Malignant transformation of abdominal wall endometriosis: a case report and literature review

Current evidence indicates that abdominal wall endometriosis (AWE) arises from iatrogenic causes, such as surgical dissemination of endometrial cells with an estimated incidence of 0.29–1.08% (1,2), and noniatrogenic mechanisms. The latter chiefly include Sampson’s theory of retrograde menstruation with subsequent implantation, wherein disease progression depends on permissive local immune and inflammatory microenvironments, and the Müllerian remnant hypothesis, which explains extrapelvic lesions via embryonic cell differentiation. Its malignant transformation is hypothesized to correlate with iron-dependent oxidative stress-induced genomic damage (3), while prolonged estrogen exposure and obesity are recognized as significant risk factors. The predominant histological subtypes of malignant AWE include clear cell carcinoma and endometrioid carcinoma. Clinically, malignant AWE primarily manifests as abdominal pain and palpable masses, occasionally accompanied by localized swelling, exudation, or ulceration (4). However, these nonspecific symptoms often lead to delayed diagnosis. Imaging modalities such as ultrasonography and magnetic resonance imaging (MRI) play pivotal roles in delineating lesion extent and differentiating benign from malignant entities, with MRI particularly excelling in characterizing tumor biology, infiltration depth, and spatial distribution, thereby informing prognostic evaluation and therapeutic planning (5). Therapeutic management centers on radical surgical resection combined with hysterectomy and bilateral salpingo-oophorectomy, supplemented by abdominal wall reconstruction when indicated (6). Paclitaxel-carboplatin regimens are effective at controlling metastasis and recurrence, although radiotherapy has limited therapeutic value. The prognosis remains suboptimal, with a median survival of 26–30 months (6,7), necessitating rigorous postoperative surveillance: quarterly follow-ups for the first 2 years, transitioning to biannual evaluations thereafter (4). Early detection of rapidly enlarging abdominal masses and adherence to standardized treatment protocols are critical determinants of clinical outcomes. The particularity of this case lies in the fact that a standard R0 procedure was not performed initially, leaving the status of pelvic organs unclear. The patient-maintained tumor-free status for 19 months during chemotherapy, achieving a recurrence interval consistent with literature reports. Subsequently, pulmonary recurrence was detected. This represents the first reported case of AWE malignant transformation recurring to the lungs with negative findings in both lymph nodes and the primary site. Currently, clinicians often struggle to promptly and accurately identify the malignant transformation of AWE, and there is a lack of authoritative consensus on its management in the academic community. Our study describes a distinctive case of clear cell carcinoma arising from the abdominal wall and attempts to summarize key aspects regarding its mechanisms, diagnosis, and treatment. We present this article in accordance with the CARE reporting checklist (available at https://gpm.amegroups.com/article/view/10.21037/gpm-2025-1-57/rc). Case presentation Main complaint: a palpable lower abdominal mass for 1 month. In May 2024, a 48-year-old female was first presented to our institution with a progressively enlarging lower abdominal mass over 1 month. She had not detected any mass in this area over the past decades. Her obstetric history included two pregnancies, one live birth, and alower uterine segment transverse cesarean section performed 20 years ago. The patient had no history of prior surgeries and no family history of gynecological cancer. Physical examination revealed an irregular, immobile, firm