CLINICAL RESEARCH
Expression of visfatin, lipocalin-2, adiponectin, and chemerin in breast cancer and their association with clinicopathological parameters
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1
Breast Unit, Department of General Surgery, University Hospital of Patras, Rio, Greece
2
Department of Cardiothoracic and Vascular Surgery, Westpfalz-Klinikum, Kaiserslautern, Germany
3
Department of Anatomy-Histology-Embryology, School of Medicine, University of Patras, Rio, Greece
4
Department of Pathology, University Hospital of Patras, Rio, Greece
These authors had equal contribution to this work
Submission date: 2025-08-31
Final revision date: 2025-11-05
Acceptance date: 2025-12-19
Publication date: 2026-01-15
Corresponding author
Vasileios Leivaditis
Department of
Cardiothoracic and
Vascular Surgery
Westpfalz Klinikum
Kaiserslautern, Germany
Arch Med Sci Atheroscler Dis 2026;11(1):1-4
KEYWORDS
TOPICS
ABSTRACT
Introduction:
Breast cancer remains the most common malignancy in women worldwide, with prognosis influenced not only by tumor-intrinsic factors but also by the tumor microenvironment. Adipokines, including visfatin, lipocalin-2, adiponectin, and chemerin, have been increasingly implicated in breast cancer biology, influencing inflammation, metabolism, angiogenesis, and the tumor microenvironment (TME). However, their precise contribution to tumor progression and their association with common prognostic markers remain unclear. The expression patterns of these adipokines were evaluated in invasive ductal carcinoma and explored their relationship with established clinicopathological parameters.
Material and methods:
Breast cancer diagnosed cases were analyzed in 2018 at the University General Hospital of Patras. Immunohistochemistry was performed for visfatin, lipocalin-2, adiponectin, and chemerin. Marker expression was correlated with estrogen receptor (ER), progesterone receptor (PR), HER2/c-ERB2, Ki67, and lymphovascular invasion (LVI).
Results:
Visfatin and adiponectin both showed significant associations between high Ki67 and LVI (p = 0.0049 and p = 0.00044, respectively). In addition, ER negativity was linked to LVI for these two adipokines (p = 0.0175 for both). By contrast, lipocalin-2 did not show significant correlations, although borderline values for ER and PR suggested a possible trend.
Conclusions:
These findings point to visfatin and adiponectin as potential indicators of aggressive breast cancer phenotypes, while lipocalin-2 may follow a different biological trajectory. Larger, prospective studies are warranted to confirm these associations and clarify underlying mechanisms.
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