Tissue Diagnosis of Hepatocellular Carcinoma

Abstract

The current American Association for the Study of Liver Diseases (AASLD) guideline provides strategies for achieving the diagnosis of hepatocellular carcinoma (HCC) based on the size of liver nodules seen on surveillance imaging. For lesions less than 1 cm in size, follow-up surveillance imaging is recommended. Lesions larger than 2 cm require typical radiological hallmark on dynamic imaging. Lesions of 1-2 cm in size require typical imaging features including intense uptake of contrast during arterial phases followed by decreased enhancement during portal venous phases on at least 2 imaging modalities. In cases of atypical radiological features of the suspected lesion, tissue diagnosis either by fine needle aspiration or biopsy should be obtained. Although fine needle aspiration could give a smaller risk of seeding than biopsy, biopsy has been preferred over cytology. Percutaneous biopsy of HCC carries a potential risk of tumor seeding along the needle tract. However the risk is low and there is no clear evidence of post transplant recurrence due to needle tract seeding. Histopathologic assessment can differentiate between premalignant lesions such as dysplastic nodules and early HCC. Atypical variants of HCC can be recognized morphologically which may have associated prognostic value. ( J CLIN EXP HEPATOL 2014;4:S67-S73) H epatocellular carcinoma (HCC) is the sixth most common cancer in the world. 1 Its incidence is expected to rise in the future due to anticipated increase in cirrhosis secondary to viral hepatitis. Over the past 2 decades, the incidence of HCC has tripled, and hepatitis C virus (HCV) related HCC is the fastest-rising cause of cancer-related death in the United States. [2][3][4] Hepatocellular carcinoma develops within an established background of chronic liver disease in 70-90% of all patients. 5 The most frequent risk factor for HCC is chronic hepatitis B virus (HBV) infection in Asia and Africa. However HCV predominates as a risk factor in Europe and Japan. 2 Other well established risk factors are alcoholism, non-alcoholic fatty liver disease and diabetes. [6][7][8] Treatment depends on early diagnosis by screening high-risk patients when HCC is small and remains localized to the liver. Various studies suggest surveillance of HCC in cirrhotic patients irrespective of its etiology. Surveillance of non-cirrhotic patients is also advocated, especially in HBV carriers with serum viral load >10,000 copies/ml 9 or HCV infected patients with bridging fibrosis. Patients with HCV infection and advanced fibrosis remain at risk for HCC even after achieving sustained virological response following antiviral treatment.The preferred imaging method for screening is ultrasonography (USG) which is well tolerated and widely available. However, the sensitivity of USG for HCC detection is low because small nodules can be missed in a cirrhotic liver. 10 Use of contrast-enhanced USG improves the diagnostic performance of USG for HCC.The most used serological test in clinical setting for screening is alpha-fetop...

Potential diagnostic value of lncRNA SPRY4-IT1 in hepatocellular carcinoma

“…Clinically, the most frequently used factor for the diagnosis of HCC is AFP, but the sensitivity is low (27). Using CT and MRI to diagnose the early stage of HCC, the sensitivity (55-91%) and specificity (77-96%) are higher (28). However, due to the different ability among doctors to identify the lesion, the accuracy is different.…”

Prognostic and Diagnostic Significance of SDPR-Cavin-2 in Hepatocellular Carcinoma

“…However, even in 15%-30% advanced patients, the AFP levels remain normal, leading to a high negative rate [9,10]. Despite the specificity and sensitivity of the early diagnosis of HCC was improved quite bit by CT and MRI, the accuracy is still determined by the ability to discriminate between tumor and non-neoplastic lesions [11]. Up to now, we are short of good early diagnostic and predictive markers for HCC [12,13].…”

LKB1 expression reverses the tumorigenicity of L02 cells

“…Notably, Nakau et al reported a high hCC prevalence in LKB1 (+/-) mice (38), suggestive of a strong LKB1 involvement in liver tumorigenesis. We demonstrated that the L02 cells possessed the capability to initiate tumor formation in immunocompromised mice after subcutaneous inoculation, and histology of the tumor tissues was markedly similar to the representative histopathology of human hCCs, including malignant cellular growth in trabecular patterns recapitulating liver cords (39). No expression of LKB1 protein was observed in these subcutaneous tumors, indicating that complete loss of LKB1 expression was required for the development of the carcinomas.…”