An analysis of the effect of statins on the risk of Non-Hodgkin's Lymphoma in the Women's Health Initiative cohort.

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Citation: Cancer Medicine. 7(5):2121-2130, 2018 05.PMID: 29608241Institution: MedStar Health Research InstituteForm of publication: Journal ArticleMedline article type(s): Journal ArticleSubject headings: *Hydroxymethylglutaryl-CoA Reductase Inhibitors/tu [Therapeutic Use] | *Leukemia, Lymphocytic, Chronic, B-Cell/ep [Epidemiology] | *Lymphoma, Follicular/ep [Epidemiology] | *Lymphoma, Large B-Cell, Diffuse/ep [Epidemiology] | *Women's Health/sn [Statistics & Numerical Data] | Aged | Cohort Studies | Female | Humans | Leukemia, Lymphocytic, Chronic, B-Cell/pc [Prevention & Control] | Lymphoma, Follicular/pc [Prevention & Control] | Lymphoma, Large B-Cell, Diffuse/pc [Prevention & Control] | Middle Aged | Risk Factors | Surveys and QuestionnairesYear: 2018ISSN:
  • 2045-7634
Name of journal: Cancer medicineAbstract: Copyright (c) 2018 The Authors. Cancer Medicine published by John Wiley & Sons Ltd.Statins have been shown to induce a phosphoprotein signature that modifies MYC (myelocytomatosis viral oncogene) activation and to have anti-inflammatory activity that may impact the risk of Non-Hodgkin's lymphoma (NHL). We analyzed the relationship between statins and risk of NHL using data from the Women's Health Initiative (WHI). The study population included 161,563 postmenopausal women ages 50-79 years from which 712 cases of NHL were diagnosed after 10.8 years of follow-up. Information on statin use and other risk factors was collected by self- and interviewer-administered questionnaires. Multivariable-adjusted HR and 95% CI evaluating the relationship between statin use at baseline, as well as in a time-dependent manner and risk of NHL, were computed from Cox proportional hazards analyses. A separate analysis was performed for individual NHL subtypes: diffuse large B-Cell lymphoma (DLBCL) (n = 228), follicular lymphoma (n = 169), and small lymphocytic lymphoma (n = 74). All statistical tests were two-sided. There was no significant association between use of statins at baseline and risk of NHL (HR 0.85, 95% C.I. 0.67-1.08). However, in the multivariable-adjusted time-dependent models, statin use was associated with a borderline lower risk of NHL (HR 0.81, 95% C.I. 0.66-1.00). Considering subtypes of NHL, statin use was associated with a lower risk of DLBCL (HR 0.62, 95% C.I. 0.42-0.91). This effect was driven by lipophilic statins (HR 0.62, 95% C.I. 0.40-0.96). In the WHI, statins were associated with a lower overall risk of DLBCL, particularly attributable to lipophilic statins. These results may have impact on primary or secondary prevention of NHL, particularly DLBCL.All authors: Anderson ML, Cirillo D, Desai P, Howard BV, Jay A, Liu S, Manson JE, Martin LW, Ray R, Safford M, Schlecht N, Simon MS, Wallace R, Wu CFiscal year: FY2018Digital Object Identifier: ORCID: Date added to catalog: 2018-05-08
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Journal Article MedStar Authors Catalog Article 29608241 Available 29608241

Copyright (c) 2018 The Authors. Cancer Medicine published by John Wiley & Sons Ltd.

Statins have been shown to induce a phosphoprotein signature that modifies MYC (myelocytomatosis viral oncogene) activation and to have anti-inflammatory activity that may impact the risk of Non-Hodgkin's lymphoma (NHL). We analyzed the relationship between statins and risk of NHL using data from the Women's Health Initiative (WHI). The study population included 161,563 postmenopausal women ages 50-79 years from which 712 cases of NHL were diagnosed after 10.8 years of follow-up. Information on statin use and other risk factors was collected by self- and interviewer-administered questionnaires. Multivariable-adjusted HR and 95% CI evaluating the relationship between statin use at baseline, as well as in a time-dependent manner and risk of NHL, were computed from Cox proportional hazards analyses. A separate analysis was performed for individual NHL subtypes: diffuse large B-Cell lymphoma (DLBCL) (n = 228), follicular lymphoma (n = 169), and small lymphocytic lymphoma (n = 74). All statistical tests were two-sided. There was no significant association between use of statins at baseline and risk of NHL (HR 0.85, 95% C.I. 0.67-1.08). However, in the multivariable-adjusted time-dependent models, statin use was associated with a borderline lower risk of NHL (HR 0.81, 95% C.I. 0.66-1.00). Considering subtypes of NHL, statin use was associated with a lower risk of DLBCL (HR 0.62, 95% C.I. 0.42-0.91). This effect was driven by lipophilic statins (HR 0.62, 95% C.I. 0.40-0.96). In the WHI, statins were associated with a lower overall risk of DLBCL, particularly attributable to lipophilic statins. These results may have impact on primary or secondary prevention of NHL, particularly DLBCL.

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