Journal of Pathology and Translational Medicine

Original Articles

Clinicopathological Analysis of Hepatocellular Adenoma According to New Bordeaux Classification: Report of Eight Korean Cases: Hyunchul Kim, Ja-June Jang, Dong-Sik Kim, Beom Woo Yeom, Nam Hee Won; Korean J Pathol. 2013;47(5):411-417. Published online October 25, 2013; DOI: https://doi.org/10.4132/KoreanJPathol.2013.47.5.411

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Background

Hepatocellular adenoma (HCA) is a rare benign tumor of the liver. A subtype classification of HCA (hepatocyte nuclear factor 1α [HNF1α]-mutated, β-catenin-mutated HCA, inflammatory HCA, and unclassified HCA) has recently been established based on a single institutional review of a HCA series by the Bordeaux group.

Methods

We used histologic and immunohistochemical parameters to classify and evaluate eight cases from our institution. We evaluated the new classification method and analyzed correlations between our results and those of other reports.

Results

Seven of our eight cases showed histologic and immunohistochemical results consistent with previous reports. However, one case showed overlapping histologic features, as previously described by the Bordeaux group. Four cases showed glutamine synthetase immunohistochemical staining inconsistent with their classification, indicating that glutamine synthetase staining may not be diagnostic for β-catenin-mutated HCA. HNF1α-mutated HCA may be indicated by the absence of liver fatty acid binding protein expression. Detection of amyloid A may indicate inflammatory HCA. HCA with no mutation in the HNF1α or β-catenin genes and no inflammatory protein expression is categorized as unclassified HCA.

Conclusions

Although the new classification is now generally accepted, validation through follow-up studies is necessary.

Citations

Citations to this article as recorded by

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Carla Henriques Agostini, Osmar Damasceno Ribeiro, Arlete Fernandes, Adriana Caroli-Bottino, Vera Lucia Pannain
Surgical and Experimental Pathology.2020;[Epub] CrossRef
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Journal of Hepatology.2018; 68(5): 1033. CrossRef
Hepatocellular adenoma: Classification, variants and clinical relevance
Paulette Bioulac-Sage, Christine Sempoux, Charles Balabaud
Seminars in Diagnostic Pathology.2017; 34(2): 112. CrossRef
A Limited Immunohistochemical Panel Can Subtype Hepatocellular Adenomas for Routine Practice
Brent K. Larson, Maha Guindi
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Hepatocellular Neoplasms Arising in Association With Androgen Use
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American Journal of Surgical Pathology.2016; 40(4): 454. CrossRef
Pigmented hepatocellular adenomas have a high risk of atypia and malignancy
Taofic Mounajjed, Saba Yasir, Patrice A Aleff, Michael S Torbenson
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SIRT1 Expression Is Associated with Good Prognosis in Colorectal Cancer: Wonkyung Jung, Kwang Dae Hong, Woon Yong Jung, Eunjung Lee, Bong Kyung Shin, Han Kyeom Kim, Aeree Kim, Baek-hui Kim; Korean J Pathol. 2013;47(4):332-339. Published online August 26, 2013; DOI: https://doi.org/10.4132/KoreanJPathol.2013.47.4.332

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Abstract PDF

Background

Silent mating type information regulation 2 homolog 1 (SIRT1), an NAD+-dependent deacetylase, might act as a tumor promoter by inhibiting p53, but may also as a tumor suppressor by inhibiting several oncogenes such as β-catenin and survivin. Deleted in breast cancer 1 (DBC1) is known as a negative regulator of SIRT1.

Methods

Immunohistochemical expressions of SIRT1, DBC1, β-catenin, surviving, and p53 were evaluated using 2 mm tumor cores from 349 colorectal cancer patients for tissue microarray.

Results

Overexpression of SIRT1, DBC1, survivin, and p53 was seen in 235 (67%), 183 (52%), 193 (55%), and 190 (54%) patients, respectively. Altered expression of β-catenin was identified in 246 (70%) patients. On univariate analysis, overexpression of SIRT1 (p=0.029) and altered expression of β-catenin (p=0.008) were significantly associated with longer overall survival. Expression of SIRT1 was significantly related to DBC1 (p=0.001), β-catenin (p=0.001), and survivin (p=0.002), but not with p53. On multivariate analysis, age, tumor stage, differentiation, and expression of SIRT1 were independent prognostic factors significantly associated with overall survival.

Conclusions

SIRT1 overexpression is a good prognostic factor for colorectal cancer, and SIRT1 may interact with β-catenin and survivin rather than p53.

