Skip to main page content
U.S. flag

An official website of the United States government

Dot gov

The .gov means it’s official.
Federal government websites often end in .gov or .mil. Before sharing sensitive information, make sure you’re on a federal government site.

Https

The site is secure.
The https:// ensures that you are connecting to the official website and that any information you provide is encrypted and transmitted securely.

Access keys NCBI Homepage MyNCBI Homepage Main Content Main Navigation
Case Reports
. 2021 Dec;12(6):3123-3132.
doi: 10.21037/jgo-21-287.

Hepatoid esophagogastric adenocarcinoma and tumoral heterogeneity: a case report

Tiago Biachi de Castria  1   2 , Laura Tang  2   3 , Marcello Moro Queiroz  1 , Beatriz Mendes Awni  1 , Viktoriya Paroder  2   3 , Ali Shamseddine  4 , Giovanni Mendonca Bariani  1 , Deborah Mukherji  4 , Charbel F Matar  4 , Gustavo Dos Santos Fernandes  1 , Ashwaq El-Olayan  5 , Fouad Sabatin  5 , Rawad Elias, Ranju Gupta, Yelena Y Janjigian  2   3 , Ghassan K Abou-Alfa  2   3
Affiliations
Case Reports

Hepatoid esophagogastric adenocarcinoma and tumoral heterogeneity: a case report

Tiago Biachi de Castria et al. J Gastrointest Oncol. 2021 Dec.

Abstract

Hepatoid adenocarcinoma of the stomach is an uncommon subtype of gastric cancer remarkably similar to hepatocellular carcinoma in histopathological analysis. It is also commonly associated with high serum alfa-fetoprotein and a poorer prognosis, despite the emergence of new therapeutic options. In recent years, next generation sequencing (NGS) technology has made it possible to identify and describe the genes and molecular alterations common to gastric cancer thereby contributing to the advancement of targeted therapies. A 62-year-old patient, with no prior risk factor for hepatocellular carcinoma (HCC), presented to the emergency room with dysphagia for solids, abdominal pain and weight loss of about 3 kilograms over 3 months. Histopathological analysis presented with disparities regarding HER2 and programmed death-ligand 1 (PD-L1) status in the primary and metastatic sites. We describe a case of a de novo metastatic, human epidermal growth factor receptor 2 (HER2) positive esophagogastric junction hepatoid adenocarcinoma. Although this is a rare subgroup of gastric cancer, treatment strategies were based in recent studies in immunotherapy and guided therapy, taking into consideration the molecular findings from the patient's tumor NGS analysis. Data about HER2 and PDL1 heterogeneity were also reviewed. Despite the aggressiveness and rarity of this histology, the patient had a good response to treatment.

Keywords: Case report; esophagogastric junction; hepatoid adenocarcinoma; heterogeneity; human epidermal growth factor receptor 2 (HER2).

PubMed Disclaimer

Conflict of interest statement

Conflicts of Interest: The authors have completed the ICMJE uniform disclosure form (available at https://dx.doi.org/10.21037/jgo-21-287). The series “Educational Case Series of the Memorial Sloan Kettering Cancer Center” was commissioned by the editorial office without any sponsorship or funding. TBC received support from Astra Zeneca, Bayer, Eli Lilly, Genentech/Roche, Ipsen, Merck KGaA, Merck Sharp & Dohme. AS received support from Roche, Merck, BMS, Sanofi, Eli Lilly and is a consultant to Roche, MSD, Merck, Sanofi, Astellas and Johnson & Johnson, and he received honoraria for lectures and presentation from Roche, Merck, BMS, MSD, Johnson & Johnson and Amgen and support for attending meetings from Merck. GMB receives research funding to his institution from mAbxience, Merck Sharp & Dohme Corp. and Bristol-Myers Squibb. DM received research support from Astellas, Pfizer, and Astra Zeneca, and honoraria/travel support from MSD, BMS, Astellas, Bayer and Janssen. GdSF received honoraria/travel support from BMS, MSD, Roche and Ipsen and advisory board support from BMS, MSD, Boeringher, Sanofi, Roche, Astelas, Bayer. GKA served as the unpaid Guest Editor for the series and he received research support from Arcus, Agios, Astra Zeneca, BioNtech, BMS, Celgene, Flatiron, Genentech/Roche, Genoscience, Incyte, Polaris, Puma, QED, Silenseed, Yiviva, and consulting support for efforts with Adicet, Astra Zeneca, Alnylam, Autem, Bayer, Beigene, Berry Genomics, Cend, Celgene, CytomX, Eisai, Eli Lilly, Exelixis, Flatiron, Genentech/Roche, Genoscience, Helio, Incyte, Ipsen, Legend Biotech, Merck, Nerviano, QED, Redhill, Rafael, Servier, Silenseed, Sillajen, Sobi, Surface Oncology, Therabionics, Vector, and Yiviva. YYJ received research support from Bayer, Bristol-Myers Squibb, Cycle for Survival, Department of Defense, Eli Lilly, Fred’s Team, Genentech/Roche, Merck, NCI, RGENIX and receives consulting fees from Astra Zeneca, Basilea Pharmaceutica, Bayer, Bristol-Myers Squibb, Daiichi-Sankyo, Eli Lilly, Imugene, Merck, Merck Serono, Michael J. Hennessy Associates, Paradigm Medical Communications, Pfizer, RGENIX, Seagen, Zymeworks Inc., and has Stock Options of RGENIX. The authors have no other conflict of interest to report.

