Abstract
Herein, we describe a case of a 60-year-old male with liver cirrhosis due to chronic hepatitis C virus (HCV) infection complicated by hepatocellular carcinoma (HCC) who underwent liver transplant at which time an incidental gall bladder adenocarcinoma (GBC) was identified. He was unsuccessfully treated for HCV in 2004 and followed by surveillance imaging which in 2011 identified a lesion suspicious for HCC. Serial imaging also identified adenomyomatosis of the gallbladder as early as 2005 which remained stable on follow-up studies. He underwent chemoembolization and then orthotopic liver transplant in 2015. Pathological evaluation of the explanted liver revealed four HCC lesions (largest measuring 1.8cm). Gross pathology of the resected gallbladder revealed a markedly thickened and fibrotic gallbladder wall with multiple pigment stones. Pathological evaluation of the resected gallbladder revealed a 12 cm moderately differentiated adenocarcinoma with the entire gallbladder wall being involved (pT2N1). To help determine the origin between the two tumors, mutational analysis was performed using next generation sequencing of 467 cancer-associated genes on both tumors. HCC contained two mutations that were not noted in the GBC, whereas the GBC carried five gene variants that were not identified within the HCC specimen. This mutual exclusivity is suggestive of distinct clonal processes and neither tumor shared a common mutation or mutated pathway that were actionable by currently available therapies. The patient was subsequently treated for HCV and maintained on immunosuppression. He was treated with adjuvant gemcitabine and cisplatin for GBC and is followed closely with surveillance imaging. In our review of the literature, only three cases of concomitant HCC and GBC have been reported. This is the first known report to present next generation sequencing data for such a case, demonstrating the utility of this technology to establish the distinct clonality of synchronous primary tumors and to identify potentially actionable mutations. This case also exemplifies the challenges in differentiating adenomyomatosis from GBC on CT imaging, especially in cases where the adenocarcinoma is microscopic and infiltrative in its pattern of growth. Though PET imaging can be useful in distinguishing between benign and malignant lesions, PET scans are not routinely ordered in pre-transplant HCC patients and were not performed in this case.Figure 1Figure 2Figure 3
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