Citations

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Experimental & Molecular Medicine.2023; 55(10): 2220. CrossRef
Association of β-Catenin, APC, SMAD3/4, Tp53, and Cyclin D1 Genes in Colorectal Cancer: A Systematic Review and Meta-Analysis
Hongfeng Yan, Fuquan Jiang, Jianwu Yang, Ying-Kun Xu
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MONICA SAVIO, VALENTINA MINOIA, PAOLA FULGHIERI, LUCIA ANNA STIVALA, VIRGINIE SOTTILE
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Amna Matly, Jean A. Quinn, Donald C. McMillan, James H. Park, Joanne Edwards
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Liz M. Garcia-Peterson, Xiaoling Li
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Molecular Biological Characteristics of Differentiated Early Gastric Cancer on the Basis of Mucin Expression.: Nari Shin, Hye Yeon Kim, Woo Kyung Kim, Min Gyung Park, Kyung Bin Kim, Dong Hoon Shin, Kyung Un Choi, Jee Yeon Kim, Chang Hun Lee, Gi Young Huh, Mee Young Sol, Do Youn Park; Korean J Pathol. 2011;45(1):69-78.; DOI: https://doi.org/10.4132/KoreanJPathol.2011.45.1.69

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Abstract PDF

BACKGROUND
It is clear that the biologic characteristics of gastric cancer are different on the basis of mucin phenotypes. However, there are unabated controversies on the exact biologic differences of mucin expression in gastric cancer.
METHODS
We analyzed various protein expressions and microsatellite instability (MSI) status based on mucin expression in 130 differentiated early gastric adenocarcinoma cases. Furthermore, we evaluated the genomic alternation in 10 selected differentiated early gastric adenocarcinoma cases using array based comparative genomic hybridization (aCGH).
RESULTS
Intestinal mucin predominant subtype showed significantly elevated p53 protein and caudal-related homeobox 2 expression, and delocalization of beta catenin expressions compared to the gastric mucin predominant subtype. On MSI status, the gastric mucin predominant subtype more frequently showed unstable status than the intestinal mucin predominant subtype. CGH study showed more frequent chromosomal gain and loss in the intestinal mucin predominant subtype than the gastric mucin predominant subtype, albeit without statistical significance. Interestingly, there were significant differences in chromosomal alternation between four mucin phenotypes.
CONCLUSIONS
Study results suggest possible different points of biologic behaviors in early differentiated gastric adenocarcinomas by mucin expression type.

Citations

Citations to this article as recorded by

Mucin Expression in Gastric Cancer: Reappraisal of Its Clinicopathologic and Prognostic Significance
Dae Hwan Kim, Nari Shin, Gwang Ha Kim, Geum Am Song, Tae-Yong Jeon, Dong-Heon Kim, Gregory Y. Lauwers, Do Youn Park
Archives of Pathology & Laboratory Medicine.2013; 137(8): 1047. CrossRef
Microsatellite Instability Status in Gastric Cancer: A Reappraisal of Its Clinical Significance and Relationship with Mucin Phenotypes
Joo-Yeun Kim, Na Ri Shin, Ahrong Kim, Hyun-Jeong Lee, Won-young Park, Jee-Yeon Kim, Chang-Hun Lee, Gi-Young Huh, Do Youn Park
Korean Journal of Pathology.2013; 47(1): 28. CrossRef

The Loss of E-cadherin is Associated with the Epigenetic Alteration of CDH1 in Breast Cancer and it is also Associated with an Abnormal beta-catenin Expression in Lobular Carcinoma.: Gwangil Kim, Ji Young Kim, Hee Jung An, Haeyoun Kang, Tae Heon Kim, Jung Yon Shim, Jin Hyung Heo, Hai Lin Park, Young Kil Choi; Korean J Pathol. 2009;43(5):400-407.; DOI: https://doi.org/10.4132/KoreanJPathol.2009.43.5.400

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Abstract PDF

BACKGROUND
APC and E-cadherin are the key molecules in the Wnt/beta-catenin pathway. We attempted to define the epigenetic alteration of APC and CDH1 (the E-cadherin gene) and the expression of Wnt-related molecules in human mammary carcinomas.
METHODS
Sixty-four mammary carcinomas, including 52 invasive ductal carcinomas (IDCs) and 12 invasive lobular carcinomas (ILCs), were evaluated using methylation-specific PCR and immunohistochemistry. We performed immunohistochemistry for E-cadherin, beta-catenin, APC, Wnt1, cyclin D1, ER, PR and C-erb B2.
RESULTS
Hypermethylation of APC and CDH1 was observed in 38 (59%) and 28 (44%) cases, respectively. CDH1 hypermethylation in ILCs was increased compared to that in IDCs (p=0.002) and it was associated with the loss of E-cadherin (p=0.02) and beta-catenin (p=0.042). APC methylation was positively correlated with the ER expression (p=0.021). Abnormal cytoplasmic localization of beta-catenin was found in 10 cases and any expression was not detected in six cases. In ILCs, the E-cadherin or beta-catenin expression was markedly decreased compared to that in IDCs (p<0.001 in both).
CONCLUSIONS
Methylation of APC or CDH1 was relatively frequent in mammary carcinomas. The loss of E-cadherin in mammary carcinoma was associated with CDH1 methylation, and abnormal beta-catenin expression was related to the loss of E-cadherin in ILC.