mass (12 cm × 10 cm × 7 cm) at the midline lower abdomen, with ill-defined margins, mild tenderness, and no erythema or signs of intestinal obstruction. Serological evaluation showed elevated tumor markers: cancer antigen 125 (CA125) was 98.6 U/mL (normal <35 U/mL) and human epididymis protein 4 (HE4) was 74.9 pmol/L (normal <70 pmol/L), whereas cancer antigen 19-9 (CA19-9) was 22.1 U/mL, within its normal limit (<37 U/mL). Contrast-enhanced computed tomography (CT) imaging revealed multiple cystic hypodense lesions within the bilateral rectus abdominis muscles, measuring 11.03 cm × 7.64 cm, with septations and no contrast enhancement (Figure 1). Eleven days after the first visit, the patient underwent radical resection, mesh hernioplasty, and abdominal wall reconstruction. Intraoperative exploration revealed an aggressively infiltrating 15 cm × 15 cm irregular mass extending from the umbilicus superiorly to the pubic symphysis inferiorly, with lateral margins reaching the anterior axillary lines. The lesion was located beneath the anterior rectus sheath, communicated with the peritoneal cavity, and demonstrated adhesions to small bowel loops and the omentum. The mass was freed, and a 5-mm negative margin around the lesion was ensured. The mass was completely excised along with partial removal of the anterior rectus sheath, rectus abdominis muscle, posterior rectus sheath, and peritoneum. Adhesions between the mass capsule and the small intestine and omentum were dissected, without resection of the small intestine or omentum. Whereas not all of the adherent portions were malignant, the mass was completely removed. Postresection biological mesh reinforcement was applied to the posterior rectus sheath. Histopathological analysis of the gray-yellow nodular mass (14 cm × 13 cm × 7 cm) revealed a cystic-solid architecture with cellular atypia and focal clear cytoplasm. Immunohistochemical staining revealed hepatocyte nuclear factor-1β (HNF-1β) (positive), Napsin A (focal+), cytokeratin (CK)7/CK (positive), Wilms tumor-1 (WT-1) (focal+), estrogen receptor (ER) (focal+), p53/p16/paired box gene 8 (PAX-8) (positive), and Ki-67 (40%+), collectively supporting a diagnosis of clear cell carcinoma with likely gynecologic origin (Figure 2). The pathological results were reviewed by three pathologists (initial review, final review, and S.L.). Postoperatively, the patient received six cycles of 21 days of chemotherapy comprising albumin-bound paclitaxel (300 mg), carboplatin (600 mg), bevacizumab (500 mg), and sintilimab (200 mg). No adverse events or accidents occurred during the treatment process. Serial tumor marker monitoring (Figure 3) demonstrated normalization of CA125 after resection, with sustained levels throughout treatment. HE4 re-elevation occurred prior to the fourth cycle but subsequently normalized. Hemoglobin, white blood cell, and platelet levels remained stable within 1 year after surgery (Figure 4). No abnormalities were detected on CT during the fourth cycle or at 1 year postoperatively (Figure 1A,1B). However, 19 months after the surgery, which was 13 months after completing chemotherapy, the patient was found to have suspected recurrence and lung metastases during a follow-up CT scan (Figure 1C,1D). We have created a timeline of the patient’s key clinical events, including the initial consultation, first surgery, diagnosis, chemotherapy, follow-up examinations, and disease recurrence (Figure 5). All procedures performed in this study were in accordance with the ethical standards of the institutional and/or national research committee(s) and with the Declaration of Helsinki and its subsequent amendments. Written informed consent was obtained from the patient for publication of this case report and accompanying images. A copy of the written consent is available for review by the editorial office of this journal.

