This study investigates the clinical characteristics and local histopathological modulators of endometriosis (E) and adenomyosis (A), focusing on their progression and transformation. The research analyzed 243 patients, including 24.7% with normal uterine tissue (control group) and 75.3% with E/A lesions. The study used histochemical and immunohistochemical staining to assess symptoms, lesion structure, neovascularization, hormone receptors, inflammatory cells, and oncoproteins. Key findings include the presence of CK7+/CK20− expression in E foci, increased CD34+ neovascularization in malignant areas, and elevated Ki67+ cell proliferation in transformed lesions. The study also identified markers of a proinflammatory microenvironment, such as CD3+, CD20+, CD68+, and tryptase+ cells, which were more abundant in malignant cases. Tumor suppressor genes p53, BCL-2, and PTEN showed altered expression in malignant lesions. The study highlights the role of inflammatory, vascular, and hormonal factors in E/A progression, leading to cellular atypia and malignant transformation. These findings suggest that proinflammatory and vascular changes may serve as future therapeutic targets for managing E and A. The study also emphasizes the importance of histopathological analysis in diagnosing and understanding the progression of these conditions.This study investigates the clinical characteristics and local histopathological modulators of endometriosis (E) and adenomyosis (A), focusing on their progression and transformation. The research analyzed 243 patients, including 24.7% with normal uterine tissue (control group) and 75.3% with E/A lesions. The study used histochemical and immunohistochemical staining to assess symptoms, lesion structure, neovascularization, hormone receptors, inflammatory cells, and oncoproteins. Key findings include the presence of CK7+/CK20− expression in E foci, increased CD34+ neovascularization in malignant areas, and elevated Ki67+ cell proliferation in transformed lesions. The study also identified markers of a proinflammatory microenvironment, such as CD3+, CD20+, CD68+, and tryptase+ cells, which were more abundant in malignant cases. Tumor suppressor genes p53, BCL-2, and PTEN showed altered expression in malignant lesions. The study highlights the role of inflammatory, vascular, and hormonal factors in E/A progression, leading to cellular atypia and malignant transformation. These findings suggest that proinflammatory and vascular changes may serve as future therapeutic targets for managing E and A. The study also emphasizes the importance of histopathological analysis in diagnosing and understanding the progression of these conditions.