In breast cancer subtypes steroid sulfatase (STS) is associated with less aggressive tumour characteristics

Keely M McNamara1, Fouzia Guestini2, Torill Sauer3,4

  • 1Department of Anatomic Pathology, School of Graduate Medicine, Tohoku University Japan, Sendai, Japan. kmcnamara@patholo2.med.tohoku.ac.jp.

Abstract

Insights

Steroid sulfatase (STS) expression in breast cancer is linked to reduced metastasis and improved survival, particularly in HER2-positive subtypes. This suggests STS plays a crucial role in breast cancer prognosis and endocrine resistance.

Area of Science:

  • Oncology
  • Endocrinology
  • Molecular Biology

Background:

  • Most breast cancers (BC) are steroid-dependent, often treated with hormonal therapy targeting aromatase or estrogen receptor alpha.
  • Alternative steroid action pathways exist but their links to BC subtypes and outcomes require further investigation.

Purpose of the Study:

  • To investigate the role of selected steroid receptors and estrogen pathways in breast cancer.
  • To correlate these factors with clinical outcomes including metastasis, relapse, and survival.

Main Methods:

  • Evaluated androgen receptor, estrogen receptor alpha/beta, glucocorticoid receptor, steroid sulfatase (STS), 17β-hydroxysteroid dehydrogenase 2 (17βHSD2), and aromatase in 139 Norwegian BC cases.
  • Utilized logistic and Cox regression analysis to examine associations with clinical outcomes.

Main Results:

  • STS expression significantly impacted distant metastasis risk (p<0.001), local relapse risk (p<0.001), HER2 subtype (p<0.015), and survival (p<0.001).
  • 17βHSD2 showed inverse, though non-significant, trends, suggesting potential benefits from alternative estrogen synthesis pathways.

Conclusions:

  • Increased intratumoral estrogen metabolism via STS correlates with lower relapse rates and better prognosis.
  • STS enrichment in HER2-overexpressing subtypes is notable, potentially influencing endocrine resistance mechanisms.

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