This case provides several important clinical insights. For women with a history of cesarean section or pelvic surgery, the development of a new abdominal wall mass should raise suspicion of malignant transformation of AWE. Given the absence of unified diagnostic criteria for this condition, clinicians should adopt a comprehensive diagnostic approach incorporating medical history, imaging studies, and pathological examination—with pathological evaluation being particularly crucial for atypical abdominal wall masses. Although no specific serological markers exist, elevated CA125 and HE4 levels may provide valuable clues regarding disease progression. The pathological diagnosis of this patient was consistent with the Sampson and Scott criteria for malignant transformation of endometriosis. The optimal management strategy involves radical surgical resection whenever possible, followed by combination therapy with chemotherapy, targeted agents, and immunotherapy, along with standardized follow-up protocols to effectively prolong patient survival. In order to better illustrate AWE malignant transformation, we have compiled a table summarizing previously reported cases (Table 1). Malignant transformation of AWE, particularly clear cell carcinoma, represents an aggressive yet relatively uncommon disease entity. Complete resection of the abdominal wall mass followed by adjuvant chemotherapy with paclitaxel and carboplatin remains the cornerstone of standard management; however, the risk of post-treatment recurrence is considerable. In recent years, the incorporation of targeted agents such as bevacizumab or immune checkpoint inhibitors, including programmed cell death protein 1 (PD-1) inhibitors like sintilimab, has demonstrated encouraging therapeutic potential. These novel approaches may offer new avenues for improving clinical outcomes and extending patient survival. Table 1 | Case | Age (years) | Chief complaint | Pathological | Treatment strategy | Clinical outcome | Reference | |---|---|---|---|---|---|---| | 2003 | 56 | AM | CCC | AWM-Ex, CT with platinum | Died 24m post-CT | (8) | | 2006 | 45 | AM | CCC | AWM-Ex, BSO, TC-CT | Died 6m post-op | (9) | | 2008 | 38 | AM | CCC | AWM-Ex, TAH, BSO, OM, TC-CT | Lymph node metastasis 8m post-op | (10) | | 2009 | 53 | AM, ASP | CCC | AWM-Ex, TAH, BSO, OM, TC-CT | Died 11m post-diagnosis | (11) | | 2010 | 59 | AM | Papillary serous carcinoma | NACT with platinum, AWM-Ex, TAH, BSO, CT, RT | No evidence of disease 12m post-op | (12) | | 2010 | 43 | AM | CCC | AWM-Ex, TAH, BSO, TC-CT, RT | Died 22m post-diagnosis | (13) | | 2012 | 51 | AM | CCC | AWM-Ex, BSO, RT | No evidence of disease 31m post-CT | (14) | | 2015 | 45 | AM | CCC | AWM-Ex | No evidence of disease 16m post-op | (15) | | 2015 | 47 | AM | CCC | AWM-Ex, BSO, OM, TC-CT | No evidence of disease 10m post-CT | (16) | | 2015 | 41 | Vaginal bleeding, AP | CCC | AWM-Ex, TAH, BSO, POM, TC-CT | R 6m post-CT, complete response after RT | (17) | | 2015 | 57 | ASP | CCC | AWM-Ex, TAH, BSO, TC-CT, RT | No evidence of disease post-CT | (17) | | 2017 | 47 | AM, pelvic pain | CCC | AWM-Ex, BSO, TC-CT | R 9m post-CT, salvage TAH and TC-CT, no evidence of disease 36m post-second operative | (18) | | 2017 | 48 | AM, cyclical AP resolved | Serous adenocarcinoma | TC-NACT, AWM-Ex, TAH, BSO, OM, TC-CT | R during cycle 6 CT | (19) | | 2019 | 48 | AM | CCC | AWM-Ex, TAH, BSO, OM, TC-CT | No evidence of disease post-cycle 4 CT | (20) | | 2020 | 45 | AM, pelvic pain | CCC | CT with TC/doxorubicin/gemcitabine | Died 7m post-diagnosis | (21) | | 2022 | 46 | AM, AP | CCC | AWM-Ex, TAH, BSO, TC-CT | No evidence of disease 32m post-CT | (22) | | 2022 | 57 | AM, AP | CCC | AWM-Ex, BSO, TC-CT | R with lymph node metastasis during cycle 6 CT | (22) | | 2023 | 48 | AM, ASP | CCC | AWM-Ex, CT with platinum, RT | No evidence of disease 12m post-CT | (23) | | 2024 | 50 | AM, cyclical AP | CCC | AWM-Ex, NACT with paclitaxel/adriamycin/cisplatin, pembrolizumab, alpelisib, everolimus | No evidence of disease 24m post-CT | (24) | | 2024 | 46 | Right flank pain, abdominal discomfort | CCC | AWM-Ex, BSO, TC-CT, bevacizumab, RT | No evidence of disease 6m post-CT | (25) | | 2025 | 48 | AM | CCC | AWM-Ex, TC-CT, bevacizumab, sintilimab | R 13m post-CT | – | AM, abdominal mass; AP, abdominal