Gastric Hepatoid Adenocarcinoma Research Articles

Hepatoid Adenocarcinoma of the Stomach with Liver and Pulmonary Metastases: A Case Report and Literature Review

Hepatoid Adenocarcinoma of the Stomach (HAS) is a rare unique subtype of Gastric Cancer (GC) with a low incidence but a high mortality rate. We report a female case of 67-years-old with APF producing hepatoid adenocarcinoma of the gastric antrum with liver and lung metastases. Abdominal CT of the patient showed multiple liver masses, which were considered as metastatic tumors and proved to be adenocarcinoma by pathological examination of a biopsy. The gastroscopy revealed antral ulcer complicated with bleeding. The biopsy results of hepatoid adenocarcinoma were consistent with the results of liver masses. Moreover, α-Fetoprotein (AFP) increased sharply to 86332 ng/mL. Thus, the diagnosis of gastric hepatoid adenocarcinoma with liver metastasis was established. In terms of treatment, liver TACE embolization was performed first, followed by radical gastrectomy and resection of liver tumor. During the operation, multiple small tumors (less than 5cm in diameter) in the liver were treated by radiofrequency ablation. The patient recovered well after surgery, with a rapid decline in AFP. Postoperative CT indicated the presence of bioactive tumors in the liver and new tumors in the lung. Lung puncture pathology suggests tumor metastasis. Liver and lung were treated with radiofrequency ablation and SOX (Oxaliplatin and Tegacil) chemotherapy. There was no significant recurrence 20 months after surgery, and personalized systematic treatment for this patient was effective. Standard treatment for gastric hepatoid adenocarcinoma has not yet been established, and personalized systematic therapy is the preferred treatment.

Differential diagnostic value of tumor markers and contrast-enhanced computed tomography in gastric hepatoid adenocarcinoma and gastric adenocarcinoma.

This study aimed to investigate the effectiveness of tumor markers and contrast-enhanced computed tomography (CE-CT) in differentiating gastric hepatoid adenocarcinoma (GHA) from gastric adenocarcinoma (GA). This retrospective study included 160 patients (44 with GHA vs. 116 with GA) who underwent preoperative CE-CT. Preoperative serum concentrations of tumor biomarkers and CT imaging features were analyzed, including alpha-fetoprotein (AFP), carcinoembryonic antigen (CEA), carbohydrate antigen 19-9 (CA19-9), carbohydrate antigen 125 (CA125), tumor location, growth pattern, size, enhancement pattern, cystic changes, and mass contrast enhancement. Multivariate logistic regression analyses were performed to evaluate useful tumor markers and CT imaging features for differentiating GHA from GA. When compared to GA, GHA showed a higher serum AFP [13.27 ng/ml (5.2-340.1) vs. 2.7 ng/ml (2.2-3.98), P <0.001] and CEA levels [4.07 ng/ml (2.73-12.53) vs. 2.42 ng/ml (1.38-4.31), P <0.001]. CT imaging showed GHA with a higher frequency of tumor location in the gastric antrum (P <0.001). GHA had significantly lower attenuation values at the portal venous phase [PCA, (82.34 HU ± 8.46 vs. 91.02 HU ± 10.62, P <0.001)] and delayed phase [DCA, (72.89 HU ± 8.83 vs. 78.27 HU ± 9.51, P <0.001)] when compared with GA. Multivariate logistic regression analyses revealed that tumor location, PCA, and serum AFP level were independent predictors of differentiation between GHA and GA. The combination of these three predictors performed well in discriminating GHA from GA, with an AUC of 0.903, a sensitivity of 86.36%, and a specificity of 81.90%. Integrated evaluation of tumor markers and CT features, including tumor location, PCA, and serum AFP, allowed for more accurate differentiation of GHA from GA.

