4.6 Article

Parents' Ages at Birth and Risk of Adult-onset Hematologic Malignancies Among Female Teachers in California

期刊

AMERICAN JOURNAL OF EPIDEMIOLOGY
卷 171, 期 12, 页码 1262-1269

出版社

OXFORD UNIV PRESS INC
DOI: 10.1093/aje/kwq090

关键词

cohort studies; hematologic neoplasms; leukemia; myeloid; acute; lymphoma; non-Hodgkin; maternal age; paternal age

资金

  1. California Breast Cancer
  2. National Institutes of Health [R01 CA77398, K05 CA136967]
  3. California Breast Cancer Research Fund [97-10500]
  4. California Department of Public Health [103885]
  5. National Cancer Institute's Surveillance, Epidemiology, and End Results Program [N01-PC-35136, N01-PC-35139, N02-PC-15105]
  6. Cancer Registries [U55/CCR921930-02]

向作者/读者索取更多资源

Although advanced parental age at one's birth has been associated with increased risk of breast and prostate cancers, few studies have examined its effect on adult-onset sporadic hematologic malignancies. The authors examined the association of parents' ages at women's births with risk of hematologic malignancies among 110,999 eligible women aged 22-84 years recruited into the prospective California Teachers Study. Between 1995 and 2007, 819 women without a family history of hematologic malignancies were diagnosed with incident lymphoma, leukemia (primarily acute myeloid leukemia), or multiple myeloma. Multivariable-adjusted Cox proportional hazards models provided estimates of relative risks and 95% confidence intervals. Paternal age was positively associated with non-Hodgkin lymphoma after adjustment for race and birth order (relative risk for age >= 40 vs. < 25 years = 1.51, 95% confidence interval: 1.08, 2.13; P-trend = 0.01). Further adjustment for maternal age did not materially alter the association. By contrast, the elevated non-Hodgkin lymphoma risk associated with advanced maternal age (>= 40 years) became null when paternal age was included in the statistical model. No association was observed for acute myeloid leukemia or multiple myeloma. Advanced paternal age may play a role in non-Hodgkin lymphoma etiology. Potential etiologic mechanisms include de novo gene mutations, aberrant paternal gene imprinting, or telomere/telomerase biology.

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