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Infectious Agents and Cancer

Genetic study links Epstein-Barr antibodies to prostate cancer

Across three datasets, genetically predicted antibody levels were linked to higher prostate cancer odds, with a pooled odds ratio of 1.074, versus 1 for no association.

Paper by Haojian Zhang, Ting Xiao
Figure 1 from Infectious Agents and Cancer
Open the figure at full size
Figure 1. Zhang et al., CC BY-NC-ND

Our read

Populations
Studied:
Mendelian randomization in prostate cancer cases and controls
What changed:
Higher Epstein-Barr antibody levels were linked to higher prostate cancer risk (odds ratio 1.074)
The catch:
The Epstein-Barr association did not survive correction for testing 37 traits

Editor of record: Boris Djordjevic · AgingResearch.News

Paper
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People with and without prostate cancer contributed genetic data to a two-sample Mendelian randomization analysis. The datasets included 79,148 cases and 61,106 controls in PRACTICAL; 15,199 cases and 131,266 controls in FinnGen; and 122,188 cases and 604,640 controls in Wang 2023’s European-ancestry subset. The analysis used inherited DNA differences as stand-ins for blood levels of antibodies, immune proteins that recognize infections.

Higher genetically predicted antibody levels against an Epstein-Barr virus protein were linked to higher prostate cancer odds in all three datasets. However, this association did not pass the stricter statistical threshold accounting for testing 37 measures. Only two polyomavirus signals passed: evidence of Merkel cell polyomavirus infection was linked to lower odds, and evidence of BK polyomavirus infection to higher odds. The authors regarded all findings as hypothesis-generating.

Why it matters

Prostate cancer is an age-related disease. The authors identified persistent Epstein-Barr infection as a candidate cause, offering a hypothesis about what may contribute to its development.

Caveats

The analysis used genetic stand-ins for infection-related blood measures, leaving open whether infection itself accounts for the cancer links.

Where the evidence stands

Cytomegalovirus infection

Humans: replicated by independent labs. Cells, worms or flies and mice: nothing yet.

C, W, M, H: cells, worms or flies, mice, humans. Dark: independent labs found the same change there. Light: one lab or one study. Outline: nothing yet.

Labs are independent when their papers share no last author and no institution.

Against: findings that point the other way from most findings on the same outcome.

Company ties: findings with an author at a company, or from a paper whose competing-interests statement declares ties to one.

  • 32 independent labs in 17 countries
  • 2 findings against
  • Funders: European Commission and others
  • 13 of 72 findings with company ties

From the paper

Result

… with a cross-cohort random-effects meta-analytic OR of 1.074 (95% CI 1.034–1.115, P = 2.1 × 10-4, I2 = 0%), and in the fully independent PRACTICAL + FinnGen meta-analysis (OR = 1.084, P = 0.002).

Results

Quoted word for word from the full text on link.springer.com.

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