CT-based radiomics nomogram for differentiating gastric hepatoid adenocarcinoma from gastric adenocarcinoma: a multicentre study

ABSTRACT Background To develop a CT-based radiomics nomogram for the high-precision preoperative differentiation of gastric hepatoid adenocarcinoma (GHAC) patients from gastric adenocarcinoma (GAC) patients. Research design and methods 108 patients with GHAC from 6 centers and 108 GAC patients matched by age, sex and T stage undergoing pathological examination were retrospectively reviewed. Patients from 5 centers were divided into two cohorts (training and internal validation) at a 7:3 ratio, the remaining patients were external test cohort. Venous-phase CT images were retrieved for tumor segmentation and feature extraction. A radiomics model was developed by the least absolute shrinkage and selection operator method. The nomogram was developed by clinical factors and the radiomics score. Results 1409 features were extracted and a radiomics model consisting of 19 features was developed, which showed a favorable performance in discriminating GHAC from GAC (AUCtraining cohort = 0.998, AUCinternal validation set = 0.942, AUCexternal test cohort = 0.731). The radiomics nomogram, including the radiomics score, AFP, and CA72_4, achieved good calibration and discrimination (AUCtraining cohort = 0.998, AUCinternal validation set = 0.954, AUCexternal test cohort = 0.909). Conclusions The noninvasive CT-based nomogram, including radiomics score, AFP, and CA72_4, showed favorable predictive efficacy for differentiating GHAC from GAC and might be useful for clinical decision-making.

Gastric hepatoid adenocarcinoma with multiple liver metastasis: a case report.

Hepatoid adenocarcinoma is a poorly differentiated alpha-fetoprotein-producing (AFP) tumor frequently located in the stomach, ovary, and pancreas. Presentation in the stomach has a high mortality rate due to late diagnosis, which offers the patient few therapeutic alternatives. On February 22, 2019, a 44-year-old woman from Lima entered the emergency department for pain in the right hypochondrium for 4 months, weight loss, nausea, and asthenia. On physical examination, hepatomegaly presented with a liver spam of 17 cm. Serology showed severe anemia and AFP of 49,800. The tomography showed multiple hypodense lesions in the liver and the presence of nodes. Endoscopy showed Bormann III gastric malignancy. Gastric biopsy determined undifferentiated epithelial malignancy; the immunohistochemical mark (+) for AFP and PAS Diastase confirmed a hepatoid gastric adenocarcinoma. A rare variant of gastric adenocarcinoma was evident, which often mimics an HCC. In this case, multiple liver metastases were observed that differed from the diagnosis of HCC, so this variant must always be taken into account when a primary gastric tumor presents with hepatic metastases.

Abstract 4747: Genomic and transcriptomic landscape of AFP-producing gastrointestinal adenocarcinoma

Abstract AFP-producing gastrointestinal adenocarcinoma (APA-GI) is a rare type of cancer, typically with hepatoid differentiation, chemotherapy resistance and poor prognosis. As the mechanisms of its AFP production and hepatoid differentiation remain unclear, the present study aims to reveal the pathogenesis of APA-GI through genomic and transcriptomic profile analysis. We firstly performed 200 × whole exome sequencing of 29 APA-GI and 8 non-APA-GI cases from our hospital, but found no significant difference in single nucleotide variants (SNV) or insertion/deletion(indels). Additionally, there was no overlap gene when compared with the known genes harbored at 20q11.21-13.12 reported in gastric hepatoid adenocarcinoma. We then performed single-cell mRNA sequencing in one APA-GI, and observed several hepatoid differentiation markers in AFP positive cells including HNF4A and HNF1A. To further determine the specific alterations of APA-GI, we divided 339 gastric cancer patients from TCGA database into AFP-low group and AFP-high group by the level of AFP transcription through a dynamic grouping method named grid search. We performed a series differentially expressed genes detections within different grouping strategies and no significant SNV or indels difference was recognized. We identified hepatoid differentiation markers (i.e. HNF4A, HNF1A and ALB, et al) in AFP-high patients in mRNA level. As the difference of hepatoid differentiation markers only occurred in the mRNA level without DNA alteration, we hypothesized that it was probably caused by epigenetic regulation. We further compared these genes with an epigenetic regulators database named EpiFactors. Finally, it showed CCCTC-Binding Factor Like (CTCFL) was stably related with AFP producing within the grid search. In conclusion, comprehensive genomic analysis of APA-GI shows significant hepatoid differentiation at the transcriptomic level without disease-specific DNA alteration. The pathogenesis of APA-GI may be associated with other mechanisms like epigenetic regulation. Further study was needed to confirm the role of epigenetic regulators we detected in the present study in the development of APA-GI. Citation Format: Jun Li, Xinlin Li, Qiancheng Ye, Yu Tian, Xiangxing Kong, Yue Liu, Xiaoming Xu, Lina Zhang, Qian Xiao, Yeting Hu, Rongzhen Xu, Jingsong Li. Genomic and transcriptomic landscape of AFP-producing gastrointestinal adenocarcinoma [abstract]. In: Proceedings of the Annual Meeting of the American Association for Cancer Research 2020; 2020 Apr 27-28 and Jun 22-24. Philadelphia (PA): AACR; Cancer Res 2020;80(16 Suppl):Abstract nr 4747.

