𝔖 Bobbio Scriptorium
✦   LIBER   ✦

Exposure to childhood infections and risk of Epstein-Barr virus–defined Hodgkin's lymphoma in women

✍ Scribed by Sally L. Glaser; Theresa H. M. Keegan; Christina A. Clarke; Muoi Trinh; Ronald F. Dorfman; Risa B. Mann; Joseph A. DiGiuseppe; Richard F. Ambinder


Publisher
John Wiley and Sons
Year
2005
Tongue
French
Weight
91 KB
Volume
115
Category
Article
ISSN
0020-7136

No coin nor oath required. For personal study only.

✦ Synopsis


Abstract

The role of Epstein‐Barr virus (EBV) in Hodgkin's lymphoma (HL) etiology remains unresolved as EBV is detected in only some HL tumors and few studies have tried to reconcile its presence with factors suggesting viral etiology (e.g., childhood social class, infection history). In a population‐based case‐control study of San Francisco Bay area women, we analyzed interview data by tumor EBV status. Among 211 young adult cases, EBV‐positive HL (11%) was associated with a single vs. shared bedroom at age 11 (OR = 4.0, 95% CI 1.1–14.4); risk was decreased for common childhood infections (OR = 0.3, 95% CI 0.1–1.0), including measles before age 10, but not with prior infectious mononucleosis (IM), which is delayed EBV infection. No study factors affected risk of young adult EBV‐negative HL. Among 57 older adult cases, EBV‐positive HL (23%) was unrelated to study factors; EBV‐negative HL was associated with a single bedroom at age 11 (OR = 3.6, 95% CI 1.5–9.1) and IM in family members (OR = 3.1, 95% CI 1.1–9.0). Thus, delayed exposure to infection may increase risk of EBV‐positive HL in young adults, but risk patterns differ in younger and older women for both EBV‐positive and ‐negative HL. Late EBV infection does not appear relevant to risk, suggesting that other pathogens impact HL etiology in affluent female populations. Inconsistency of findings with prior studies may reflect failure of study risk factors to proxy meaningful exposures, risk differences by gender, or selection or misclassification bias. Null findings for EBV‐negative HL indicate that etiologic models should be reconsidered for this common form. © 2005 Wiley‐Liss, Inc.


📜 SIMILAR VOLUMES


Non-Hodgkin's lymphoma in four children
✍ David Nadal; Rosmarie Caduff; Eva Frey; Shabir Hassam; Dieter R. Zimmermann; Jea 📂 Article 📅 1994 🏛 John Wiley and Sons 🌐 English ⚖ 668 KB

Background. Reports on lymphoid malignancy and its treatment in children infected with human immunodeficiency virus (HIV) are limited. Methods. Antibodies to Epstein-Barr virus (EBV) were detected by indirect immunofluorescence. DNA was extracted from peripheral blood lymphocytes or biopsy specimen

Childhood exposure to simian virus 40-co
✍ Eric A. Engels; Leonard H. Rodman; Morten Frisch; James J. Goedert; Robert J. Bi 📂 Article 📅 2003 🏛 John Wiley and Sons 🌐 French ⚖ 79 KB

## Abstract Persons with acquired immunodeficiency syndrome (AIDS) have increased risk for non‐Hodgkin's lymphoma (NHL). Recent studies have reported the detection of DNA sequences from simian virus 40 (SV40), a macaque polyomavirus that contaminated early poliovirus vaccines, in a large proportion

Epstein-Barr virus infection and associa
✍ Ohshima, Koichi; Suzumiya, Junji; Tasiro, Kotaro; Mukai, Yasuo; Tanaka, Tosihiro 📂 Article 📅 1996 🏛 John Wiley and Sons 🌐 English ⚖ 930 KB

Sixty cases of B-cell nodal nonHodgkin's malignant lymphoma (B-ML), and 46 cases of T-cell nodal lymphoma (T-ML) were surveyed for Epstein-Barr virus (EBV) genomes, RNA, and associated proteins. We used a Southern blot analysis, polymerase chain reaction (PCR), and EBV-encoded small RNA-1 (EBER-1) i

Composite Hodgkin's and Non-Hodgkin's ly
✍ Jeannette Guarner; Carlos Del Rio; Lynn Hendrix; Elizabeth R. Unger 📂 Article 📅 1990 🏛 John Wiley and Sons 🌐 English ⚖ 520 KB

A 44-year-old man infected with human immunodeficiency virus had Hodgkin's disease, mixed cellularity, and malignant non-Hodgkin's lymphoma, diffuse large cell type. Colorimetric in-situ hybridization showed the Epstein-Barr virus (EBV] genome in the cells of the large cell non-Hodgkin's lymphoma an