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Query: UMLS:C1864663 (HCC)
 2,985 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The antiproliferative activity of flavone acetic acid (LM 975) was investigated on human adenocarcinoma cell lines (HCC-P2998, HCC-M1544, HCC-M1410, HT 29, LoVo), on a murine colon adenocarcinoma cell line (Colon 26), on murine pancreatic adenocarcinoma cells growing in primary culture (Pan 03) and on human normal fibroblasts (N1). No cytotoxic effects were found against human normal fibroblasts. LM 975 was active against murine adenocarcinoma Pan 03 and Colon 26, known to be sensitive in vivo too and, to variable extents, on human adenocarcinoma cell lines. LM 975 in vitro cytotoxic potency was relatively low. The high concentrations (1.0-1.4 mM) required to obtain a cytotoxic effect are, however, pharmacologically reasonable since they are comparable with drug plasma levels in mice or in patients treated with tolerable doses. After a relatively short LM 975 treatment (2 h) DNA, RNA and protein synthesis were inhibited in different proportions. In more sensitive cells LM 975 appeared to inhibit RNA synthesis more than DNA and protein synthesis. Inhibition of macromolecule synthesis after 2 h exposure was completely reversed in 24 h recovery. After 2 h treatment no detectable DNA breakage was found by the alkaline elution method, thus corroborating the idea that this compound does not act by causing DNA damage.
Eur J Cancer Clin Oncol 1987 Oct
PMID:Antiproliferative properties of flavone acetic acid (NSC 347512) (LM 975), a new anticancer agent. 367 16

The question of whether HBV causes HCC has to date best been answered by epidemiologic studies, in particular prospective analysis such as the ongoing study in Taiwan. The mechanism whereby HBV may cause HCC by genetic or epigenetic means, acting alone or in concert with other agents, is still moot . To date, studies of HBV gene expression have not shown the presence of a transforming gene or an oncogene associated with this virus. The finding of integrated HBV DNA in most HCC of carriers is highly suggestive of a causal role of the virus in the pathogenesis of neoplasia. In order to be more certain, it will be necessary to show that expression of integrated HBV genes or of cellular genes, as a result of HBV infection, causes neoplastic transformation of cells. Failure to date to demonstrate that HBV DNA induces neoplastic transformation of eukaryotic cells in culture may be simply due to an inadequate experimental model. The majority of these experiments have used fibroblasts or monkey kidney cells as the recipient cell, whereas cultured human hepatocytes might be more suitable. Whatever role HBV eventually is shown to have in the pathogenesis of HCC, molecular biologic techniques will have in great measure contributed to that knowledge. The use of these powerful new methods will permit studies of the replication of HBV and possible elucidation of how this virus affects the hepatocyte during persistent infection and will in time lead to a better understanding of cell and molecular events leading to development of hepatic malignancy.
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PMID:Hepatitis B virus and hepatocellular carcinoma: molecular biology and mechanistic considerations. 608 62

The authors concurrently determined four markers consisting of novel gamma-GTP isoenzyme (Novel gamma-GTP), variant alkaline phosphatase (VAALP), basic fetoprotein (BFP) and CEA in addition to AFP in 144 patients having HCC. Serum AFP levels below 400ng/ml, a condition commonly seen in sera of hepatobiliary diseases other than HCC were obtained in 60 our of patients, or 42%. There was little correlation among positivities of these markers, and the diagnostic usefulness was increased by combination assay of these markers, except in the case of CEA. Specific diagnosis of HCC could be made in 78% by a combination of Novel gamma-GTP and VAALP in addition to AFP. Moreover, diagnosis of an existing malignancy could be made in 87% by BFP in addition to AFP, Novel gamma-GTP and VAALP. Positive ratios of BFP and CEA increased in proportion to staging, whereas those of AFP and Novel gamma-GTP were independent of the stage and relatively high even in patients within the early stage. In general, incidences of these markers were relatively lower in patients having small HCC, however, markers of a secreting type such as AFP and Novel gamma-GTP were relatively useful for early diagnosis of HCC.
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PMID:[Tumor markers of hepatocellular carcinoma with special reference to diagnostic efficacy of combination of these markers and relation to its stages]. 619 67

A review of 205 primary hepatic cancers from different geographic areas reveals that HCC which forms the vast majority (86%) of these, commonly presents as the trabecular variety (76%). The compact and pseudoglandular forms are rare (18% and 6%). Relatively fewer cases of undifferentiated cancer, hepatoblastoma and cholangiocarcinoma are encountered. HCC is often associated with the presence of hepatitis B virus surface antigen (HBsAg) in the liver. This is particularly true of the trabecular variety (81%). A proportion of the compact variety as well as undifferentiated cancers do not appear to be related to HBV infection. Cholangio carcinomas are considered to be related to infection by liver flukes. Hepatoblastomas occur in infancy and childhood and show no known aetiologic association. Aflatoxin may be aetiologically related to same cases of HCC. Continued use of oral contraceptives can occasionally induce HCC.
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PMID:Relationship between histology and aetiological factors in primary liver cancer. 625 13

