The Involvement of Gas6/sAXL Signaling Pathway in Patients with Idiopathic Granulomatous Mastitis

Abstract Background:Idiopathic granulomatous mastitis (IGM) is an uncommon, benign, chronic inflammatory breast disease. There are several hypotheses about the etiology of IGM. The interaction between growth arrest-specific protein 6 (Gas6)/Tyro, AXL, and Mer (TAM) affects the regulation of innate immune reactions and promotes the induction of phagocytosis and a reduction in proinflammatory cytokine expression. We analyzed the potential implications of the Gas6/sAXL signaling pathway, which is essential for the inflammatory response to the pathophysiology of IGM, the cause of which is yet unknown. Methods: This study included 37 patients. Nineteen of these patients achieved a complete response solely through medical treatment (Group R), while the remaining 18 comprised individuals who, following medical treatment, did not achieve a complete response and necessitated supplementary surgery (Group NR). Logistic regression analysis was used to define predictive factors. The optimal cutoff values of the predictive prognostic factors for resistance to treatment were identified using receiver operating characteristic (ROC) curve analysis. Results: No significant differences were detected between the two groups in terms of lesion size, age, parity, attack frequency, white blood cell count, presence of accompanying axillary lymphadenopathy (LAP), or smoking history (p>0.05). Significant differences were detected in terms of Gas6, sAXL, and the presence of accompanying abscess (p<0.05). Conclusions:Decreased Gas6 and sAXL levels can be explained by two mechanisms. Inflammation may have developed due to Gas6 deficiency. The finding that low Gas6 levels are an independent risk factor for IGM treatment resistance will be a new method for treating this disease.