462 controls. We calculated odds ratios (OR) and 95% confidence intervals (CI) for sun exposure measures for joint variant-exposure effects. Results: The association with NHL risk for time in the midday sun within the last decade was dependent upon Ex11 + 32 T > C genotype. Compared to TT carriers who reported < 7 h/week of sun exposure, CC subjects with < 7 h/week of sun exposure had an increased risk of NHL (OR = 1.9, 95% CI 0.8-4.4, Pinteraction = 0.16), while the relative risks for other CC carriers approached unity with increasing level of sun exposure. This pattern of effects was especially apparent for follicular lymphoma (for CC genotype and < 7 h/week of exposure: OR 6.3, 95% CI 1.9-22, Pinteraction = 0.004), and was consistently observed across measures of reported sun exposure for different periods of life. As IVS10 + 283G > A is correlated with Ex11 + 32T > C in our population (r2 = 0.95), results were equivalent for those with the IVS10 + 283 AA genotype. No evidence of interaction with cytokine gene variants was observed. Conclusions: Our results suggest that the inverse association between UV exposure and NHL risk may be mediated by the vitamin D pathway. Further investigation of this finding in other studies is warranted.

Original languageEnglish (US)
Pages (from-to)989-999
Number of pages11
JournalCancer Causes and Control
Volume18
Issue number9
DOIs
StatePublished - Nov 2007

Fingerprint

Calcitriol Receptors
Solar System
Non-Hodgkin's Lymphoma
Genes
Genotype
Vitamin D
Interleukin-4
Interleukin-10
Population
Case-Control Studies
Joints
Odds Ratio
Confidence Intervals
Interviews
Cytokines

Keywords

  • Genetic
  • Non-Hodgkin lymphoma
  • Polymorphism
  • Sunlight
  • Vitamin D

ASJC Scopus subject areas

  • Oncology
  • Epidemiology
  • Cancer Research

Cite this

Sun exposure, vitamin D receptor gene polymorphisms and risk of non-Hodgkin lymphoma. / Purdue, Mark P.; Hartge, Patricia; Davis, Scott; Cerhan, James R; Colt, Joanne S.; Cozen, Wendy; Severson, Richard K.; Li, Yan; Chanock, Stephen J.; Rothman, Nathaniel; Wang, Sophia S.

In: Cancer Causes and Control, Vol. 18, No. 9, 11.2007, p. 989-999.

Research output: Contribution to journalArticle

Purdue, MP, Hartge, P, Davis, S, Cerhan, JR, Colt, JS, Cozen, W, Severson, RK, Li, Y, Chanock, SJ, Rothman, N & Wang, SS 2007, 'Sun exposure, vitamin D receptor gene polymorphisms and risk of non-Hodgkin lymphoma', Cancer Causes and Control, vol. 18, no. 9, pp. 989-999. https://doi.org/10.1007/s10552-007-9039-z
Purdue, Mark P. ; Hartge, Patricia ; Davis, Scott ; Cerhan, James R ; Colt, Joanne S. ; Cozen, Wendy ; Severson, Richard K. ; Li, Yan ; Chanock, Stephen J. ; Rothman, Nathaniel ; Wang, Sophia S. / Sun exposure, vitamin D receptor gene polymorphisms and risk of non-Hodgkin lymphoma. In: Cancer Causes and Control. 2007 ; Vol. 18, No. 9. pp. 989-999.
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abstract = "Objective: Recent findings suggest that ultraviolet (UV) radiation exposure may reduce risk of developing non-Hodgkin lymphoma (NHL), but the biologic basis for this relationship remains unclear. We analyzed data from our US population-based case-control study of NHL to investigate whether our previously reported inverse association with sun exposure was dependent upon variants in the vitamin D receptor gene (IVS10 + 283G > A (BsmI), Ex11 + 32T > C (TaqI)), and genes linked to UV-induced immune modulation (IL4, IL10, IL12A, IL12B, TNF). Methods: UV exposure data was collected from an in-person interview with 551 cases and 462 controls. We calculated odds ratios (OR) and 95{\%} confidence intervals (CI) for sun exposure measures for joint variant-exposure effects. Results: The association with NHL risk for time in the midday sun within the last decade was dependent upon Ex11 + 32 T > C genotype. Compared to TT carriers who reported < 7 h/week of sun exposure, CC subjects with < 7 h/week of sun exposure had an increased risk of NHL (OR = 1.9, 95{\%} CI 0.8-4.4, Pinteraction = 0.16), while the relative risks for other CC carriers approached unity with increasing level of sun exposure. This pattern of effects was especially apparent for follicular lymphoma (for CC genotype and < 7 h/week of exposure: OR 6.3, 95{\%} CI 1.9-22, Pinteraction = 0.004), and was consistently observed across measures of reported sun exposure for different periods of life. As IVS10 + 283G > A is correlated with Ex11 + 32T > C in our population (r2 = 0.95), results were equivalent for those with the IVS10 + 283 AA genotype. No evidence of interaction with cytokine gene variants was observed. Conclusions: Our results suggest that the inverse association between UV exposure and NHL risk may be mediated by the vitamin D pathway. Further investigation of this finding in other studies is warranted.",
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AU - Hartge, Patricia