Gastric Hepatoid Adenocarcinoma: Differentiation From Gastric Adenocarcinoma With Dynamic Contrast-Enhanced Computed Tomographic Findings.

This study aimed to describe the computed tomographic (CT) findings of gastric hepatoid adenocarcinoma (GHA) and determine features distinguishing it from gastric adenocarcinoma (GA). Computed tomographic images of pathologically verified GHA (n = 11) and GA (n = 38) were retrospectively reviewed. α-Fetoprotein (AFP), carcinoembryonic antigen (CEA), and CT findings were assessed in our study. Computed tomographic findings included the location, distribution, growth pattern, ulceration, thickness of gastric wall, enhancement pattern, and the ratio of lesion attenuation to aorta CT attenuation. Short diameter of the metastatic lymph nodes, mean short diameter of metastatic lymph nodes, and the ratio of the number of enlarged lymph node on CT to the number of metastatic lymph nodes pathologically were measured and calculated. Data were compared using the χ and Student t tests; significant CT criteria were identified using receiver operating characteristic curve. α-Fetoprotein, CEA, and CT findings, including the longest short diameter, the mean short diameter, the ratio of the number of enlarged lymph node on CT to the number of metastatic lymph nodes pathologically, the lesion in arterial phase minus portal venous phase, and the lesion/aorta ratio, were statistically significant predictors for the differentiation of GHA from GA (P < 0.05). When only the aforementioned CT findings were used as criteria, the sensitivity and specificity for diagnosing GHA were 82.86% and 90.91%, respectively. When AFP, CEA, and CT findings were used as criteria, sensitivity of 97.14% and specificity of 90.91% were achieved. Elevated serum AFP level and CT findings could distinguish GHA and GA with a high degree of accuracy.

Gastric hepatoid adenocarcinomas are a genetically heterogenous group; most tumors show chromosomal instability, but MSI tumors do exist

The Cancer Genome Atlas Research Network classified gastric adenocarcinoma into four molecular subtypes: (1) Epstein-Barr virus-positive (EBV), (2) microsatellite-instable (MSI), (3) chromosomal instable (CIN), and (4) genomically stable (GS). The molecular subtypes of gastric hepatoid adenocarcinomas are still largely unknown. We analyzed 52 hepatoid adenocarcinomas for the expression of surrogate markers of molecular subtypes (MLH1, p53, and EBER in situ hybridization) and some biomarkers (p21, p16, Rb, cyclin D1, cyclin E, β-catenin, Bcl-2, IMP3, ARID1A and HER2), and mutations of TP53, CTNNB1, KRAS, and BRAF. We analyzed 36 solid-type poorly differentiated adenocarcinomas as a control group. Hepatoid adenocarcinomas were categorized as follows: EBV group (EBER-positive), no cases (0%); MSI group (MLH1 loss), three cases (6%); "CIN or GS" (CIN/GS) group (EBER-negative, MLH1 retained), 49 cases (94%). In the CIN/GS group, most of the tumors (59%) had either p53 overexpression or TP53 mutation and a coexisting tubular intestinal-type adenocarcinoma component (90%), suggesting that most hepatoid adenocarcinomas should be categorized as a true CIN group. Hepatoid adenocarcinomas showed relatively frequent expressions of HER2 (score 3+/2+: 21%/19%). Hepatoid adenocarcinomas showed shorter survival, more frequent overexpressions of p16 (67%) and IMP3 (98%) than the control group. None of hepatoid adenocarcinomas had KRAS or CTNNB1 mutations except for one case each, and no hepatoid adenocarcinomas had BRAF mutation. In conclusion, gastric hepatoid adenocarcinomas are a genetically heterogenous group. Most hepatoid adenocarcinomas are "CIN," but a small number of hepatoid adenocarcinomas with MSI do exist. Hepatoid adenocarcinomas are characterized by overexpressions of p16 and IMP3.

