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Background <p>The process of transformation from Benign Prostatic Hyperplasia (BPH) to Prostate Cancer (PCa) is highly debatable; however, there is convincing information that it takes place in the background of inflammation. Multifocal high-grade prostatic intraepithelial neoplasia (HPIN), intraductal carcinoma (IDC-P), atypical intraductal proliferation (AIP), atypical adenomatous hyperplasia (AAH)/ adenosis, and proliferative inflammatory atrophy (PIA) are considered as precursor lesions during such transformation by Working Group 1 at the ISUP Cancer Precursors Meeting in September 2024. We specifically emphasize the need for further investigation of the inflammatory process, where stromal epithelial activity, angiogenesis, and mast cells are involved.</p> <p>In this study, we investigated the role of vascular endothelial growth factor (VEGF), and MCs during its progression from BPH to PCa. Additionally, we investigated the relationship between MCs and Gleason Grade Group (GG), as well as other prognostic variables.</p> Methods <p>Retrospectively, 100 PCa patients whose pathology included areas of BPH and multifocal HPIN close to cancerous tissue. All the specimens were stained with CD117 as an MC marker and VEGF to evaluate for angiogenesis. </p> Results <p>While there was overall intense MC infiltration in all areas of BPH in general, it was relatively less intense in areas of carcinomatous tissue. Nevertheless, MC infiltration intensified with higher GG. Similarly, with increasing MC infiltration in cancerous and HPIN tissues, VEGF staining also intensified, specifically in glandular areas. In HPIN areas, the relationship between MCs and VEGF was intermediate between BPH and cancerous areas, representing a progression.</p> Conclusion <p> Stromal changes, stromal-epithelial interactions, and coexisting inflammatory changes are important elements in the development of BPH and PCa. We specifically investigated the intratumoral MC population and glandular VEGF staining intensity with increasing GG; thus, assessing the role of MCs and VEGF in tumor progression towards cancer development. MCs and VEGF staining characteristics in HPIN areas emphasize the efficient role these elements play in the transition of tissues from BPH to HPIN and eventually to PCa.</p>

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Benign prostatic hyperplasia to HPIN to carcinoma; the impact of mast cells and VEGF

  • 期刊论文

  • 出版模式：

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  • 发表日期：

    2026年1月21日

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  • Oya Nermin Sivrikoz,
  • Aşkın Eroğlu,
  • Bilgin Öztürk,
  • İncila Öztop,
  • Salahattin M. Sanal

摘要

Background

The process of transformation from Benign Prostatic Hyperplasia (BPH) to Prostate Cancer (PCa) is highly debatable; however, there is convincing information that it takes place in the background of inflammation. Multifocal high-grade prostatic intraepithelial neoplasia (HPIN), intraductal carcinoma (IDC-P), atypical intraductal proliferation (AIP), atypical adenomatous hyperplasia (AAH)/ adenosis, and proliferative inflammatory atrophy (PIA) are considered as precursor lesions during such transformation by Working Group 1 at the ISUP Cancer Precursors Meeting in September 2024. We specifically emphasize the need for further investigation of the inflammatory process, where stromal epithelial activity, angiogenesis, and mast cells are involved.

In this study, we investigated the role of vascular endothelial growth factor (VEGF), and MCs during its progression from BPH to PCa. Additionally, we investigated the relationship between MCs and Gleason Grade Group (GG), as well as other prognostic variables.

Methods

Retrospectively, 100 PCa patients whose pathology included areas of BPH and multifocal HPIN close to cancerous tissue. All the specimens were stained with CD117 as an MC marker and VEGF to evaluate for angiogenesis.

Results

While there was overall intense MC infiltration in all areas of BPH in general, it was relatively less intense in areas of carcinomatous tissue. Nevertheless, MC infiltration intensified with higher GG. Similarly, with increasing MC infiltration in cancerous and HPIN tissues, VEGF staining also intensified, specifically in glandular areas. In HPIN areas, the relationship between MCs and VEGF was intermediate between BPH and cancerous areas, representing a progression.

Conclusion

Stromal changes, stromal-epithelial interactions, and coexisting inflammatory changes are important elements in the development of BPH and PCa. We specifically investigated the intratumoral MC population and glandular VEGF staining intensity with increasing GG; thus, assessing the role of MCs and VEGF in tumor progression towards cancer development. MCs and VEGF staining characteristics in HPIN areas emphasize the efficient role these elements play in the transition of tissues from BPH to HPIN and eventually to PCa.