scholarly journals Diagnostic Role of Aldoketoreductase family 1B10 (AKR1B10) in Hepatocellular Carcinoma and Benign Hepatic Lesions

QJM ◽  
2020 ◽  
Vol 113 (Supplement_1) ◽  
Author(s):  
L M Farid ◽  
M H Abdelrahman ◽  
S A Sammour ◽  
N A Hegazy ◽  
E Ibrahim ◽  
...  

Abstract Background Hepatocellular carcinoma is the most common primary liver cancer. It is the second most common cause of cancer deaths. The majority of HCCs arise in chronically diseased livers with cirrhotic background. Several benign lesions might be found in a cirrhotic liver along with hepatocellular carcinoma (HCC), and may exhibit typical or atypical imaging features. Distinction between benign hepatocellular nodular lesions, such as hepatic adenoma, and focal nodular hyperplasia, from HCC is of crucial clinical importance in determining appropriate therapy and assessing the prognosis.AKR1B10 is a promising marker that is recently used in the HCC diagnosis. Aim of the Work is to study the immuno-histochemical expression of Aldoketoreductase family 1B10 (AKR1B10) in hepatocellular carcinoma and benign hepatic lesions, to assess its role in the diagnosis of hepatocellular carcinoma and in differentiating it from different benign hepatic lesions. Materials and Methods Hepatocellular carcinoma (HCC(T)):(109), corresponding non tumor tissue with and without cirrhosis (NT):(80), benign hepatic lesions (Focal Nodular Hyperplasia(FNH):(6) and Hepatic Adenoma(HCA)) (6) and Hepatic Cirrhosis (Cs) without HCC (16). Results AKR1B10 was over expressed in 82.6% (90/109) of studied HCC cases, negative expression in studied corresponding non-tumor hepatic tissue (NT) in 92.5% (74/80), complete negativity of AKR1B10 was observed in studied benign hepatic lesions 100% (0/12) and also negative expression in 81.3% (13/16) of included hepatic cirrhosis without HCC. Conclusion AKR1B10 is a promising marker in the diagnosis of HCC and distinguishing it from other benign hepatic lesions.

2015 ◽  
Vol 139 (4) ◽  
pp. 537-542 ◽  
Author(s):  
Benjamin J. Swanson ◽  
Martha M. Yearsley ◽  
William Marsh ◽  
Wendy L. Frankel

Context The correct histologic diagnosis of mass lesions of the liver can be difficult, especially in biopsy samples. Reticulin, glypican-3, and glutamine synthetae are stains that can help distinguish hepatocellular carcinoma, hepatic adenoma, and focal nodular hyperplasia. Objective To evaluate the utility of a triple stain of reticulin, glypican-3, and glutamine synthetae in distinguishing hepatocellular carcinoma, hepatic adenoma, and focal nodular hyperplasia. Design Whole tissue sections and tissue microarrays were evaluated with a triple stain of reticulin, followed by glutamine synthetae (diaminobenzidine, brown chromogen) and glypican-3 (alkaline phosphatase, red chromogen). The 109 cases evaluated included whole tissue section hepatocellular carcinoma (n = 16), tissue microarray hepatocellular carcinoma (n = 19), whole tissue section hepatic adenoma (n = 15), tissue microarray hepatic adenoma (n = 13), whole tissue section focal nodular hyperplasia (n = 13; 12%), tissue microarray focal nodular hyperplasia (n = 13), as well as nonmalignant liver parenchyma adjacent to hepatocellular carcinoma (n = 20). All cases were scored for reticulin being intact or lost, positive or negative staining for glypican-3, and diffuse, maplike, perivenular, or negative staining for glutamine synthetae. Results The combination of intact reticulin with either glypican-3 negativity or negative glutamine synthetae was 92% sensitive and 95% specific in the distinction of tissue microarray hepatic adenoma from hepatocellular carcinoma. For the distinction of tissue microarray focal nodular hyperplasia and hepatic adenoma, maplike glutamine synthetae was most useful and was 85% sensitive and 100% specific. Conclusions The triple stain of reticulin, glypican-3, and glutamine synthetae is useful in the differentiation of hepatocellular carcinoma, hepatic adenoma, and focal nodular hyperplasia on biopsy specimens. Furthermore, this triple stain is advantageous to single stains and can help when aberrant staining patterns are observed.


2006 ◽  
Vol 5 (3) ◽  
pp. 206-211 ◽  
Author(s):  
Javier Lizardi-Cervera ◽  
Lorena Cuéllar-Gamboa ◽  
Daniel Motola-Kuba

2018 ◽  
Vol 31 (9) ◽  
pp. 470 ◽  
Author(s):  
Henrique Donato ◽  
Luísa Andrade ◽  
Nina Bastati ◽  
Augusta Cipriano ◽  
Ahmed Ba-Ssalamah ◽  
...  

Introduction: Multiacinar regenerative nodules are benign hepatocellular nodules related to vascular disturbances of the liver. They strongly resemble conventional focal nodular hyperplasia but are connected to different clinical settings, typically chronic liver disease. The purpose of the present study was to describe the key imaging features of these lesions and compare them with a control arm of focal nodular hyperplasia.Material and Methods: A blinded consensus review of liver magnetic resonance consisting of 26 cases of multiacinar regenerative nodules and 25 cases of focal nodular hyperplasia was performed. Lesion size, shape, margins, structure, T1 and T2 signal intensity, diffusion and contrast-enhanced features (including hepatobiliary phase), presence of a central scar and of a peripheral hypointense rim were compared between the two groups.Results: Significant differences between multiacinar regenerative nodules and focal nodular hyperplasia included size (median 2.35 cm, IQR: 2.13, vs 6.00 cm, IQR: 5.20, respectively, p < 0.001), presence of a peripheral hypointense rim after contrast (n = 9 vs n = 2 cases, p = 0.038) and of a central scar (n = 9 vs n = 20, p = 0.002). There were no other significant differences.Discussion: Overall multiacinar regenerative nodules and focal nodular hyperplasia have very similar imaging features but lack of a central scar and presence of a hypointense rim should suggest a diagnosis of multiacinar regenerative nodules.Conclusions: Recognition of the imaging findings of multiacinar regenerative nodules can explain some atypical cases of focal nodular hyperplasia, avoiding unnecessary biopsies. They may also be the trigger to investigate an unsuspected underlying liver vascular abnormality.


1983 ◽  
Vol 84 (5) ◽  
pp. 994-1002 ◽  
Author(s):  
P. Kerlin ◽  
G.L. Davis ◽  
D.B. McGill ◽  
L.H. Weiland ◽  
M.A. Adson ◽  
...  

2020 ◽  
Vol 24 (3) ◽  
pp. 389-403
Author(s):  
Lauren Myers ◽  
Joseph Ahn

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