Abstract

Primary hepatic adenosquamous carcinoma (ASC) is a rare pathologic type of liver cancer. It is identified as a liver tumor containing both adenocarcinoma and squamous cell carcinoma originated from the same stem cell. ASC is considered to have a higher grade malignancy than primary hepatocellular carcinoma (HCC). Now, we reported such a case. A previously healthy 74-year-old woman presented with health checkup. The results of laboratory examinations were shown as below: carcinoembryonic antigen (CEA), 16.75 ng/mL, saccharide antigen 199 (CA199), 876.40 U/mL. Abdominal contrast-enhanced computed tomography showed a mass located in the left liver, and a space-occupying lesion was found in the left hepatic duct along with dilated distal bile ducts. The parenchyma of the lesion was obviously enriched after being potentiated. The hilar structure was clear and there was no evidence of lymph node metastasis or distant metastasis (Figure 1A). The patient then underwent left hemihepatic resection, cauda lobectomy, and intraperitoneal dissection. Histologic examination and immunohistochemical staining confirmed the diagnosis of left hepatic adenosquamous carcinoma (Figure 1B-D). Postoperative examination revealed the expression of CA199 was significantly reduced (73.00 U/mL), the results of CEA and biochemical examination were normal. After the operation, the patient did not receive subsequent therapy and died of tumor recurrence about 21 months later. ASC may arise from squamous metaplasia of adenocarcinoma cells. Some scholars believe that chronic inflammation and continuous stimulation of various congenital biliary cysts can cause metaplastic changes of the bile duct epithelium, which leads to the occurrence of liver ASC. Therefore, ASC of the liver is considered to be a rare subtype of cholangiocarcinoma (CCC).1 ASC can occur in lung, stomach, colon, gallbladder, pancreas, bladder, and uterus. It mostly occurs alone and always lacks specificity in clinical manifestations, such as abdominal pain, fever, jaundice, weight loss, and so on. Patients usually have no history of hepatitis or cirrhosis.2 ASC of the liver has typical pathological features.3 In general, tumor cells are arranged in nests, with some glandular tubular structures and keratinized beads. Cytoplasm is abundant, atypia and nuclear fission can be observed, which are consistent with the pathological features of our case. The serum tumor markers of primary hepatic squamous cell carcinoma (SCC)/ASC are significantly different from those of HCC patients. In some patients of ASC or SCC, CA199 has a relatively high expression. While alpha fetal protein (AFP), as a typical tumor marker of HCC, is seldom expressed. Therefore, tumor markers may provide reference for early detection and disease monitoring of hepatic ASC. At present, it is difficult to distinguish ASC from CCC, based solely on tumor indicators.4 Surgical excision is the preferred treatment when surgical conditions are available. In some cases, appropriate chemotherapy, radiotherapy, or biological therapy can be supplemented according to specific conditions.4 Compared with CCC, primary hepatic ASC is more resectable, but the overall prognosis is still poor due to the specific biological behavior of ASC.5 In our case, the result was still poor after aggressive therapy. The exact mechanism of rapid progression of ASC is still not clear and may be related to multi-influence factors such as malignant characteristics of tumors and postoperative negative treatment. Increasing the rate of early diagnosis often helps improve the prognosis of patients. The authors declare no potential conflict of interest.

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