pain; ASP, abdominal scar pain; AWE, abdominal wall endometriosis; AWM-Ex, abdominal wall mass excision; BSO, bilateral salpingo-oophorectomy; CCC, clear cell carcinoma; CT, chemotherapy; m, month; NACT, neoadjuvant chemotherapy; OM, omentectomy; POM, partial omentectomy; post-op, post-operative; R, recurrence; RT, radiotherapy; TAH, transabdominal hysterectomy; TC, paclitaxel + carboplatin; TC-CT, paclitaxel + carboplatin chemotherapy. Endometriosis is a gynecological disorder that is pathologically defined by the presence of endometrial tissue outside the uterine cavity and is characterized by estrogen dependence, high recurrence rates, and malignant transformation potential. While predominantly affecting pelvic structures (e.g., ovaries and uterosacral ligaments), it may exceptionally manifest at cesarean section scars as AWE (26). Current evidence suggests that AWE can be attributed to both iatrogenic and non-iatrogenic factors. Surgical procedures may increase the likelihood of endometriosis in patients by spreading endometrial cells. Epidemiological studies have reported a 0.29–1.08% incidence of AWE following cesarean delivery (1,2). Malignant transformation is estimated to occur in 0.7% to 1.5% of all cases of endometriosis (27), and this event typically manifests approximately 21 years after the initial surgical procedure (7). Non-medical factors mainly include Sampson’s theory and Müllerian remnant hypothesis. Sampson’s theory is the most widely accepted hypothesis concerning the pathogenesis of endometriosis. It proposes that during menstruation, fragments of shed endometrial tissue may reflux through the fallopian tubes into the pelvic cavity, subsequently adhering to and implanting on the peritoneum or ovarian surface. Within an estrogen-dependent environment, these implants continue to proliferate, forming ectopic lesions (28). However, since retrograde menstruation is highly prevalent among women of reproductive age while only a subset develop the condition, contemporary research emphasizes the critical role of “soil” factors—such as impaired immune clearance, local inflammatory microenvironment, and genetic susceptibility—in disease onset. The Müllerian remnant hypothesis offers a complementary explanation for certain atypical forms of endometriosis, such as thoracic or nasal cases. This hypothesis suggests that residual Müllerian duct cells from embryonic development may disperse to pelvic or distant sites, where, under the influence of sex hormones and other stimuli, these pluripotent cells can differentiate into endometrium-like tissue, thereby giving rise to ectopic lesions (29). Obesity is recognized as a critical risk factor for endometriosis malignant transformation (30) and is mediated primarily through two mechanisms: surgical compromise due to adiposity-related impairment of uterine incision closure and inadequate subcutaneous irrigation, which increases the risk of endometrial cell implantation, and estrogen biosynthesis driven by adipose-derived aromatase activity, which converts androgens to estrogens, thereby inducing atypical hyperplasia within AWE lesions. Additional risk factors include prolonged estrogen exposure, early-onset endometriosis diagnosis, and chronic disease duration (22). Clinically, malignant AWE primarily presents with abdominal pain and palpable masses (ranging from 3 to 25 cm) (27), occasionally accompanied by cyclic/irregular pain, localized hyperpigmentation, swelling, exudation, ulceration, or bleeding. Notably, classical endometriosis symptoms such as dysmenorrhea, dyspareunia, urinary urgency, and diarrhea are infrequent. There is a lack of specific serological biomarkers for the malignant transformation of AWE. Therefore, the early diagnosis of malignant transformation of AWE still faces numerous challenges in clinical practice (4). However, markedly elevated CA125 may indicate increased malignant potential in endometriosis (31). A serum CA125 level over 200 U/mL is often used as a cutoff for possible malignant transformation of ovarian endometriomas. The sensitivity of the CA125 level was lower in patients with abdominal wall endometriomas than in those with ovarian endometriomas. The sensitivity of serum CA125 for diagnosing abdominal wall endometriomas is reportedly only 21.43% (4). Furthermore, CA125 