&lt;p&gt;Establishment and characterization of the GC-030-35 cell line derived from gastric hepatoid adenocarcinoma&lt;/p&gt;

PurposeGastric hepatoid adenocarcinoma is a rare subtype of primary gastric cancer and is a high-grade form of malignancy. However, the pathogenesis and molecular biology of gastric hepatoid adenocarcinoma remain poorly understood. The aim of this study was to establish and characterize a new human gastric hepatoid adenocarcinoma cell line, GC-030-35.Materials and methodsThe GC-030-35 cell line was established from tumor cells from a 58-year-old Chinese man with gastric hepatoid adenocarcinoma. The cultured cells underwent immunocytochemistry and flow cytometry to confirm the tumor cell phenotype. RNA sequencing was performed to analyze the differences in gene expression between GC-030-35 cells compared with normal gastric epithelial cells. A zebrafish assay was performed. Gene enrichment analysis and interrogation of the bioinformatics databases, the Gene Ontology (GO) database and the Kyoto Encyclopedia of Genes and Genomes (KEGG) database, were used for pathway analysis.ResultsFlow cytometry analysis of the GC-030-35 cells showed a positive expression rate for CD44+ of 10.7%, high cell clonality, an average plating efficiency of 32%, cell-doubling time of 29.2 hours, and cell proliferation for >15 generations in serial culture. The zebrafish assay showed the ability of the GC-030-35 cells to proliferate, promote angiogenesis, and metastasize. RNA sequencing identified the functional clustering of 6,601 differentially expressed genes of GC-030-35, which were significantly different when compared with nonneoplastic gastric epithelial cells. Pathway enrichment analysis and interrogation of the GO and KEGG bioinformatics databases identified genes for microbial metabolism in diverse environments (63 genes), metabolism of xenobiotics by cytochrome P450 (CYP450; 25 genes), and the drug metabolism cytochrome P450 (28 genes).ConclusionA human gastric hepatoid adenocarcinoma cell line, GC-030-35, was developed and characterized by comparison with normal gastric epithelial cells. Bioinformatics and gene analysis data showed that the CYP450 gene was significantly differentially expressed by GC-030-35 cells.

