Delphine Casabonne1,2, Esther Gracia3,4,5, Ana Espinosa3,4,5,6, Mariona Bustamante3,4,6,7, Yolanda Benavente8,3, Claudia Robles8, Laura Costas8,3, Esther Alonso9, Eva Gonzalez-Barca10, Adonina Tardón3,11, Trinidad Dierssen-Sotos3,12, Eva Gimeno Vázquez13,14, Marta Aymerich15, Elies Campo15, José J Jiménez-Moleón3,16,17, Rafael Marcos-Gragera18, Gemma Castaño-Vinyals3,4,5,6, Nuria Aragones3,19,20, Marina Pollan3,19,20, Manolis Kogevinas3,4,5,6,21, Carmen Urtiaga22, Pilar Amiano3,23, Victor Moreno3,24, Silvia de Sanjose8,3. 1. Unit of Infections and Cancer (UNIC), Cancer Epidemiology Research Programme, IDIBELL, Institut Català d'Oncologia, Av. Gran Via 199 - 203, 2º, 08907, L'Hospitalet De Llobregat, Barcelona, Spain. dcasabonne@iconcologia.net. 2. CIBER Epidemiología y Salud Pública (CIBERESP), 28029, Madrid, Spain. dcasabonne@iconcologia.net. 3. CIBER Epidemiología y Salud Pública (CIBERESP), 28029, Madrid, Spain. 4. Centre for Research in Environmental Epidemiology (CREAL), 08003, Barcelona, Spain. 5. Universitat Pompeu Fabra (UPF), 08002, Barcelona, Spain. 6. Hospital del Mar Medical Research Institute (IMIM), Barcelona, Spain. 7. Center for Genomic Regulation (CRG), 08003, Barcelona, Spain. 8. Unit of Infections and Cancer (UNIC), Cancer Epidemiology Research Programme, IDIBELL, Institut Català d'Oncologia, Av. Gran Via 199 - 203, 2º, 08907, L'Hospitalet De Llobregat, Barcelona, Spain. 9. Department of Pathology, Hospital Universitari de Bellvitge, 08907, L'Hospitalet De Llobregat, Barcelona, Spain. 10. Hematology, IDIBELL, Institut Català d' Oncologia, 08907, L' Hospitalet De Llobregat, Barcelona, Spain. 11. Oncology Institute (IUOPA), University of Oviedo, 33006, Oviedo, Austria. 12. Faculty of Medicine, University of Cantabria- IDIVAL, 39011, Santander, Spain. 13. Department of Clinical Hematology, Hospital del Mar, 08003, Barcelona, Spain. 14. Grup de Recerca Aplicada en Neoplasies Hematològiques-PSMAR, Barcelona, Spain. 15. Hematopathology Unit, Pathology Department, Hospital Clínic, University of Barcelona, Institute of Biomedical Research August Pi i Sunyer (IDIBAPS), 08036, Barcelona, Spain. 16. Department of Preventive Medicine and Public Health, University of Granada, 18071, Granada, Spain. 17. Instituto de Investigación Biosanitaria de Granada, Servicio Andaluz de Salud/Universidad de Granada, 18012, Granada, Spain. 18. Epidemiology Unit and Girona Cancer Registry, Oncology Coordination Plan, Department of Health, Autonomous Government of Catalonia, Catalan Institute of Oncology, Girona Biomedical Research Institute (IdiBGi), 17007, Girona, Spain. 19. National Center for Epidemiology, Carlos III Institute of Health, 28029, Madrid, Spain. 20. Instituto de Investigación Sanitaria (IIS), 28222, Puerta De Hierro Majadahonda, Spain. 21. National School of Public Health, 115 21, Athens, Greece. 22. Public Health Division of Gipuzkoa, Basque Health Department, 20013, San Sebastian, Spain. 23. Public Health Division of Gipuzkoa, BioDonostia Research Institute, Basque Health Department, 20013, San Sebastian, Spain. 24. Cancer Prevention and Control Program, IDIBELL, Institut Català d'Oncologia, University of Barcelona, 08907, L'Hospitalet De Llobregat, Barcelona, Spain.
Abstract
PURPOSE: There is currently no convincing epidemiological evidence that fruit and vegetable consumption, the primary source of vitamin C, plays a role in chronic lymphocytic leukaemia (CLL) aetiology. We hypothesized that variations in vitamin C dietary intake as well as in genetic variability in vitamin C transporter gene SLC23A2 could explain some inconsistencies in the literature. METHODS: Fruit/vegetable/vitamin C consumption from food frequency questionnaires and six low-penetrance genetic susceptibility polymorphisms in vitamin C transporter gene SLC23A2 (rs1715364, rs6133175, rs1776948, rs6139587, rs369270 and rs6052937) were examined in 434 CLL cases and 1257 randomly selected controls from primary care centres with genetic data of whom 275 cases and 1094 controls having both diet and genetic information. Logistic regression models were used to estimate odds ratio (OR) and 95 % confidence intervals (CI). RESULTS: CLL patients were more likely to have a higher fruit consumption than controls (highest versus lowest quartile in g/day OR: 1.48; 95 % CI: 1.00 to 2.18; P = 0.03), whereas no associations were found with vegetable or total vitamin C intake. Based on log-additive models, rs6133175_A > G (OR: 1.19, 95 % CI: 1.00 to 1.41; P = 0.05) and rs1776948_T > A (OR: 1.20; 95 %CI: 1.01 to 1.41; P = 0.04) were associated with CLL. The haplogenotype analysis (rs1715364, rs6133175) supported the genotype results. No gene-diet interactions in CLL remained statistically significant after correction for multiple testing. CONCLUSIONS: These data suggest that both fruit intake and genetic marker in SLC23A2 may play an independent role in CLL biology.
PURPOSE: There is currently no convincing epidemiological evidence that fruit and vegetable consumption, the primary source of vitamin C, plays a role in chronic lymphocytic leukaemia (CLL) aetiology. We hypothesized that variations in vitamin C dietary intake as well as in genetic variability in vitamin C transporter gene SLC23A2 could explain some inconsistencies in the literature. METHODS: Fruit/vegetable/vitamin C consumption from food frequency questionnaires and six low-penetrance genetic susceptibility polymorphisms in vitamin C transporter gene SLC23A2 (rs1715364, rs6133175, rs1776948, rs6139587, rs369270 and rs6052937) were examined in 434 CLL cases and 1257 randomly selected controls from primary care centres with genetic data of whom 275 cases and 1094 controls having both diet and genetic information. Logistic regression models were used to estimate odds ratio (OR) and 95 % confidence intervals (CI). RESULTS: CLL patients were more likely to have a higher fruit consumption than controls (highest versus lowest quartile in g/day OR: 1.48; 95 % CI: 1.00 to 2.18; P = 0.03), whereas no associations were found with vegetable or total vitamin C intake. Based on log-additive models, rs6133175_A > G (OR: 1.19, 95 % CI: 1.00 to 1.41; P = 0.05) and rs1776948_T > A (OR: 1.20; 95 %CI: 1.01 to 1.41; P = 0.04) were associated with CLL. The haplogenotype analysis (rs1715364, rs6133175) supported the genotype results. No gene-diet interactions in CLL remained statistically significant after correction for multiple testing. CONCLUSIONS: These data suggest that both fruit intake and genetic marker in SLC23A2 may play an independent role in CLL biology.
Entities:
Keywords:
Chronic lymphocytic leukaemia; Fruit intake; Polymorphism; SLC23A2; Vegetable intake; Vitamin C intake
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