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Hispanic Ethnicity Differences in Birth Characteristics, Maternal Birth Place, and Risk of Early-Onset Hodgkin Lymphoma: A Population-Based Case-Control Study
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9-02-
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Source: Cancer Epidemiol Biomarkers Prev. 31(9):1788-1795
Details:
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Alternative Title:Cancer Epidemiol Biomarkers Prev
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Personal Author:
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Description:Background:
Hispanic ethnicity differences in the risk of early-onset Hodgkin lymphoma (HL) diagnosed at < 40 years are understudied. We conducted a population-based case-control study to evaluate associations between birth characteristics and early-onset HL with a focus on potential ethnic differences.
Methods:
This study included 1,651 non-Hispanic White and 1,168 Hispanic cases with HL endorsing a range of races diagnosed at the age of 0-37 years during 1988-2015 and 140,950 controls without cancer matched on race/ethnicity and year of birth from the California Linkage Study of Early-Onset Cancers. Odds ratios (OR) and 95% confidence intervals (CI) were estimated from multivariable logistic regression models.
Results:
Having a foreign-born mother versus a United States-born mother (i.e., the reference group) was associated with an increased risk of early onset HL among non-Hispanic Whites (OR=1.52, 95% CI:1.31-1.76; P<0.01) and a decreased risk among Hispanics (OR=0.78, 95% CI:0.69-0.88; P<0.01). Among both race groups, risk of early onset HL increased with birthweight and maternal age (all P-trends<0.01). Among Non-Hispanic Whites, each 5-year increase in maternal age (OR = 1.11; 95% CI, 1.04-1.18; P-trend < 0.01) and paternal age (OR=1.07, 95% CI:1.02-1.13; P-trend=0.01) was associated with increased risk of early onset HL. Compared to female Hispanics, male Hispanics had an increased risk of early onset HL (OR =1.26, 95% CI:1.12-1.42; P<0.01).
Conclusion:
Maternal birthplace may play a role in risk of early-onset HL that differs by ethnicity.
Impact:
The ethnic differences observed between certain birth characteristics, maternal birthplace and early onset HL raise questions about the underlying biological, generational, lifestyle, residential, and genetic contributions to the disease.
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Pubmed ID:35709749
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Pubmed Central ID:PMC9444874
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