elevation is nonspecific and may also be correlated with other gynecologic or gastrointestinal malignancies, necessitating comprehensive differential diagnosis (32). In this case, CA125 was only slightly elevated at the initial onset of the disease. During postoperative monitoring and even with recent lung metastasis recurrence, CA125 levels have remained consistently within the normal range. In contrast, HE4 showed a more noticeable trend of variation, though it was only mildly above the normal range and exhibited no significant correlation with chemotherapy or recurrence milestones. Imaging plays an important role in the diagnosis and treatment of the malignant transformation of AWE. Ultrasonography serves as a first-line screening and surveillance tool due to its accessibility and cost-effectiveness, typically revealing iso-/hyperechoic masses within the abdominal wall soft tissue with peripheral vascularity (33); the presence of solid components within cystic AWE lesions should raise suspicion for malignancy. On CT and positron emission tomography (PET)/CT, malignant AWE typically manifests as irregularly shaped, heterogeneously enhancing masses on contrast imaging. MRI has emerged as the cornerstone for diagnostic evaluation, delineating precise tumor morphology and invasion depth. Malignant AWE on MRI presents as irregular masses infiltrating the adipose, fascial, and muscular layers, occasionally extending into the peritoneum. Characteristic signal patterns include hypointense/isointense on T1-weighted imaging, hyperintense on T2-weighted imaging, and restricted diffusion on diffusion-weighted imaging with reduced apparent dispersion coefficient values (34). Contrast-enhanced MRI further revealed septal enhancement within the lesions. Considering the differential diagnosis in MRI, preoperative differentiation between an abdominal wall hernia and an abdominal tumor is essential. Points for differentiation include: (I) MRI imaging characteristics: the presence of high-signal hemorrhagic foci on T1-weighted images (which remain high-signal on fat-suppressed sequences) serves as strong evidence suggestive of an endometriotic origin (35). The direct visualization of hernia contents, such as bowel loops or omental fat, is a definitive imaging feature for diagnosing a hernia. (II) Assessment of tumor aggressiveness: for masses suspected of malignant transformation or sarcoma, MRI must meticulously describe the extent of invasion into surrounding structures, including the skin, muscle layers, peritoneum, and deeper tissues. This assessment is crucial for surgical planning (36). Histopathologically, AWE malignancies predominantly manifest as clear cell carcinoma (50%) and endometrioid carcinoma (30%) (10). AWE-associated clear cell carcinoma (AWECC) exhibits tubular-cystic, papillary, or solid architectures and is often admixed. Histologic hallmarks include flattened eosinophilic “hobnail cells” with moderate-to-severe cytologic atypia (34). Immunohistochemical profiling has revealed positivity for HNF-1β, Napsin A, alpha-methylacyl-CoA racemase, cytokeratin 7, and p53 (37). Endometrioid carcinoma is characterized by labyrinthine or cribriform glandular structures lined by stratified columnar epithelial and an ithelium with pseudostratified nuclei and moderate atypia. Destructive stromal invasion and inflammatory infiltrates are frequently observed (34). Immunoreactivity for p53, cyclin-dependent kinase inhibitor 2A (p16), phosphatase and tensin homolog (PTEN), and insulin-like growth factor II messenger RNA (mRNA)-binding protein 3 (IMP-3) supports this diagnosis (27). The key genomic alterations in these cancers include frequent co-occurring mutations in ARID1A [a switch/sucrose non-fermentable (SWI/SNF) complex subunit] and PI3K pathway changes. Recent evidence also implicates PTEN inactivation in early malignant transformation and deficient mismatch repair (MMR) status in pathogenesis (38). Wepy et al. suggested that Napsin A was identified as a risk factor for EAOC. Their sequencing analysis revealed pathogenic variants in genes including ATM, BRCA2, KRAS, AKT, CTNNB1, PTEN, and ARID1A. TP53 was wild-type in all cases, and MMR proficiency was maintained (39). The diagnostic criteria for malignant transformation of endometriosis were established