Surgical case reports · 2025
Sarcomatoid Carcinoma in a Resected Hepatic Metastasis of Esophageal Squamous Cell Carcinoma after Chemotherapy.
Клинический случайСтатьяНазвание и аннотация: Перевод в очереди
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Kimura Kotaro, Kinoshita Yoshihiro, Okada Naoya, Yamabuki Takumi, Kawaguchi Saki, Goto Chiho, Koyama Ryouto, Asai Yusuke, Naito Zen, Yamamoto Hiroyuki, Suzuki Tomohiro, Tsunetoshi Yusuke, Kyogoku Noriaki, Katagiri Hirokatsu, Kato Kentaro, Takada Minoru, Ambo Yoshiyasu, Omori Yuko
Аннотация
INTRODUCTION: Sarcomatoid carcinoma is a rare histological variant of carcinoma characterized by a mesenchymal-like morphology, often arising through the epithelial-mesenchymal transition. Although sarcomatoid carcinoma is occasionally observed in primary esophageal carcinosarcoma, its diagnosis at metastatic sites is rare.
CASE PRESENTATION: A man in his 60s was diagnosed with esophageal squamous cell carcinoma with synchronous liver and cutaneous metastases. A cutaneous nodule in the abdomen was surgically resected and pathologically confirmed to be metastatic squamous cell carcinoma. Owing to the unresectable nature of the tumor, the patient underwent 10 cycles of combined pembrolizumab and fluorouracil + cisplatin therapy, followed by 20 cycles of S-1 monotherapy owing to immune-related adverse events. This treatment resulted in a complete clinical response of the primary esophageal tumor and a significant reduction in most liver metastases. However, one liver metastasis in the left lateral segment exhibited progressive disease, requiring surgical resection. Pathological examination of the hepatic lesion revealed a well-demarcated lobulated tumor with necrosis and hemorrhage. Microscopically, the tumor comprised polygonal-to-short, spindle-shaped atypical cells with pleomorphism, frequent mitotic figures, and sinusoidal infiltration. Immunohistochemically, the hepatic lesion exhibited diffuse vimentin positivity, partial Cam5.2, and scattered INSM-1 expression, suggesting a mesenchymal transition of the carcinoma with partial neuroendocrine differentiation. CK AE1/AE3, CK5/6, and p40 were negative. p53 and BRM/SMARCA2 showed a complete loss of expression. A retrospective analysis of esophageal and cutaneous lesions revealed a progressive loss of BRM/SMARCA2 expression across different metastatic sites, supporting the hypothesis of epithelial-mesenchymal transition-driven transformation during hepatic metastasis. Despite surgical intervention, multiple hepatic recurrences were detected within 2 months postoperatively, highlighting the aggressive nature of sarcomatoid carcinoma and the limitations of surgery alone in controlling this disease.
CONCLUSIONS: This case highlights the rare phenomenon of histological transformation of squamous cell carcinoma to sarcomatoid carcinoma within a metastatic site, emphasizing the importance of surgical resection for both diagnosis and treatment. The loss of BRM/SMARCA2 may have contributed to the epithelial-mesenchymal transition-driven transformation and, together with neuroendocrine differentiation, may have played a role in the tumor's aggressiveness. Histological reassessment of chemotherapy-resistant lesions is crucial for elucidating tumor evolution and optimizing future therapeutic strategies.
CASE PRESENTATION: A man in his 60s was diagnosed with esophageal squamous cell carcinoma with synchronous liver and cutaneous metastases. A cutaneous nodule in the abdomen was surgically resected and pathologically confirmed to be metastatic squamous cell carcinoma. Owing to the unresectable nature of the tumor, the patient underwent 10 cycles of combined pembrolizumab and fluorouracil + cisplatin therapy, followed by 20 cycles of S-1 monotherapy owing to immune-related adverse events. This treatment resulted in a complete clinical response of the primary esophageal tumor and a significant reduction in most liver metastases. However, one liver metastasis in the left lateral segment exhibited progressive disease, requiring surgical resection. Pathological examination of the hepatic lesion revealed a well-demarcated lobulated tumor with necrosis and hemorrhage. Microscopically, the tumor comprised polygonal-to-short, spindle-shaped atypical cells with pleomorphism, frequent mitotic figures, and sinusoidal infiltration. Immunohistochemically, the hepatic lesion exhibited diffuse vimentin positivity, partial Cam5.2, and scattered INSM-1 expression, suggesting a mesenchymal transition of the carcinoma with partial neuroendocrine differentiation. CK AE1/AE3, CK5/6, and p40 were negative. p53 and BRM/SMARCA2 showed a complete loss of expression. A retrospective analysis of esophageal and cutaneous lesions revealed a progressive loss of BRM/SMARCA2 expression across different metastatic sites, supporting the hypothesis of epithelial-mesenchymal transition-driven transformation during hepatic metastasis. Despite surgical intervention, multiple hepatic recurrences were detected within 2 months postoperatively, highlighting the aggressive nature of sarcomatoid carcinoma and the limitations of surgery alone in controlling this disease.
CONCLUSIONS: This case highlights the rare phenomenon of histological transformation of squamous cell carcinoma to sarcomatoid carcinoma within a metastatic site, emphasizing the importance of surgical resection for both diagnosis and treatment. The loss of BRM/SMARCA2 may have contributed to the epithelial-mesenchymal transition-driven transformation and, together with neuroendocrine differentiation, may have played a role in the tumor's aggressiveness. Histological reassessment of chemotherapy-resistant lesions is crucial for elucidating tumor evolution and optimizing future therapeutic strategies.