Research progress of the clinically uncommon gastric carcinoma

Gastric cancer is one of the most important diseases that endangers people's health. Beside gastric adenocarcinoma, gastric carcinoma also includes the following types: adenosquamous carcinoma, squamous carcinoma, gastric neuroendocrine tumor, gastric hepatoid adenocarcinoma, AFP-producing gastric cancer, EBV-associated gastric cancer, lymphoepithelioma-like carcinoma, undifferentiated-type gastric cancer, gastric carcinosarcoma and so on. The adenosquamous carcinoma, squamous carcinoma of stomach, gastric hepatoid adenocarcinoma, AFP-producing gastric cancer and gastric carcinosarcoma mainly occurred in old men, while the linitisplastica gastric cancer was common in young women. It refers to the gastric cancers that are clinically rare and have lower incidence, unique histological and pathological features, however, without obviously clinical manifestations. The clinically uncommon gastric cancers are easy to be misdiagnosed or missed, and further to miss the optimal opportunity for treatment due to the unclearly specific pathogenesis and disease progression. With the development of studies on the clinically uncommon gastric carcinoma, although people have a further knowledge of its pathologic features, methods of diagnosis and treatment, the diagnosis and treatment standards for the clinically uncommon gastric cancer has not yet been established and unified. The therapeutic principle of the clinically uncommon gastric cancers is also the radical surgery, radiotherapy and chemotherapy as the main comprehensive treatment supplemented by individualized treatment. With lucubrating the pathogenesis of them, specific diagnostic methods and treatment measures are new hope for improving the diagnosis and treatment of the clinically uncommon gastric cancers. So, the further researches on the clinically uncommon gastric cancers and exploring their etiology, pathogenesis, histological and pathological features have important significance to their diagnosis and treatment. This article makes a summary of the clinically uncommon gastric cancers with the aspects of epidemiology, histology, pathology, diagnosis, treatment, to provide reference to clinical diagnosis and scientific studies.

Chemotherapy of metastatic hepatoid adenocarcinoma: Literature review and two case reports with cisplatin etoposide.

Hepatoid adenocarcinoma (HAC) is a rare and aggressive cancer subtype with a poor prognosis under metastatic conditions. Currently, there is no specific chemotherapy treatment protocol for advanced stages of the disease. This review evaluates two cases of HAC of gastric cardia with synchronous liver metastasis, which were successfully treated by chemotherapy with cisplatin (25 mg/m2 each day) (day 1 to day 3) and etoposide (100 mg/m2) (day 1 to day 3), every three weeks. A structured literary evaluation and reviewed pertinent articles are additionally presented to analyse the different approaches for the treatment of metastatic HAC (mHAC). The two described case reports demonstrated good partial responses to treatment and one of the two patients exhibited a good prognosis after a 9-year follow-up. A total of 20 case reports concerning the use of chemotherapy in mHAC were presented in the literature, 11 of which were regarding gastric HACs. The two aforementioned cases result in a total of 22 reports, 11 of which exhibited objective responses to chemotherapy, 8 patients demonstrated a partial response and 3 a complete response. The cisplatin-based regimen concerned 55% (12/22) patients and enabled 9 (75%) to exhibit a partial or complete response. A total of three patients exhibited a good prognosis in the long-term follow-up, all of them treated with a cisplatin-based regimen. It was demonstrated that the usual digestive regimens were not efficient in the treatment of HAC. In the absence of prospective trials, it may be hypothesized that cisplatin-based chemotherapy may be the most efficient first-line treatment in mHAC, with a 75% patient response, in accordance with the literature and follow-up cases.

Clinicopathologic characteristics and prognosis of gastric hepatoid adenocarcinoma

