A 78-year-old woman treated for colon cancer at another hospital was referred to our hospital for further evaluation of abnormal imaging findings. She was diagnosed with colon cancer (stage II) 2 years ago. She underwent a right hemicolectomy and received adjuvant chemotherapy for 6 months. After treatment, there was no evidence of disease during regular follow-up. However, a hepatic mass was detected on computed tomography (CT) performed for surveillance of colon cancer recurrence 3 months ago. She did not have any other risk factors for HCC, such as alcoholism and metabolic disorders. We did not check the serologic test for viral hepatitis at the initial evaluation because she was referred from another medical center during the follow-up period and had no history of hepatitis. As she had been treated for colon cancer, liver metastasis of colon cancer was most suspected clinically at that time. Dynamic liver magnetic resonance imaging (MRI) and positron emission tomography-computed tomography (PET-CT) was also performed. Although imaging studies were conducted fully, the differentiation between metastasis and primary liver cancer was still unclear. The patient wanted a second opinion and thus visited our hospital. At the initial inspection, she had no specific symptoms or abnormal findings on physical examination. On initial laboratory examination, her complete blood count profile revealed a WBC count of 5.33×10³/μL, a hemoglobin level of 12.3 g/μL, and platelet count of 239×10³/μL, which were within the normal ranges. Liver function tests also showed nearly normal results, with a serum bilirubin level of 0.4 mg/ dL, albumin level of 4.8 g/dL, prothrombin time international normalized ratio of 1.01, aspartate aminotransferase level of 44 IU/L, and alanine aminotransferase level of 34 IU/L. Serum levels of alpha-fetoprotein (AFP) and protein induced by vitamin K absence or antagonist-II (PIVKA-II) were 3.0 ng/mL (reference range: 0.0–9.0 ng/mL) and 34 mAU/mL (reference range: 0–35 mAU/mL), respectively. Considering the history of colon cancer, we performed a carcinoembryonic antigen (CEA) assessment also, level 3.06 ng/mL (reference range: 0.0–5.0 ng/mL).

An abdominal CT scan that detected a hepatic mass first revealed a 3.6-cm-sized lobulated mass in segment VII of the liver. It showed peripheral rim enhancement in contrast images (Fig. 1). The background features of the liver parenchyma were not remarkable. As the CT scan did not involve dynamic phase images, it was limited for evaluating the lesion precisely. Dynamic liver MRI showed heterogeneous enhancement in the arterial phase and wash-out in the portal phase. Hyperintensity was observed in T2-weighted images (Fig. 2). PET-CT showed FDG uptake in the hepatic mass without evidence of any other lesions (Fig. 3).

Although there were typical findings for HCC based on imaging studies, liver metastasis of colon cancer could not be definitively ruled out due to the clinical history. We planned surgical resection for diagnosis and treatment. The patient underwent a volume-preserving right hemihepatectomy, and the tumor was completely resected. Gross findings of the specimen exhibited a lobulated round mass (Fig. 4). Hematoxylin and eosin (H&E) staining revealed moderately differentiated hepatic tumor cells, which represented trabecular patterns of polygonal cells with distinct cell membranes, abundant granular eosinophilic cytoplasm, and a higher nuclear-cytoplasmic ratio. Moreover, there was an infiltration of a large number of lymphocytes, known as the lymphoepithelioma-like pattern (Fig. 5). The immunohistochemical staining results suggested that the tumor cells originated in the liver, as arginase-1 was positive, while cytokeratin 7 and 19 (CK7 and CK19) and epithelial membrane antigen (EMA) were negative. T-lymphocyte infiltration was demonstrated through diffuse staining of the cluster of differentiation 3 and 8 (CD3 and CD8). Programmed death-ligand 1 (PD-L1) was positive with a 90% tumor proportion score. Epstein-Barr virus-encoded RNA (EBER) in situ hybridization (ISH) was negative (Fig. 6). The pathology of the liver parenchyma showed mild inflammation and periportal fibrosis. Based on the above findings, we made a diagnosis of lymphocyte-rich HCC characterized by infiltration of lymphocytes into hepatic tumor cells. As the patient did not undergo a serologic screening test for hepatitis, we checked the viral markers of hepatitis B and C virus (HBV and HCV) after surgery, and she was found positive for anti-HCV antibody and HCV-RNA. Therefore, she had this risk factor for HCC that was detected retrospectively. She recovered well without complications and was discharged 10 days after surgery.