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Hepatocellular carcinomas can be further divided into distinct subtypes that provide important clinical information and biological insights. These subtypes are distinct from growth patterns and are on based on morphologic and mole...
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Hepatocellular carcinomas can be further divided into distinct subtypes that provide important clinical information and biological insights. These subtypes are distinct from growth patterns and are on based on morphologic and molecular findings. There are 12 reasonably well-defined subtypes as well as 6 provisional subtypes, together making up 35% of all hepatocellular carcinomas. These subtypes are discussed, with an emphasis on their definitions and the key morphologic findings.
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Deleted in Liver Cancer (DLC) proteins belong to the family of RhoGAPs and are believed to operate as negative regulators of the Rho family of small GTPases. So far, the role of the first identified member from the DLC family, DLC...
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Deleted in Liver Cancer (DLC) proteins belong to the family of RhoGAPs and are believed to operate as negative regulators of the Rho family of small GTPases. So far, the role of the first identified member from the DLC family, DLC1, was established as a tumor suppressor in hepatocellular carcinoma. The function of its close family relative, DLC2 is unequivocal. In the present study we attempted to determine whether the loss of DLC2 is a common feature of hepatocellular carcinoma tissue. We examined two types of hepatocellular carcinomatypical and fibrolamellar one. Our analysis revealed that DLC2 protein is not diminished in cancer tissue when compared to non-cancerous liver specimens. What is more, we observed DLC2 to be more abundantly expressed in cancer tissue, particularly in tumors with the inflammation background. In addition, we found that DLC2 gene status was diploid in virtually all tumor samples examined. Our results indicate that DLC2 is not diminished in hepatocellular carcinoma cells. It appears that members of the DLC family, although structurally highly related, may function differently in cancer cells.
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Cirrhotomimetic hepatocellular carcinoma is a recognized pattern exhibiting cirrhosis-like growth and a reputation for evading pretransplant detection. Five cases encountered from our institution were retrospectively reviewed. Cli...
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Cirrhotomimetic hepatocellular carcinoma is a recognized pattern exhibiting cirrhosis-like growth and a reputation for evading pretransplant detection. Five cases encountered from our institution were retrospectively reviewed. Clinicopathologic and literature reviews were performed. All five patients were male, aged?50–66. Diffuse, innumerable nodules were seen grossly, exhibiting predominantly well-to-moderate differentiation with pseudoglandular and trabecular patterns microscopically. By immunohistochemistry, the tumor was diffusely positive for Glypican-3, showed sinusoidal capillarization by CD34 and slightly increased MIB-1 proliferation index. At up to 3.25?years of follow-up, our cohort of cirrhotomimetic hepatocellular carcinoma?had no recurrence in 60% (3/5), solitary recurrence in 20% (1/5) and one patient had died of disease in?20% (1/5). Literature review suggests that these tumors recurred at a frequency of 50% (19 of 38 patients).
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Tanaka and colleagues report on the contribution of hepatitis C virus (HCV)–related hepatocellular carcinoma (HCC) to changes in HCC incidence in Osaka, Japan. Between 1981 and 2003, incidence of HCC among men age 50 to 59 years,...
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Tanaka and colleagues report on the contribution of hepatitis C virus (HCV)–related hepatocellular carcinoma (HCC) to changes in HCC incidence in Osaka, Japan. Between 1981 and 2003, incidence of HCC among men age 50 to 59 years, 60 to 69 years, and 70 to 79 years peaked in 1986, 1995, and 2000, respectively, with marked downward trends thereafter. Trends were similar in women. The rates of HCV-associated HCC decreased, but those of HCC unrelated to HCV did not change, suggesting that the decrease in HCC rates is related to the decreasing incidence of HCV.
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Hepatocellular carcinoma (HCC) is the third leading cause of cancer-related deaths worldwide, and its incidence continues to increase. Despite improvements in both medical and surgical therapies, HCC remains associated with poor o...