To investigate the clinicopathological characteristics, diagnosis, treatment and prognosis of gastric hepatoid adenocarcinoma(HAS). Retrospective analysis of clinicopathological data of 24 cases with gastric HAS diagnosed by surgery and pathology in Chinese PLA General Hospital from January 2013 to May 2016 were carried out. All the patients underwent preoperative serum alpha fetoprotein (AFP), carcinoembryonic antigen (CEA), endoscopy and imaging examination (CT or B-mode ultrasonography), and those with elevated AFP were excluded from liver cancer, cirrhosis, endodermal sinus tumor and other diseases. The follow-up ended in June 2016 or the death of the patient. The survival was from the operation to the death of the patient or the end of follow-up. There were a total of 24 cases with gastic HAS, accounting for 1.03%(24/2 326) of the total number of patients with gastric cancer diagnosed at the same time in our center. There were 19 males and 5 females, the ratio of male to female was 3.8:1.0, the mean age of the patients was 55.9 (31 to 72) years, and 2 of them had liver metastasis. The first symptom in 50% (12/24) patients was epigastric pain, in 25%(6/24) was abdominal distension with vomiting, and the rest included dysphagia (12.5%, 3/24), hematemesis (8.3%, 2/24) and melena (4.2%, 1/24). Preoperative serum levels of AFP and CEA were elevated in 10 (41.7%) and 5 patients (20.8%) respectively. All the patients underwent surgical treatment, including 23 cases with D2 radical resection of gastric cancer and R0 resection, and the other of palliative gastrojejunostomy. Lesions of HAS located in gastric antrum in 11 cases (45.8%), in cardia in 7 cases (29.2%), and in gastric body in 6 cases (25%). Tumor maximum diameter of 10 cases was larger than 5 cm, and the average diameter was 5.7(1.0 to 12.0) cm. Postoperative pathological TNM staging: stage I(b was in 1 cases, stage II( in 7 cases, stage III( in 14 cases, stage IIII( in 2 cases; lymph node metastasis in stage N1-3 in 20 cases (83.3%). Poorly-differentiated tumors were found in 21 cases (87.5%), and no well-differentiated tumors were found. There were 11 cases (45.8%) with formation of intravascular tumor thrombi. In immunohistochemistry, AFP positive expression was found in 11 cases(45.8%). Seventeen HAS cases (70.8%, 17/24) received postoperative SOX(oxaliplatin + S-1) or XELOX (oxaliplatin + capecitabine) as adjuvant chemotherapy, 5 cases postoperative immune therapy, and 2 cases postoperative traditional Chinese medicine. All the patients were followed up for 0.7 to 42.0 months (median 8 months). A total of 9 patients died, of whom, 1 case underwent gastrojejunostomy because of liver and peritoneal metastasis before operation, and died 20 days after surgery; 4 cases died of multiple liver metastases after 1.5 to 12.0 months with survival of 3 to 18 months; 3 cases presented local recurrence after 2 to 17 months with survival of 6 to 22 months; 1 cases had peritoneal metastasis after 12 month with survival of 26 months. HAS is a rare type of gastric cancer with poor prognosis. The diagnosis is mainly based on histopathology, and radical resection is the mainstay treatment.

Gastric hepatoid adenocarcinoma resulting in a spontaneous gastric perforation: a case report and review of the literature

BackgroundGastric hepatoid adenocarcinoma (GHAC) is an atypical form of gastric cancer (GC) that has similar tissue morphology to hepatocellular carcinoma and frequently produces alpha-fetoprotein. We present an exceedingly rare case of GHAC resulting in a spontaneous gastric perforation.Case presentationA 61-year-old man presented at our institution complaining of abdominal and back pain. A computed tomography scan revealed a spontaneous gastric perforation with a solitary liver tumor and lymph node swelling. Following a diagnosis of advanced-stage GC with a gastric perforation, perforative peritonitis, multiple lymph node metastases, and a solitary metastasis of the lateral segment of the liver, the patient underwent distal gastrectomy. Histopathology of the resected specimen revealed that the tumor cells were arranged in a hepatoid pattern. On immunohistochemical staining, the tumor cells were positive for alpha-fetoprotein and Sal-like protein 4. Thus, the patient was diagnosed with GHAC. Hepatic resection of the solitary liver metastasis was performed. However, recurrence occurred and the patient achieved complete response following tegafur/gimeracil/oteracil-based chemotherapy.ConclusionsGHAC is a highly malignant histological subtype of GC. We reported on an extremely rare case of GHAC resulting in a spontaneous gastric perforation and reviewed the literature, including epidemiological data, treatment regimens, and the association between GHAC and alpha-fetoprotein-producing GC.

