• 대한유전성대사질환학회지
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• 제13권1호
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• pp.48-53
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• 2013

Tyrosinemia I (fumarylacetoacetate hydrolase deficiency) is an autosomal recessive inborn error of tyrosine metabolism that produces liver failure in infancy or a more chronic course of liver disease with cirrhosis, often complicated by hepatocellular carcinoma in childhood or early adolescence. We studied a 37-year-old woman with tyrosinemia I whose severe liver disease in infancy and rickets during childhood were resolved with dietary therapy. From 14 years of age, she resumed unrestricted diet with the continued presence of the biochemical features of tyrosinemia, yet maintained normal liver function. In adult years, she accumulated only a small amount of succinylacetone. Despite this evolution to a mild biochemical and clinical phenotype, she eventually developed hepatocellular carcinoma. Her fumarylacetoacetate hydrolase genotype consists of a splice mutation, IVS6-1G>T, and a novel missense mutation, p.Q279R. Studies of resected liver revealed the absence of hydrolytic activity and immunological expression of fumarylacetoacetate hydrolase in tumour. In the non-tumoral areas, however, 53% of normal hydrolytic activity and immunologically present fumarylacetoacetate hydrolase were found. This case demonstrates the high risk of liver cancer in tyrosinemia I even in a seemingly favorable biological environment. In this study of tyrosinemia I, Case 2 with negative succinylacetone accumulation and the recovery of acute liver failure was compared with Case 1. Diet restriction and NTBC treatment are crucial to prevent hepatocellular carcinoma until liver transplant can take place and cure the condition. Further studies are needed to examine cases where liver cancer did not result despite clinical symptoms/signs of tyrosinemia type I.

• 호스피스학술지
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• 제7권2호
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• pp.6-14
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• 2007

Purpose: Hepatocellular carcinoma is the 3rd leading cause of cancer death in Korea and its prognosis is very poor. We aimed to investigate the clinical characteristics of terminal patients with hepatocellular carcinoma on admission into a hospice unit, and to know if they had received appropriate hospice and palliative care. Methods: We retrospectively reviewed the medical records in 62 patients with hepatocellular carcinoma who had admitted, received palliative care, and died in a hospice unit between January 2003 and December 2005. Results: The median age of patients was 56.5 years with 50 men(80.65%) and 12 women(19.35%) and gender ratio(male to female) was 417. Child-Pugh class A, B, and C were 6(9.68%), 22(35.38%), and 34(58.84%) respectively. We divided the patients into two groups and compared, the terminal HCC patients with class C as group I and those with class A & B as group 2. The median time from hospice referral to death was significantly short in group 1 with 15.5 days compared to group 2 with 53 days. Statistically more prevalent symptoms in group I were ascites, dyspnea, peripheral edema, and hepatic encephalopathy with abnormal laboratory findings (jaundice, hypoalbuminemia, or renal insufficiency). There, however, was no significant difference in complications and managements during admission between group 1 and 2. Conclusion: Most terminal HCC patients were often accompanied with chronic liver disease. The length of hospice and palliative care for above patients was not enough to attend them. Therefore, we suggest that proper education and information should be provided to physicians, patients, and their family members for effective hospice and palliative care.

• Journal of Yeungnam Medical Science
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• 제13권2호
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• pp.302-307
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• 1996

급속조영 전산화단층촬영에서 다른 간종괴와 감별이 어려운 간세포암의 경우 AFP 수치의 상승과 HBsAg 양성은 간세포암을 시사하는 유용한 지표이며 종괴의 모양과 조영양상을 같이 고려한다면 간종괴의 감별진단에 많은 도움을 주리라 생각한다.

