Background <p>Human papillomavirus (HPV) has been investigated as a potential risk factor in breast cancer, but the literature remains inconsistent. Although biological mechanisms involving HPV <i>E6/E7</i> oncogene activity provide biological plausibility for viral involvement, reproducible evidence in breast tumors is lacking. This study aimed to determine whether high-risk HPV is detectable or transcriptionally active in breast cancer tissues from young women negative for <i>BRCA1/BRCA2</i> mutations.</p> Methods <p>This retrospective, single-center study included women younger than 50 years with confirmed <i>BRCA1</i>/<i>BRCA2</i>-negative breast cancer. Formalin-fixed, paraffin-embedded tumor specimens were analyzed for high-risk HPV DNA using a PCR-based assay targeting HPV-16, HPV-18, and pooled high-risk genotypes. A subset of tumors with sufficient residual FFPE material and laboratory acceptance for FFPE-based RNA testing also underwent high-risk HPV <i>E6/E7</i> mRNA analysis to assess transcriptional activity.</p> Results <p>Ninety women contributed 91 breast cancer specimens. Demographic, reproductive, and pathological features were consistent with typical early-onset breast cancer. High-risk HPV DNA was not detected in any tumor specimen. All mRNA analyses were also negative, indicating absence of transcriptionally active viral oncogene expression.</p> Conclusions <p>High-risk HPV was neither detectable nor transcriptionally active in breast cancer tissues from young <i>BRCA1/BRCA2</i>-negative women. These findings do not support a role for high-risk HPV in breast carcinogenesis in this population.</p>

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Absence of high-risk human papillomavirus in breast cancer tissues from young BRCA1/BRCA2-negative women

  • Eren Kaya,
  • Edis Kahraman,
  • Akif Enes Arikan,
  • Fatma Tokat,
  • Cihan Uras,
  • Serkan Erkanlı

摘要

Background

Human papillomavirus (HPV) has been investigated as a potential risk factor in breast cancer, but the literature remains inconsistent. Although biological mechanisms involving HPV E6/E7 oncogene activity provide biological plausibility for viral involvement, reproducible evidence in breast tumors is lacking. This study aimed to determine whether high-risk HPV is detectable or transcriptionally active in breast cancer tissues from young women negative for BRCA1/BRCA2 mutations.

Methods

This retrospective, single-center study included women younger than 50 years with confirmed BRCA1/BRCA2-negative breast cancer. Formalin-fixed, paraffin-embedded tumor specimens were analyzed for high-risk HPV DNA using a PCR-based assay targeting HPV-16, HPV-18, and pooled high-risk genotypes. A subset of tumors with sufficient residual FFPE material and laboratory acceptance for FFPE-based RNA testing also underwent high-risk HPV E6/E7 mRNA analysis to assess transcriptional activity.

Results

Ninety women contributed 91 breast cancer specimens. Demographic, reproductive, and pathological features were consistent with typical early-onset breast cancer. High-risk HPV DNA was not detected in any tumor specimen. All mRNA analyses were also negative, indicating absence of transcriptionally active viral oncogene expression.

Conclusions

High-risk HPV was neither detectable nor transcriptionally active in breast cancer tissues from young BRCA1/BRCA2-negative women. These findings do not support a role for high-risk HPV in breast carcinogenesis in this population.