A continuous human cell line was established from a hepatocellular carcinoma of an HBsAg-positive Japanese male. The cell line, designated HCC-M, grows as an adhering monolayer with a doubling time of 24 h in medium RPMI-1640 supplemented with 10% FCS and grows with 30% clonal efficiency in soft agar. The cells have been shown by light and electron microscopy to be of epithelial type. When they were transplanted subcutaneously into the back of athymic nude mice (BALB/c, nu/nu), tumors developed at the sites of inoculation, which were shown to be hepatocellular carcinoma, similar in morphology to the original tumor from which they were derived. HCC-M had a chromosome mode of 63 with five identifiable marker chromosomes. HCC-M produced albumin at the 10th passage but this property was lost by the 30th passage. This cell line has not secreted alpha-fetoprotein. Hepatitis B viral particles or HBsAg have not been demonstrated in the cells from the primary culture nor in several subsequent subcultures tested.
Int J Cancer 1983 Aug 15
PMID:Establishment of a cell line (HCC-M) from a human hepatocellular carcinoma. 630 92

Hepatitis C and B viruses are associated with hepatocellular carcinoma in Europe, Asia and Southern Africa. A study of hepatitis C and hepatitis B virus infection was carried out on 70 patients with HCC, from the National Cancer Institute, Cairo University. Sera from patients were tested for anti-HCV and HBsAg markers. Twenty patients (30%) were anti HCV positive alone, 15 (21.4%) were HBsAg positive alone, 28 (40%) were positive for both anti-HCV and HBsAg and the remaining 6 patients (8.6%) were negative for the two markers. The total positivity for anti-HCV and for HBsAg in these patients was 70% and 61.4% respectively. The comparable figures in a recent study on 90 blood donors from Egypt, were 24.4% for anti-HCV and 4.4% for HBSAg. These data suggest a possible link between HCV and HBV infection and the development of hepatocellular carcinoma in Egypt, as has been found elsewhere in the world.
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PMID:Hepatitis C and B viruses, and their association with hepatocellular carcinoma in Egypt. 750 48

A clinicopathologic analysis of 93 hepatectomies of < 3 cm small hepatocellular carcinoma (small-HCC) over the last ten years was made, which accounted for 8.5% in 1096 resected HCC during the same period. Serum AFP levels of > or = 400 micrograms/L in patients with small-HCC accounted for 40.3%. The rate of capsule formation was 58.1%, and the incidences of tumor direct invasion, cancer thrombus as well as tumor satellites were 33.3%, 28% and 3.2%, respectively. The 5-year postoperative survival rate of patients with small-HCC was 77.9%. It is proposed that the essential features of < 3 cm small-HCC are: (1) expanding growth pattern and capsule formation in majority of the cases; (2) the lesions are limited, seldom occurring long-distance (> 2 cm) invasion; (3) the incidence of cancer thrombus and satellites are lower; and (4) the majority of < 3 cm small-HCC are of diploid DNA content, showing a relatively slow growth. It is considered that < 3 cm small- HCC basically reflects the pathobiologic features of early HCC, and is an important opportunity of achieving radical therapeutic effect after the resection.
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PMID:[Clinicopathologic features of small hepatocellular carcinoma--an analysis of ninety-three cases]. 751 35

A thorough understanding of the incidence, clinical presentation, treatment, prognosis, and psychosocial issues surrounding children with solid tumors enables the nurse to actively participate on the health care team. Although significant advances over the past two-and-a-half decades to improve the outcomes of children with cancer have occurred, there remains room for continued improvement, especially among children with advanced-stage nephroblastoma, neuroblastoma, HCC, and teratoma.
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PMID:Solid tumors in children. 752 19

Our patient presented with a large liver mass, an extremely elevated AFP level, and an almost certain diagnosis of HCC. However, extensive evaluation and biopsies failed to demonstrate malignancy, and the available evidence strongly suggests that the patient has an adult polycystic disease without renal involvement, and that the mass was the result of hemorrhage and degenerative changes in one of his cysts. Polycystic diseases can involve only one lobe, as it appears in this case. Only about 10-15% of patients with polycystic disease have symptoms due to the liver disease, while 30-50% have associated renal disease. Thus, our patient is unusual in several respects. However, his liver mass has decreased in size, he feels well, and his biochemical abnormalities have returned to normal. Despite a classic presentation for HCC, this case underscores the necessity for a thorough evaluation, especially for patients without major risk factors for hepatocellular carcinoma.
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PMID:A 22-year-old man with a liver mass and markedly elevated serum alpha fetoprotein. 753 71

Thirteen cases of combined hepatocellular (HCC) and cholangiocellular carcinoma (CCC) were examined. In addition to routine pathology, immunoreactivities for carcinoembryonic antigen, alpha-fetoprotein (AFP), cytokeratin (Cam 5.2 and AE1), epithelial membrane antigen (EMA) and tumor-associated glycoprotein 72 (B72.3) were also examined. The average age of the 13 cases was 64.8 years, which lay between the average ages of pure HCC and CCC cases. They were categorized as separate type (2), collision type (6), and intermingled type (5). AE1 and EMA were the best markers to differentiate the CCC from the HCC area. B72.3 immunoreactivity was detected only in CCC (46%). There were no transitional features between HCC and CCC in two cases of the separate type and two cases of the collision type. However, focal transitional features from HCC to CCC were observed in all cases of the intermingled type and in four of six cases of the collision type. In one case of the intermingled type, many cancer cells contained both bile and mucus simultaneously, and revealed dual immunoreactivities. The conclusions are: 1) the combined type is generated from two sources; one is the intrahepatic double cancer (thoroughly separate type and a part of the collision type) and another is the stem cell origin with diverse phenotypes (intermingled type and a part of the collision tumor); and 2) AE1 was the most helpful marker to differentiate the CCC area from HCC, and other markers, e.g. AFP for HCC and EMA, CEA, and B72.3 for CCC, were also supportive but somewhat limited in the differential diagnosis.
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PMID:An immunohistochemical analysis of 13 cases with combined hepatocellular and cholangiocellular carcinoma. 753 81


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