• Nutrition Research and Practice
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• 제2권2호
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• pp.80-84
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• 2008

Beneficial effects of dehydroepiandrosterone (DHEA) supplement on age-associated chronic diseases such as cancer, cardiovascular disease, insulin resistance and diabetes, have been reported. However, its mechanism of action in hepatocellular carcinoma in vivo has not been investigated in detail. We have previously shown that during hepatocellular carcinogenesis, DHEA treatment decreases formation of preneoplastic glutathione S-transferase placental form-positive foci in the liver and has antioxidant effects. Here we aimed to determine the mechanism of actions of DHEA, in comparison to vitamin E, in a chemically-induced hepatocellular carcinoma model in rats. Sprague-Dawley rats were administered with control diet without a carcinogen, diets with 1.5% vitamin E, 0.5% DHEA and both of the compounds with a carcinogen for 6 weeks. The doses were previously reported to have anti-cancer effects in animals without known toxicities. With DHEA treatment, cytosolic malate dehydrogenase activities were significantly increased by ${\sim}5$ fold and glucose 6-phosphate dehydrogenase activities were decreased by ${\sim}25%$ compared to carcinogen treated group. Activities of Se-glutathione peroxidase in the cytotol was decreased siguificantly with DHEA treatment, confirming its antioxidative effect. However, liver microsomal cytochrome P-450 content and NADPH-dependent cytochrome P-450 reductase activities were not altered with DHEA treatment. Vitamin E treatment decreased cytosolic Se-glutathione peroxidase activities in accordance with our previous reports. However, vitamin E did not alter glucose 6-phosphate dehydrogenase or malate dehydrogenase activities. Our results suggest that DHEA may have decreased tumor nodule formation and reduced lipid peroxidation as previously reported, possibly by increasing the production of NADPH, a reducing equivalent for NADPH-dependent antioxidant enzymes. DHEA treatment tended to reduce glucose 6-phosphate dehydrogenase activities, which may have resulted in limited supply for de novo synthesis of DNA via inhibiting the hexose monophophaste pathway. Although both DHEA and vitamin E effectively reduced preneoplastic foci in this model, they seemed to fimction in different mechanisms. In conclusion, DHEA may be used to reduce hepatocellular carcinoma growth by targeting NADPH synthesis, cell proliferation and anti-oxidant enzyme activities during tumor growth.

• Asian Pacific Journal of Cancer Prevention
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• 제13권8호
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• pp.3815-3819
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• 2012

The CD4+CD25+ regulatory T cell (Treg) is a special kind of T cell subset. Studies have showed that Treg cells are involved in a number of physiological processes and pathologic conditions such as autoimmune diseases, transplantation tolerance and cancer. Tregs with unique capacity for immune inhibition can impair anti-tumour immunity and help tumor cells to escape from immune surveillance. The aim of our study was to investigate whether Tregs are involved in hepatocellular carcinoma (HCC). A BABL/C mouse with HCC in situ model was established to evaluate the Treg existence in carcinoma tissues and the changes of Tregs in spleen using flow cytometry and immunohistochemistry methods. Granzyme B expression in carcinoma tissues was analyzed by immunohistochemistry to investigate the tumor local immune status.The proportion of CD4+CD25+/CD4+ spleen lymphocytes of tumor bearing mice ($18.8%{\pm}1.26%$) was found to be significantly higher than that in normal mice ($9.99%{\pm}1.90%$) (P<0.01 ). Immunohistochemistry of spleen tissue also confirmed that there was an increase in Treg in tumor-bearing mice, while in carcinomas it showed Treg cells to be present in tumor infiltrating lymphocyte areas while Granzyme B was rarely observed. Anti-tumour immunity was suppressed, and this might be associated with the increase of Tregs. Our observations suggest that the CD4+CD25+Treg/CD4+ proportion in spleen lymphocytes can be a sensitive index to evaluate the change of Tregs in hepatocellular carcinoma mice and the Treg may be a promising therapeutic target for cancer.