Clinicopathological Characteristics of Gastric Hepatoid Adenocarcinoma

Clinicopathological Characteristics of Gastric Hepatoid Adenocarcinoma

Gastric hepatoid adenocarcinoma: a report of 25 patients

Objective To study the clinicopathological features and prognosis of Gastric hepatoid adenocarcinoma (GHA) and aims to guide future clinical practice. Method We retrospectively studied the clinical data of 25 patients with pathologically confirmed GHA who were admitted to our hospital from January 2003 to December 2015. Results There were 19 males and 6 females. The average age was 61.2 years. The clinical manifestations were non-specific. Pathologically, majority of GHA presented with ulcerative type, poor differentiation and extensive vascular cancerous embolus. Preoperative liver metastases were found in 12 patients, and postoperative liver metastases in 15 patients. Conclusions GHA is a special primary gastric adenocarcinoma which possesses both hepatocellular carcinoma-like and adenocarcinoma-like histology. GHA is characterized by a significantly elevated serum AFP and early hepatic metastasis. GHA is therefore often misdiagnosed as primary hepatocellular carcinoma. The main treatment option remains to be surgical resection, and the prognosis is poor. Key words: Gastric hepatoid adenocarcinoma; Primary hepatocarcinoma; Differential diagnosis; Treatment; Prognosis

A Rare Case of Gastric Hepatoid Adenocarcinoma Rapidly Progressing to Fulminant Liver Failure

Introduction: Hepatoid adenocarcinoma (HAC) is a rare type of extrahepatic tumor, morphologically resembling hepatocellular carcinoma, and most commonly recognized in East Asians. We present a Latin American patient who was found to have gastric HAC with liver metastases complicated by rapidly progressive liver failure. Case Presentation: A 65 year-old Guatemalan male with history of Type 2 diabetes mellitus presented with epigastric pain, melenic stools and weight loss. Laboratory values on admission revealed a hemoglobin of 6.1 g/mL, alanine aminotransferase of 139 U/L, aspartate aminotransferase of 179 U/L, total bilirubin of 3.5 mg/dL, alkaline phosphatase of 185 U/L, and INR of 1.2. Alpha feto-protein (AFP) level was elevated to 4,438 ng/mL. Other tumor markers were negative. A CT scan showed extensive thrombosis of the superior mesenteric vein extending to the portal vein, diffuse nodular circumferential wall thickening of the gastric body, moderate ascites, and enlarged lymph nodes. MRI demonstrated one 1.6 cm, nonenhancing lesion in the right lobe of the liver without evidence of cirrhosis. Esophagastroduodenoscopy revealed an ulcerating, friable mass extending along the lesser curvature from the gastric body to the antrum and involving the duodenal bulb. Gastric and liver biopsies showed poorly differentiated adenocarcinoma with immunohistochemistry of the stomach and liver positive for AFP and CEA (Figure 1) but negative for Arginase-1 (Figure 2). The diagnosis was consistent with HAC. Over a two-month period, the patient developed jaundice, tense ascites, and encephalopathy. Repeat imaging showed multiple liver lesions. Aminotransferases continued to trend up, and the bilirubin rose to 34 mg/dL and INR to 2.5. The patient ultimately died from liver failure.Figure 1Figure 2Discussion: HAC has an extremely poor prognosis. Koide et al (AJG, 1999) described AFP producing gastric cancers as richly neovascular, highly proliferative, and weakly apoptotic. In our case, the fulminant liver failure was secondary to extensive portal vein thrombosis and rapid development of liver metastases. We theorize that such rapidly progressive course is attributed to the tumor's biological behavior as a high-grade malignancy. We suggest that diagnosis should be suspected in cases with gastric tumor, liver lesions and elevated AFP, as early diagnosis relies on high index of suspicion.

Gastric hepatoid adenocarcinoma: a specific type of gastric adenocarcinoma easily misdiagnosed as hepatocellular carcinoma

Gastric hepatoid adenocarcinoma (GHA) is a rare but important sub-type of gastric adenocarcinoma characterized by high serum α-fetoprotein, early lymphatic and hepatic metastasis, and poor prognosis. Clinically, the presentation could be atypical, liver neoplasm could be the initial finding. With similar clinicopathological presentation as hepatocellular carcinoma (HCC), prompt and correct diagnosis can be a challenge, especially in endemic areas with a high incidence of HCC. Once diagnosed, surgical removal remains the treatment of choice. This review focus on advancement on the biological, histological and immunohistological features, and the clinicopathological presentation of GHA. Key words: Gastric hepatoid adenocarcinoma; Hepatocellular carcinoma; Differential diagnosis; Treatment; Prognosis

Clinicopathologial features of gastric hepatoid adenocarcinoma.

