Hepatocellular carcinoma in a transplanted donor liver and colon cancer developing in a patient with a complex background: A case report

Abstract

The development of tumors in livers transplanted from hepatitis B virus (HBV)-negative donors to patients with hepatitis B and cirrhosis is rare. The present study describes the case of a woman in her 60s who developed hepatocellular carcinoma (HCC) in her grafted liver, 19 years after transplantation, as well as a metachronous colorectal tumor. The pathological findings, including clinical, immunohistochemical and molecular results, are described in the present case report. The liver tumor was a conventional HCC and the colorectal tumor comprised a tubular adenocarcinoma. Immunohistochemistry of both tumors showed a loss of expression of mutL homolog 1 and postmeiotic segregation increased 2 in the tumor cells, confirming microsatellite instability-high (MSI-H) status. Furthermore, a molecular study detected the presence of genes located on the Y chromosome in the normal and tumor tissues of the liver, proving that the HCC occurred in the grafted liver. The present report also discusses that prolonged use of immunosuppressive drugs to prevent post-transplant rejection, poorly controlled diabetes mellitus and MSI-H may have contributed to the risk of tumor development.

Keywords: HBV; HCC; MSI; colon cancer; diabetes mellitus; immunosuppressant; transplantation.

Figure 1.

(A) Abdominal enhanced computed tomography and (B) T1-weighted magnetic resonance tomography before the first operation. The images show a nodule with early enhancement in the segment four area, in the arterial phase. Arrowheads indicate the tumor.

Figure 2.

(A) Abdominal enhanced computed tomography and (B) T1-weighted magnetic resonance tomography of the recurrent tumor. The images show a nodule with early enhancement in the segment eight area, in the arterial phase. Arrowheads indicate the tumor.

Figure 3.

Macroscopic and histological findings of the primary tumor. (A) A relatively well-defined, bright yellowish nodule exposed on the cut surface. (B) The tumor, comprising a hepatocellular carcinoma with a trabecular pattern. The tumor cells having distinct Mallory-Denk bodies in their cytoplasm (arrowheads).

Figure 4.

Macroscopic and histological findings of the second tumor. (A) Loupe figure of the pathological specimen. The tumor showing fused multinodular lesions (insert). Well-defined, yellowish multi-nodular tumor exposed on the cut surface. (B) The tumor showing similar histological findings to the primary liver tumor. The tumor cells having round to oval and deeply eosinophilic hyaline bodies in their cytoplasm (arrowheads).

Figure 5.

Macroscopic and histological findings of the cecal tumor. (A) A slightly elevated tumor, located in the cecum (arrowhead). (B) Histology, the tumor was moderately differentiated tubular adenocarcinoma. Tumor tissue revealing fused glands (arrowheads) and irregular branching (*).

Figure 6.

Capillary electrogram of the polymerase chain reaction products of genes located on the Y chromosome and amplified from primary and normal liver tissue. Both electrograms feature similar peaks, suggested SRY-a-Y, AMEL-Y, SRY-b-Y, and STS-Y gene products.

Figure 7.

Capillary electrogram of polymerase chain reaction products for D17S938, as a microsatellite marker. The peak derived from normal liver tissue was not obtained from the primary and second liver tumors (arrowheads).

Figure 8.

Immunohistochemistry for MLH1 in the liver and colon cancers. (A) Primary, (B) recurrent hepatocellular carcinoma and (C) colon carcinoma. Nuclear expression of MLH1 detected lymphocytes and vascular endothelial cells as internal controls but was not detected in the tumor cells.