AU - Davis, Scott

AU - Cerhan, James R

AU - Colt, Joanne S.

AU - Cozen, Wendy

AU - Severson, Richard K.

AU - Li, Yan

AU - Chanock, Stephen J.

AU - Rothman, Nathaniel

AU - Wang, Sophia S.

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N2 - Objective: Recent findings suggest that ultraviolet (UV) radiation exposure may reduce risk of developing non-Hodgkin lymphoma (NHL), but the biologic basis for this relationship remains unclear. We analyzed data from our US population-based case-control study of NHL to investigate whether our previously reported inverse association with sun exposure was dependent upon variants in the vitamin D receptor gene (IVS10 + 283G > A (BsmI), Ex11 + 32T > C (TaqI)), and genes linked to UV-induced immune modulation (IL4, IL10, IL12A, IL12B, TNF). Methods: UV exposure data was collected from an in-person interview with 551 cases and 462 controls. We calculated odds ratios (OR) and 95% confidence intervals (CI) for sun exposure measures for joint variant-exposure effects. Results: The association with NHL risk for time in the midday sun within the last decade was dependent upon Ex11 + 32 T > C genotype. Compared to TT carriers who reported < 7 h/week of sun exposure, CC subjects with < 7 h/week of sun exposure had an increased risk of NHL (OR = 1.9, 95% CI 0.8-4.4, Pinteraction = 0.16), while the relative risks for other CC carriers approached unity with increasing level of sun exposure. This pattern of effects was especially apparent for follicular lymphoma (for CC genotype and < 7 h/week of exposure: OR 6.3, 95% CI 1.9-22, Pinteraction = 0.004), and was consistently observed across measures of reported sun exposure for different periods of life. As IVS10 + 283G > A is correlated with Ex11 + 32T > C in our population (r2 = 0.95), results were equivalent for those with the IVS10 + 283 AA genotype. No evidence of interaction with cytokine gene variants was observed. Conclusions: Our results suggest that the inverse association between UV exposure and NHL risk may be mediated by the vitamin D pathway. Further investigation of this finding in other studies is warranted.

AB - Objective: Recent findings suggest that ultraviolet (UV) radiation exposure may reduce risk of developing non-Hodgkin lymphoma (NHL), but the biologic basis for this relationship remains unclear. We analyzed data from our US population-based case-control study of NHL to investigate whether our previously reported inverse association with sun exposure was dependent upon variants in the vitamin D receptor gene (IVS10 + 283G > A (BsmI), Ex11 + 32T > C (TaqI)), and genes linked to UV-induced immune modulation (IL4, IL10, IL12A, IL12B, TNF). Methods: UV exposure data was collected from an in-person interview with 551 cases and 462 controls. We calculated odds ratios (OR) and 95% confidence intervals (CI) for sun exposure measures for joint variant-exposure effects. Results: The association with NHL risk for time in the midday sun within the last decade was dependent upon Ex11 + 32 T > C genotype. Compared to TT carriers who reported < 7 h/week of sun exposure, CC subjects with < 7 h/week of sun exposure had an increased risk of NHL (OR = 1.9, 95% CI 0.8-4.4, Pinteraction = 0.16), while the relative risks for other CC carriers approached unity with increasing level of sun exposure. This pattern of effects was especially apparent for follicular lymphoma (for CC genotype and < 7 h/week of exposure: OR 6.3, 95% CI 1.9-22, Pinteraction = 0.004), and was consistently observed across measures of reported sun exposure for different periods of life. As IVS10 + 283G > A is correlated with Ex11 + 32T > C in our population (r2 = 0.95), results were equivalent for those with the IVS10 + 283 AA genotype. No evidence of interaction with cytokine gene variants was observed. Conclusions: Our results suggest that the inverse association between UV exposure and NHL risk may be mediated by the vitamin D pathway. Further investigation of this finding in other studies is warranted.

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