Figures

Figure 1
Figure 1
Pathology high magnification views. Histopathological tissue analysis from liver biopsy revealed a tubular and hepatoid adenocarcinoma (A,B; ×100). Immunohistochemistry stained positive for Hepatocyte (C; ×100) and HER2 3+ (D; ×400).
Figure 2
Figure 2
CT scan liver views. Chronic liver disease (liver enlargement and splenomegaly). Several liver lesions with early arterial phase enhancement (A) and rapid washout (B, blue arrows), suspicious for hepatocellular carcinoma. Enlarged gastrohepatic node (C).
Figure 3
Figure 3
Pathology high and low magnification. Histopathological tissue analysis from esophagogastric junction biopsy revealed a poorly cohesive adenocarcinoma, signet-ring type (A,B; ×100). There was also a focal tubular and hepatoid features (C,D; ×400).
Figure 4
Figure 4
Liver lesion and lymph node regression after first line chemotherapy with FOLFOX and trastuzumab. Nearly homogeneous enhancement of the liver with disappearance of hypervascular areas of enhancement on arterial phase (A) and just a few residual areas of washout on the portal venous phase (B). Previously enlarged gastrohepatic node (C, blue arrow) has decreased in size and attenuation (D, blue arrow).
Figure 5
Figure 5
Timeline of the case report. AFP, alfa-fetoprotein; CT, computed tomography; FLOT, docetaxel, oxaliplatin, leucovorin and 5-fluoracil; FOLFOX, 5-fluoruracil, oxaliplatin and leucovorin; RECIST, Response Evaluation Criteria in Solid Tumours.
See this image and copyright information in PMC

References

    1. Liu X, Cheng Y, Sheng W, et al. Analysis of clinicopathologic features and prognostic factors in hepatoid adenocarcinoma of the stomach. Am J Surg Pathol 2010;34:1465-71. 10.1097/PAS.0b013e3181f0a873 - DOI - PubMed
    1. Lin CY, Yeh HC, Hsu CM, et al. Clinicopathologial features of gastric hepatoid adenocarcinoma. Biomed J 2015;38:65-9. 10.4103/2319-4170.126860 - DOI - PubMed
    1. Qu BG, Bi WM, Qu BT, et al. PRISMA-Compliant Article: Clinical Characteristics and Factors Influencing Prognosis of Patients With Hepatoid Adenocarcinoma of the Stomach in China. Medicine (Baltimore) 2016;95:e3399. 10.1097/MD.0000000000003399 - DOI - PMC - PubMed
    1. Yano T, Kishimoto T, Tomaru U, et al. Further evidence of hepatic transdifferentiation in hepatoid adenocarcinomas of the stomach: quantitative analysis of mRNA for albumin and hepatocyte nuclear factor-4alpha. Pathology 2003;35:75-8. - PubMed
    1. Fujii H, Ichikawa K, Takagaki T, et al. Genetic evolution of alpha fetoprotein producing gastric cancer. J Clin Pathol 2003;56:942-9. 10.1136/jcp.56.12.942 - DOI - PMC - PubMed

Publication types