Abstract A49: Meta-analysis of vitamin D-binding protein and cancer risk
Notice bibliographique
Résumé
Abstract Antiproliferative effects of 1,25-dihydroxyvitamin D, the biologically active form of vitamin D, are well established in various cell types, including normal and malignant cells, by influencing cell differentiation, cell growth and apoptosis. In addition meta-analyses of epidemiological studies showed that serum 25-hydroxyvitamin D (25OHD) and vitamin D receptors polymorphisms (VDRs) are associated with cancer risk. The biological effects of vitamin D are mediated by an abundance of the vitamin D binding protein (DBP) and VDRs. The gene for the vitamin D–binding protein, known as ‘‘group-specific component’’ (Gc), is also a logical candidate in the vitamin D pathway because its major function is to transport vitamin D metabolites in the blood to different target organs. Variants in this gene have been shown to alter plasma concentrations of 25OHD and several studies investigated Gc SNPs and DBP in association with cancer risk with controversial results. Thus we carried out a comprehensive literature search and meta-analysis to investigate these associations. A systematic literature search was performed following a pre-defined protocol and using validated search strategies up to April 2014. We included for 24 independent studies for a total of 38,331 cases and 25,050 controls, from several countries Australia, Canada and USA, Finland, Germany, the Netherlands, Spain, UK, China and Iran. Data collected concern the following cancer sites: skin (n. of estimates=1), bladder (n=2), breast (n=3), colon-rectum (n=5), endometrium (n=1), liver (n=1), esophagus (n=1), stomach (n=1), melanoma (n= 3), pancreas (n= 2), prostate (n= 5) and kidney (n=1). Through random effect models we calculated the Summary Odd Ratios (SORs) for serum DBP (n. of estimates=6) and the following polymorphisms: rs2282679 (n. of estimates=7), rs12512631 (n=4), rs7041 (n=17), rs4588 (n=12), rs1155563 (n=5) and rs1352844 (n=3). We found a significant 8% increase cancer risk at any site for rs4588 variant (dominant model) and a non significant decrease risk at increasing level of DBP: SOR= 0.94 (0.86-1.02) per an increase of 1000 nmol/L. We evaluated also departure from Hardy-Weinberg equilibrium (HWE) in controls and sensitivity analyses excluding studies that do not respect HWE did not show important changes in results. No indication of publication bias was found. In conclusion we found some interesting associations indicating a possible role of DBP in cancer etiology. Further studies should consider also the role of the ‘free’ unbound part of 25OHD, that drives many of the non-classical actions of vitamin D, and it is dependent on the concentration of DBP. References: -Lauridsen AL, Vestergaard P, Hermann AP, et al. Plasma concentrations of 25-hydroxy-vitamin D and 1,25-dihydroxy-vitamin D are related to the phenotype of Gc (vitamin D-binding protein): a cross-sectional study on 595 early postmenopausal women. Calcif Tissue Int 2005. -Sinotte M, Diorio C, Berube S, Pollak M, Brisson J. Genetic polymorphisms of the vitamin D binding protein and plasma concentrations of 25-hydroxyvitamin D in premenopausal women. Am J Clin Nutr 2009. -Gandini S, Boniol M, Haukka J et al. Meta-analysis of observational studies of serum 25-hydroxyvitamin D levels and colorectal, breast and prostate cancer and colorectal adenoma. Int J Cancer. 2011. -Autier P and Gandini S. Vitamin D supplementation and total mortality: a meta-analysis of randomized controlled trials. Arch Intern Med. 2007. -Raimondi S, Johansson H, Maisonneuve P, and Gandini S. Review and meta-analysis on vitamin D receptor polymorphisms and cancer risk. Carcinogenesis. 2009. Citation Format: Sara Gandini, Tagliabue Elena, Sara Raimondi. Meta-analysis of vitamin D-binding protein and cancer risk. [abstract]. In: Proceedings of the Thirteenth Annual AACR International Conference on Frontiers in Cancer Prevention Research; 2014 Sep 27-Oct 1; New Orleans, LA. Philadelphia (PA): AACR; Can Prev Res 2015;8(10 Suppl): Abstract nr A49.
Récupéré en direct depuis OpenAlex et désinversé. Les résumés ne sont pas conservés dans cette base de données : les index inversés représentent 8,6 Go des 9,3 Go de texte de la base, et le serveur dispose de 13 Go libres.
Comment cette classification a été obtenuedéplier
Prédiction distillée sur la base complète
Imitation des enseignantsNi prévalence calibrée, ni vérité terrain. Validation humaine à venir. Apprise à partir de 10 348 étiquettes directes de Codex et de 10 348 étiquettes directes de Gemma. Le mode candidate est l'union des têtes enseignantes seuillées; le consensus est leur intersection. Ces sorties portent le statut machine_predicted_unvalidated et ne sont ni des étiquettes humaines ni des étiquettes directes de modèles de pointe.
Scores Codex et Gemma par catégorie
| Catégorie | Codex | Gemma |
|---|---|---|
| Métarecherche | 0,005 | 0,001 |
| Méta-épidémiologie (sens strict) | 0,000 | 0,000 |
| Méta-épidémiologie (sens large) | 0,001 | 0,000 |
| Bibliométrie | 0,001 | 0,002 |
| Études des sciences et des technologies | 0,000 | 0,000 |
| Communication savante | 0,000 | 0,000 |
| Science ouverte | 0,000 | 0,000 |
| Intégrité de la recherche | 0,000 | 0,001 |
| Charge utile insuffisante (le modèle a refusé de juger) | 0,002 | 0,000 |
Scores machine (provisoires)
Les deux têtes enseignantes du modèle étudiant, lues sur ce travail. Un score ordonne la base pour la relecture; il n'affirme jamais une catégorie, et le statut de validation accompagne chaque rangée tel quel.
Scores de référence d'un modèle non mature (critères de maturité non atteints, 7 itérations). Un score ordonne; il n'affirme jamais une catégorie.
score_only:v0-immature-baseline · tel quel depuis la passe de notation : score_only signifie que le nombre peut ordonner les travaux, et qu'aucune étiquette de catégorie n'en découleClassification
machine, non validéePrédiction automatique; un appel candidat d’une seule tête enseignante, pas un consensus.
Le détail, modèle par modèle et score par score, se trouve en fin de page sous « Comment cette classification a été obtenue ».