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Hepatocellular carcinoma (HCC) is the third leading cause of cancer-related deaths worldwide, and its incidence continues to increase. Despite improvements in both medical and surgical therapies, HCC remains associated with poor outcomes due to its high rates of recurrence and mortality. Approximately 50% of patients require systemic therapies that traditionally consist of tyrosine kinase inhibitors. Recently, however, immune checkpoint inhibitors have revolutionized HCC management, providing new therapeutic options. Despite these major advances, the different factors involved in poor clinical responses and molecular pathways leading to resistance following use of these therapies remain unclear. Alternative strategies, such as adoptive T cell transfer, vaccination, and virotherapy, are currently under evaluation. Combinations of immunotherapies with other systemic or local treatments are also being investigated and may be the most promising opportunities for HCC treatment. The aim of this review is to provide updated information on currently available immunotherapies for HCC as well as future perspectives.?The Author(s) 2022. Published by Baishideng Publishing Group Inc. All rights reserved.
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Pedunculated hepatocellular carcinoma (P-HCC) is a rare subtype of HCC. P-HCC may occur in patients without underlying liver cirrhosis and can be present with negative serum tumor markers. With a growing worldwide incidence of non...
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Pedunculated hepatocellular carcinoma (P-HCC) is a rare subtype of HCC. P-HCC may occur in patients without underlying liver cirrhosis and can be present with negative serum tumor markers. With a growing worldwide incidence of nonalcoholic fatty liver disease, non-cirrhotic HCC will likely become more prevalent. We report a patient presenting to the hospital with nonspecific symptoms of weight loss, abdominal discomfort, and early satiety. Abdomen palpation found a large firm mass in the right middle abdomen. Computed tomography imaging showed a large right abdominal mass without evidence of liver attachment. The patient underwent a diagnostic laparotomy where a single 17 cm exophytic mass originating from the left liver lobe was found and resected. Clear margins were attained, and pathology demonstrated HCC. Early diagnosis of HCC is critical to achieving curative treatment, and physicians should keep P-HCC in mind when presented with a similar patient.
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Purpose We aimed to distinguish between fibrolamellar hepatocellular carcinoma and scirrhous hepatocellular carcinoma histopathologically. Methods and results In this review, fibrolamellar hepatocellular carcinoma and scirrhous he...
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Purpose We aimed to distinguish between fibrolamellar hepatocellular carcinoma and scirrhous hepatocellular carcinoma histopathologically. Methods and results In this review, fibrolamellar hepatocellular carcinoma and scirrhous hepatocellular carcinoma two specific and rare variants of hepatocellular carcinoma, which are difficult to diagnose histopathologically are discussed. Conclusion The clinical, radiological, gross, histopathological, immunohistochemical, and molecular features of these two tumors, which are defined by the World Health Organization (WHO), are mentioned.
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The macrotrabecular (MT) pattern of hepatocellular carcinoma (HCC) has been suggested to represent a distinct HCC subtype. We retrospectively reviewed 231 HCC cases. Detailed pathologic evaluation for histologic patterns, includin...
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The macrotrabecular (MT) pattern of hepatocellular carcinoma (HCC) has been suggested to represent a distinct HCC subtype. We retrospectively reviewed 231 HCC cases. Detailed pathologic evaluation for histologic patterns, including MT-pattern, was performed for each case and recorded as percentage involved at 10% intervals. MT-pattern was defined as having trabeculae >6 cells thick. After excluding all recognized HCC subtypes, remaining cases were deemed conventional HCC (CV-HCC) and served as controls. HCCs with a component of >= 10%, >= 30% and >= 50% MT-pattern were identified in 41 (17.7%), 24 (10.4%) and 4 (1.7%) cases, respectively. The clinicopathologic features of HCCs with 10% to 29% MT-pattern (n=17, 7.4%) were largely similar to CV-HCC. No significant difference was observed between the 30% and 49% (n=20) and >= 50% (n=4) MT groups, hence these were combined for further analysis as MT-HCC. MT-HCCs (>= 30% MT-pattern) were larger tumors (5.5 vs. 3.1 cm), were less likely to be associated with cirrhosis (54% vs. 79%), were more likely to have hepatitis B (21% vs. 5%) and less likely hepatitis C infection (33% vs. 58%) compared with CV-HCC. MT-HCC was associated with the presence of anaplastic tumor cells (42% vs. 14%), higher alpha-fetoprotein level, higher AJCC stage, and higher histologic grade. Compared with patients with CV-HCC, patients with MT-HCC had poorer overall survival. Patients with MT-HCC who underwent primary resection or transplantation had a higher recurrence rate and worse recurrence-free survival. Our findings suggest that >= 30% MT-pattern could be used as the more appropriate cut-off for defining MT-HCC, which represents a unique and aggressive HCC histologic subtype.