Gastric hepatoid adenocarcinoma (GHA), a rare type of primary gastric cancer, is characterized by hepatocellular carcinoma-like histology. As details of this disease remain unknown, the aim of this study was to evaluate the clinicopathological features of GHA. From January 2001 to December 2010, 4563 patients were diagnosed with primary gastric cancer at Chang Gung Memorial Hospital, Linkou Medical Center. Ten (0.22%) of these patients were diagnosed with GHA. The clinicopathological characteristics of these patients were collected retrospectively. The median age at diagnosis was 65.5 years, and six patients (60%) were male. Seven patients had lymph node metastasis and five had distant metastasis, with the liver as the most common site (four cases). Serum alpha-fetoprotein (AFP) levels were elevated in seven of eight patients (median: 359.2 ng/ml; range: 4.3-6535.6 ng/ml). Endoscopically, six tumors were classified as Borrmann's type III cancer with the appearance of fungating mass lesion with a purple, berry-like surface. Of the five patients without distant metastasis, all received curative-intent surgery and four received adjuvant chemotherapy. Four patients with distant metastasis received either palliative operation or chemotherapy, and one patient received neither operation nor chemotherapy due to a poor performance status. The median survival time was 7.2 months (range: 0.7-131.8 months), and the 5-year survival rate was 20%. There was survival benefit in the chemotherapy groups. GHA is a rare subtype of gastric cancer which is prone to lymph node and liver metastasis. Most GHAs appear as Borrmann's type III fungating mass lesion with a purple, berry-like surface. Although the prognosis of advanced stage GHA is poor, chemotherapy might provide some benefit.

Ex vivo hepatectomy and partial liver autotransplantation for hepatoid adenocarcinoma: A case report.

We previously reported the case of a 56-year-old male who underwent surgical treatment for gastric hepatoid adenocarcinoma and splenic metastasis. The present study reports the case of the same patient who underwent successful ex vivo hepatectomy and partial liver autotransplantation. Computed tomography scans demonstrated that the tumor was located in the left and caudate lobes of the liver, with hepatic vein and inferior vena cava involvement, and right portal vein compression. To clarify the association between the vessels and the tumor, a three-dimensional imaging technique was used to reconstruct the liver architecture. During the surgery, the whole liver was removed with the retrohepatic vena cava, which was replaced with a prosthetic graft without a veno-venous bypass; a portacaval shunt for the anhepatic phase was performed simultaneously. The surgery lasted 9 h, and the anhepatic phase lasted 4 h. Blood loss during the surgery was recorded at 1,500 ml. The time taken for recovery was 21 days post-surgery, and at 20 months, the patient was disease-free. To the best of our knowledge, this is the first case of ex vivo liver resection performed for hepatic metastasis of hepatoid adenocarcinoma to be reported.

Case Series of Gastric Hepatoid Adenocarcinoma

Case Series of Gastric Hepatoid Adenocarcinoma

Magnetic resonance imaging diffusion-weighted imaging for diagnosis of a gastric hepatoid adenocarcinoma

A 63-year-old man consulted his general practitioner (GP) for bdominal pain in March 2010. Laboratory examination revealed n elevated alpha-fetoprotein and the GP referred the patient for uspected hepatocellular carcinoma. A computed tomography scan howed no tumour. Magnetic resonance imaging (MRI) confirmed he absence of hepatic tumour but showed irregular thickening of tomach wall on T2-weighted image with an increased signal on igh b-value (1000 s/mm2) in diffusion-weighted imaging (Fig. 1). pper endoscopy revealed a large ulcerated tumour of the distal tomach. Biopsy samples revealed hepatoid adenocarcinoma (HAC) nd the patient underwent subtotal gastrectomy. The tumour was a