Citations

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Wnt/β-catenin signaling pathway activation reverses gemcitabine resistance by attenuating Beclin1-mediated autophagy in the MG63 human osteosarcoma cell line
Hao Tao, Feng Chen, Haifei Liu, Yanling Hu, Yingzhen Wang, Haiyan Li
Molecular Medicine Reports.2017; 16(2): 1701. CrossRef

beta-Catenin Expression in Gastric Carcinogenesis.: Haeyoun Kang, Yon Rak Choi, Hoguen Kim; Korean J Pathol. 2001;35(5):376-382.

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Abstract PDF: BACKGROUND
The molecular pathogenesis of gastric carcinoma is not yet well characterized. The purpose of this study is to assess the role of beta-catenin in gastric carcinogenesis.
METHODS
We analyzed beta-catenin expression using immunohistochemistry on 68 gastric adenomas and 34 gastric adenocarcinomas, and compared the result with pathological and molecular types of tumors and E-cadherin expression.
RESULTS
Nuclear expression of beta-catenin was noted more frequently in gastric adenomas than in carcinomas (40% vs. 21%, 0.05< or = P<1). There was no significant relationship between nuclear beta-catenin expression and histologic degree of adenoma, histologic type of carcinoma or microsatellite instability. E-cadherin expression showed significantly more frequent decrease in the membrane stainability of carcinomas compared to adenomas (P<0.01).
CONCLUSIONS
The frequent nuclear beta-catenin expression in gastric adenomas suggests that the beta-catenin alteration might play an early role in gastric carcinogenesis.

Correlation of the Nuclear beta-catenin Expression with the Clinicopathological Parameters of Hepatocellular Carcinoma.: Hyoung Jong Kwak, Ha Na Choi, Sung Ho Hwang, Keum Ha Choi, Ho Sung Park, Kyu Yun Jang, Myoung Ja Chung, Myoung Jae Kang, Dong Geun Lee, Woo Sung Moon; Korean J Pathol. 2008;42(4):208-214.

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Abstract PDF: BACKGROUND
Hepatocellular carcinoma (HCC) is the most common primary malignant tumor of the human liver. However, the molecular changes and mechanisms that regulate the development and progression of HCC remain unclear. Beta-catenin is known as a multi-functional protein that acts as a regulator of the cadherin-mediated cell-cell adhesion system and also in the Wingless/Wnt signal transduction pathway. The aim of this study was to investigate the expression of beta-catenin and its possible role in HCC.
METHODS
We investigated the expression of beta-catenin, Ki-67, TP53, alpha-smooth muscle actin and CD34 by performing immunohistochemical staining for 61 specimens of HCC and their adjacent non-tumorous tissue. We also examined the relationship between the nuclear expression of beta-catenin and the clinicopathologic parameters.
RESULTS
The altered expression of beta-catenin was not detected in the nontumorous liver tissue. The nuclear expression of beta-catenin was observed in approximately 16% (10/61) of the HCC specimens. Double immunohistochemical staining for beta-catenin and E-cadherin showed a close relationship between nuclear translocation of beta-catenin and the loss of the membranous E-cadherin expression. Significant correlation was found between the nuclear translocation of beta-catenin and the tumor size, tumor necrosis and the presence of microvessel invasion and intrahepatic metastasis (p<0.05).
CONCLUSIONS
This data indicates that nuclear translocation of beta-catenin could play a role in the growth and progression of HCC.

Prognostic Significance of Abnormal beta - catenin Expression in Breast Carcinoma.: Won Ae Lee; Korean J Pathol. 2005;39(2):114-119.

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Abstract PDF: BACKGROUND
The subcellular localization and activity of beta-catenin are tightly regulated within the cell. The aim of this study was to analyze the aberrant beta-catenin expression in breast carcinomas and to determine its clinical significance.
METHODS
Fifty five cases of breast carcinoma were immunostained with monoclonal antibodies against beta-catenin. Normal expression of -catenin was defined as exclusive membranous staining. Abnormal expression of beta-catenin was reclassified into 3 categories: complete or partial loss of membranous staining (LOM) without cytoplasmic staining and nuclear staining, LOM with cytoplasmic staining and without nuclear staining, and LOM with nuclear staining and with/without cytoplasmic staining. RESULTS: Normal membranous beta-catenin expression was detected in 25 (45.5%) of 55 cases of breast carcinoma. Thirty cases with abnormal -catenin expression comprised 9 cases (16.1%) showing LOM without cytoplasmic and/or nuclear staining, 20 cases (36.4%) showing LOM with cytoplasmic staining and without nuclear staining, and one case (1.8%) showing LOM with nuclear and cytoplasmic staining. Abnormal beta-catenin expression was significantly correlated with lymph node metastasis (p=0.03). LOM with cytoplasmic and/or nuclear expression was significantly correlated with poor disease free survival by univariate (p=0.03) and multivariate analyses (p=0.03). In addition, it was correlated with poor overall survival with a borderline significance (p=0.059).
CONCLUSIONS
This study suggests that the cytoplasmic and/or nuclear expression of beta-catenin can be used as a biologic marker for predicting disease recurrence and poor patients' survival in breast carcinomas.

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