• Radiation Oncology Journal
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• 제31권4호
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• pp.267-272
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• 2013

Although significant advances in the treatment of intrahepatic lesions, it is reported that the prognosis for patients with hepatocellular carcinoma (HCC) who have extrahepatic metastasis remains poor. We report a patient with lung, liver, brain, bone and subcutaneous metastasis from HCC who has survived more than 7 years maintaining relatively good performance status as a result of repeated therapies. A 55-year-old male patient with HCC underwent right lobectomy of the liver and cholecystectomy in September 2006. He received wedge resection for lung metastasis twice (July 2009, January 2011) and Gamma Knife stereotactic radiosurgery for brain metastasis (April 2011). Over the last 3 years, he has developed metastasis in subcutaneous tissues, muscle, and bone with pain. He has undergone 7 courses of radiotherapies for subcutaneous tissues, muscle, and bone metastasis and been prescribed sorafenib and he is still capable of all self-care.

• Asian Pacific Journal of Cancer Prevention
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• 제14권3호
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• pp.1769-1772
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• 2013

A case-control study of the association of miR-499A>G rs3746444 with risk of hepatocellular carcinoma (HCC)was conducted. Patients with HCC and healthy control subjects were recruited for genotyping of miR-499A>G using duplex polymerase-chain-reaction with confronting-two-pair primer(PCR-RFLP) analysis. The MiR-499 GG genotype was associated with a decreased risk of HCC as compared with the miR-499 AA genotype (adjusted OR=0.74, 95%CI=0.24-0.96). Similarly, the GG genotype showed a 0.45-fold decreased HCC risk in a recessive model. The MiR-499 G allele was significantly associated with decreased risk of HCC among patients infected with HBV in a dominant model (OR=0.09, 95%CI= 0.02-0.29). In conclusion, the MiR-499A>G rs3746444 polymorphism is associated with HCC risk in the Chinese population, and may be useful predictive marker for CAD susceptibility.

• Asian Pacific Journal of Cancer Prevention
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• 제14권3호
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• pp.1579-1583
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• 2013

Intercellular adhesion molecule-1 (ICAM-1) is a member of the immunoglobulin superfamily, its main function being to participate in recognition and adhesion between cells. ICAM-1 is considered closely related to occurrence, development, metastasis and invasion process of hepatocellular carcinoma (HCC). A variety of inflammatory cytokines and stimulus affect its expression through the nuclear factor-kappa B (NF-${\kappa}B$) signal transduction pathway. In the initial stage of inflammation, hepatocirrhosis and tumor development, ICAM-1 is expressed differently, and has varied effects on different cells to promote occurrence of malignancy and metastasis. ICAM-1 has diagnostic significance for AFP-negative or suspected HCC, and may be a prognositic significance. It is thus widely used in studies as a biomarker which reflects cancer cells metastasis as well as curative effect of drugs. Many new treatments of HCC may be based on the effects of ICAM-1 on different levels of function.

• Asian Pacific Journal of Cancer Prevention
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• 제13권12호
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• pp.5955-5958
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• 2012

Hepatocellular carcinoma (HCC), the sixth most prevalent cancer worldwide, continues to have high prevalence in many countries of Asia. The main challenge is the high prevalence of chronic hepatitis and aflatoxin, for example in China. HBV vaccination should be the major preventive tactic in Asian countries. The burden of HCC is low in Iran because most cases are due to HBV and this infection was less common. Although in Iran, a mass vaccination program started in 1993, its impact on decreasing the burden of HCC due to HBV can only be expected in future decades.

• Journal of Korean Neurosurgical Society
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• 제47권6호
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• pp.461-463
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• 2010

We report a case of an acute spontaneous epidural hematoma (EDH) due to skull base metastasis in a 46-year-old male patient with hepatocellular carcinoma (HCC). The patient presented with the acute onset of severe headache followed by unconsciousness, and computed tomography showed a large EDH in the right temporal and parietal lobes with midline shift. Emergency evacuation of the EDH was performed, and the hemorrhage was determined to be secondary to skull base metastasis of HCC.