by Sampson and Scott between 1925 and 1953 and require four key elements: histologic continuity between endometriosis and malignant lesions, absence of primary tumors at other sites, histologic consistency with endometrial origin, and coexistence of tumor and endometrial tissues within the same lesion (40,41). The therapeutic management of AWE-associated malignanciesremains non-standardized due to their rarity; although current case reports predominantly advocate radical surgical resection combined with chemotherapy, it has been recommended that achieving a negative margin of 5–10 mm is typically considered adequate (27). Given frequent large tumor dimensions (3–20 cm) (4), abdominal wall reconstruction via myocutaneous flaps or mesh augmentation is often needed, alongside routine hysterectomy and bilateral salpingo-oophorectomy to eliminate estrogen-driven progression. Inguinal lymphadenectomy is indicated for radiologically confirmed nodal metastasis, as inguinal nodes represent the most common metastatic site. For patients who are not candidates for radical resection, neoadjuvant chemotherapy may be considered. This approach not only reduces the size of the lesion, making surgery safer and more conducive to complete tumor removal, but also helps control micrometastases that are difficult to detect through imaging, thereby lowering the risk of postoperative recurrence and distant metastasis. The adjuvant chemotherapy regimen typically consisted of taxane combined with carboplatin, which mirrors the standard treatment for epithelial ovarian cancer (27). First-line chemotherapy includes 6‒8 cycles of paclitaxel-carboplatin regimens (42). However, systemic chemotherapy primarily suppresses metastatic spread with limited efficacy against local recurrence (21,22), whereas radiotherapy shows minimal benefit (42). Currently, there is no direct strong evidence supporting the use of immunotherapy and targeted therapy for the malignant transformation of AWE. However, similar studies on ovarian clear cell carcinoma and endometriosis-associated clear cell carcinoma have provided indirect evidence that combination therapy with vascular endothelial growth factor A (VEGF-A) and PD-1 inhibitors may offer clinical benefit (43,44). Based on this rationale, we administered sintilimab and bevacizumab to this patient. The prognosis for AWECC remains dismal, with median survival ranging from 26.1 to 30 months across studies (6,7). The overall prognosis for malignant transformation of AWE is poor, characterized by a high recurrence rate, with the majority of relapses occurring within 2 years after surgery (4), approximately one quarter of women died within 13 months of diagnosis (45). In clinical practice, a multimodal therapy centered on surgical resection and combined with chemotherapy is the standard approach. However, due to limitations in the available data, it has not been quantitatively demonstrated that this multimodal treatment significantly improves survival compared to surgery alone. The Multidisciplinary Team is also essential for formulating a personalized and sequential treatment plan, particularly in determining the optimal order of surgery and systemic therapy (21). Current follow-up protocols recommend quarterly evaluations for 2 years postoperatively, transitioning to semiannual assessments thereafter (4). Prognostic factors may be related to platinum resistance. Other factors include locally advanced stage, tumor size, endometriosis-related clear cell carcinoma (compared with endometrioid carcinoma), and tumor grade, all of which are associated with a poor prognosis (27). In addition to the abdominal wall, endometriosis has also been found to involve the intestines, liver, and lungs. Intestinal endometriosis can cause bowel obstruction when it penetrates the full thickness of the intestinal wall and may also undergo malignant transformation (46). The majority of intestinal endometriosis occurs in the sigmoid colon and rectum, with a smaller portion found in the ileum and cecum. In the latter, the tumor types are often sarcomas or mixed Müllerian tumors, rather than the endometrioid carcinomas commonly seen in colorectal sites. Common symptoms of intestinal endometriosis include abdominal or pelvic pain, melena, and abdominal or pelvic masses (47). Malignant transformation of intestinal endometriosis can be easily confused with primary colorectal cancer, but differentiation can be achieved using markers such as CK7, CK20, caudal type homeobox 2 (CDX2), CD10, ER, and progesterone receptor (PR) (48). Pulmonary endometriosis typically manifests as recurrent hemoptysis, chest pain, dyspnea, spontaneous pneumothorax, and hemothorax that coincide with the menstrual cycle. Its characteristic pathological features include ectopic endometrial glands, stroma, and hemosiderin deposits (49). Hepatic endometriosis often presents as abdominal pain. Its imaging features and specific clinical symptoms vary widely, making preoperative diagnosis challenging. For treatment, patients typically undergo cystectomy or various degrees of liver resection (50). This case report has certain limitations. First, it is a singlecase, singlecenter report and therefore lacks largesample data. Second, although followup results showing pulmonary metastasis 13 months after completion of chemotherapy have been obtained, the treatment strategy for this recurrence has not yet been explored.

In this case, the patient was not definitively diagnosed with AWECC before surgery and was not initially treated by the gynecology department. The hernia surgeon also did not examine the gynecological organs, which led to the inability of gynecologists during postoperative consultation to determine whether the abdominal wall mass originated from the uterus or adnexa. The purpose of presenting this case is to remind physicians not to overlook the possibility of malignant transformation in AWE in similar scenarios. The key insight of this article is that, because no gynecologist was involved during the patient’s initial surgery, the standard surgical procedure for malignant AWE was not performed (this also constitutes a major difference from other cases). The subsequent treatment of this patient described in our case, including combination chemotherapy with paclitaxel and carboplatin, experimental targeted therapy and immunotherapy represented by bevacizumab and sintilimab, as well as the close follow-up plan, may provide references for the treatment and follow-up of similar cases. Research limitationspersist due to the scarcity of AWE malignancy cases, necessitating future efforts to consolidate case data and extrapolate insights from extrapelvic endometriosis to optimize prevention, diagnosis, and therapeutic strategies. Acknowledgments None. Footnote Reporting Checklist: The authors have completed the CARE reporting checklist. Available at https://gpm.amegroups.com/article/view/10.21037/gpm-2025-1-57/rc Peer Review File: Available at https://gpm.amegroups.com/article/view/10.21037/gpm-2025-1-57/prf Funding: The study was supported by Conflicts of Interest: All authors have completed the ICMJE uniform disclosure form (available at https://gpm.amegroups.com/article/view/10.21037/gpm-2025-1-57/coif). The authors have no conflicts of interest to declare. Ethical Statement: The authors are accountable for all aspects of the work in ensuring that questions related to the accuracy or integrity of any part of the work are appropriately investigated and resolved. All procedures performed in this study were in accordance with the ethical standards of the institutional and/or national research committee(s) and with the Declaration of Helsinki and its subsequent amendments. Written informed consent was obtained from the patient for publication of this case report and accompanying images. A copy of the written consent is available for review by the editorial office of this journal. Open Access Statement: This is an Open Access article distributed in accordance with the Creative Commons Attribution-NonCommercial-NoDerivs 4.0 International License (CC BY-NC-ND 4.0), which permits the non-commercial replication and distribution of the article with the strict proviso that no changes or edits are made and the original work is properly cited (including links to both the formal publication through the relevant DOI and the license). See: https://creativecommons.org/licenses/by-nc-nd/4.0/.

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Malignant transformation of abdominal wall endometriosis: a case report and literature review. Gynecol Pelvic Med 2026;9:40.