Endometrial adenocarcinoma arising from adenomyosis: A case report and literature review.

[BACKGROUND] Endometrial carcinoma arising from adenomyosis (EC-AIA) is remarkably uncommon, and its underlying molecular mechanisms are not yet fully elucidated. This knowledge gap is particularly significant given that most reported EC-AIA cases are well-differentiated and hormone receptor-positive, creating a critical need to characterize the rare, aggressive variants and their clinical implications.

[OBJECTIVE] This study aims to address this gap by presenting a unique case of poorly differentiated endometrioid adenocarcinoma with adenomyosis, exploring their potential association, and to synthesize current understanding through literature review to inform clinical decision-making.

[CASE PRESENTATION] A 45-year-old woman with a history of adenomyotic lesion resection presented with abnormal uterine bleeding. Postoperative pathology confirmed poorly differentiated endometrioid adenocarcinoma (International Federation of Gynecology and Obstetrics IIIC2 stage), with immunohistochemistry showing estrogen receptor/progesterone receptor (PR) negativity, p53 mutation pattern, and nonspecific molecular profile. Concurrent adenomyosis (0.6 cm) was identified, though direct histological transition between adenomyosis and carcinoma was not established. The patient underwent cytoreductive surgery and platinum-based chemotherapy.

[DISCUSSION] Our analysis reveals that the relationship between adenomyosis and endometrial carcinoma remains debated. This case (characterized by high-grade histology, hormone receptor negativity, and widespread metastases) provides crucial evidence diverging from the classic EC-AIA profile (typically well-differentiated and hormone-sensitive), implying a distinct malignant transformation mechanism. These findings challenge the conventional understanding of EC-AIA and highlight the spectrum of its clinical presentations.

[CONCLUSION] This study underscores that the management of suspected malignant transformation of adenomyosis requires multidisciplinary evaluation. More importantly, our findings demonstrate that aggressive treatment should be initiated even without definitive pathological confirmation when clinical suspicion is high. The significance of this work lies in its contribution to recognizing the heterogeneous nature of EC-AIA, urging future research to focus on elucidating molecular mechanisms and developing personalized therapeutic strategies for these aggressive variants.