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It has been reported that miR-21 is upregulated in hepatocellular carcinoma (HCC), and overexpressed miR-21 plays a key role in promoting cell cycle progression, reducing cell death and favoring angiogenesis and invasion. Overexpr...
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It has been reported that miR-21 is upregulated in hepatocellular carcinoma (HCC), and overexpressed miR-21 plays a key role in promoting cell cycle progression, reducing cell death and favoring angiogenesis and invasion. Overexpression of hepatocellular carcinoma, downregulated 1 (HEPN1) exhibits an antiproliferative effect on HepG2 cells, suggesting that silencing of HEPN1 may contribute to carcinogenesis of hepatocytes. In silico analysis revealed that HEPN1 may be a potential target of miR-21. Using quantitative reverse transcription PCR and Western blot, we found that HEPN1 was strikingly downregulated in both mRNA (fold change was 33.5, P<0.0001) and protein levels in human HCC tumor tissues, in comparison with the adjacent non-tumor tissues. More importantly, the expression level of HEPN1 was inversely correlated with the expression of miR-21 in HCC (R-2=0.442, P<0.0001). The combination between the 3' untranslated region (UTR) of HEPN1 with miR-21 was experimentally verified by a miRNA luciferase reporter approach. The suppressed cell proliferation upon stimulation of miR-21 inhibitor could be partially abolished by knocking down HEPN1, so inhibition of miR-21 expression in HCC cells profoundly suppressed cell proliferation partially by upregulating HEPN1 expression. Taken together, the current study suggested an underlying mechanism that miR-21 directly target HEPN1 and inhibit its expression during the carcinogenesis of HCC. HEPN1 may thus be a candidate as a therapeutic target for patients with HCC.
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Living donor liver transplant (LDLT) is one of the important modalities to treat hepatocellular carcinoma (HCC) in Asian countries. LDLT for HCC consists of >50% of the total LDLT at Seoul National University Hospital (SNUH). Mila...
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Living donor liver transplant (LDLT) is one of the important modalities to treat hepatocellular carcinoma (HCC) in Asian countries. LDLT for HCC consists of >50% of the total LDLT at Seoul National University Hospital (SNUH). Milan or University of California San Francisco (UCSF) criteria were not considered as absolute selection criteria for LDLT at SNUH. We experienced that some patients with beyond Milan criteria have long-term survival after LDLT. On the contrary, LDLT showed poorer outcome than deceased donor LT (DDLT) in patients with within UCSF criteria in our series. There are several reasons for higher recurrence rate in LDLT such as fast-track selection and rapid regeneration in LDLT. Therefore, the feasibility of conventional criteria based on tumor size and number to predict HCC recurrence after LDLT seemed somewhat different from that of DDLT. We identified significant pre-operative biological factors such as AFP, PIVKAII, and PET positivity. Combination of those biological factors predicted HCC recurrence better than conventional criteria based on size and number. All patients with three risk factors showed 100% recurrence. This group should be excluded regardless of Milan criteria. There have been debates in expanding the criteria in LDLT. Some centers still stick on the expanded criteria that are estimated to yield a 5-year survival of approximately 50%. However, there was no completely tailored criterion to predict HCC recurrence exactly. The survival after recurrence was also different from case by case. Furthermore, the introduction of m-TOR inhibitor and targeted agent improved survival after recurrence. Based on these ideas, we experimentally expanded our indication to the far advanced HCC (HCC larger than 10 cm or more than 10 numbers or with macrovascular invasion preoperatively). The patients with far advanced HCC have usually poor prognosis. However, the selected patients with low AFP (<200 ng/ml), 2-year recurrence free survival was 54.5%.In conclusion, we are now expanding the criteria selectively up to patients with macrovascular invasion if there are no other effective treatment options and the expected survival and risk after LT is acceptable in both recipient and donor. The current absolute contraindication for LDLT in SNUH is extrahepatic metastasis.
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