Serum Oncostatin M Levels are Associated with Insulin Resistance and Clinical Severity in Iraqi Women with Breast Cancer: A Case-Control Study

Hussein Naeem Abd Ali; Hanaa Addai Ali

doi:10.31557/APJCC.2026.11.5.719

Authors

Hussein Naeem Abd Ali Department of Chemistry, Faculty of Science, University of Kufa, Najaf 54001 Iraq.
Hanaa Addai Ali Department of Chemistry, Faculty of Science, University of Kufa, Najaf 54001 Iraq.

DOI:

https://doi.org/10.31557/APJCC.2026.11.5.719

Keywords:

Breast cancer, Oncostatin, insulin resistance, Biomarkers, Metabolic Dysregulation, Iraqi population

Abstract

Introduction: Breast cancer (BC) is a diverse disease characterized by the uncontrolled growth of mammary cells, resulting in tumors with invasive and metastatic capabilities. The advancement of this disease is affected by intricate signaling networks, as Oncostatin (OSM) is a pleiotropic cytokine that regulates inflammation, proliferation, and differentiation. This study aimed to evaluate serum Oncostatin M (OSM) levels in Iraqi women with breast cancer and investigate its correlation with insulin resistance (IR) and disease progression across different clinical stages. Furthermore, the study explores the potential of the OSM pathway as a future therapeutic target.

Materials and Methods: In a case-control design, 90 newly diagnosed triple-negative BC patients (Stages I–IV) were compared with 90 age-matched healthy controls. Serum OSM and insulin were measured using ELISA, while fasting serum glucose (FSG) and liver enzymes (ALT, AST, ALP) were determined spectrophotometrically. Metabolic indices, including HOMA-IR, HOMA-β, and HOMA-S%, were calculated.

Results: Serum Oncostatin M (OSM) levels were significantly elevated in BC patients (120.46 ±pm 18.97 pg/ mL) compared to healthy controls (70.16 ±12.50 pg/mL; P < 0.001). A stepwise progressive increase in OSM was observed alongside advancing tumor stages (I–IV). BC patients exhibited marked metabolic and hepatic disruption, evidenced by significantly higher FSG, insulin, HOMA-IR, and liver enzymes, with a concomitant decrease in HOMA-S% (P < 0.001). Strong positive correlations were found between OSM and both HOMA-IR (r = 0.733) and insulin (r = 0.721). ROC analysis demonstrated excellent performance for OSM (AUC = 0.927), with 89.7% sensitivity and 84.3% specificity at an exploratory cut-off of 99.46 pg/mL.

Conclusion: Serum Oncostatin M (OSM) serves as a significant marker of progression in Iraqi women with breast cancer, correlating strongly with insulin resistance. Our findings highlight OSM as a key indicator of the metabolic-inflammatory axis; Further longitudinal studies are warranted to validate its potential as a therapeutic target.