Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0019204 (hepatocellular carcinoma)
 71,386 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

c-Hc-4 has been established and maintained for more than seven years. The hepatocellular carcinoma originated in 45-year old man with liver cirrhosis. The cell grew in vitro forming a sheet of monolayered cells and firmly attaching to the inner surface of cultured flasks. Morphologically they showed epithelial-like pattern. The doubling time was about 20 hours. Their modal chromosome number was 58. Serial heterologous transplantation in nude mice was successful. The histological finding was almost the same patterns as those in the primary tumor. The cultured cells produced alpha-fetoprotein (AFP) and carcinoembryonic antigen (CEA).
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PMID:[Establishment of the human hepatocellular carcinoma cell line and its characteristics]. 285 42

Recent studies in our laboratory have shown that five established rat hepatoma cell lines provide a wide spectrum of tumor-associated aldehyde dehydrogenase (ALDH) activity representative of the range of activities of this enzyme seen in primary rat hepatocellular carcinomas. Four newly established rat hepatoma cell lines, RLT-2M, RLT-3C, RLT-9F, and RLT-5G, were derived from a primary hepatocellular carcinoma. The primary tumor was induced by a single injection of diethylnitrosamine (15 microM/g body weight) to a 1-d-old female S-D rat followed at weaning by chronic phenobarbital treatment. RLT-2M was established from outgrowths of minced tumor pieces. RLT-3C, RLT-9F, and RLT-5G were cloned from RLT-2M by the serial endpoint dilution. All four lines have been maintained in culture for over 100 passages. The ALDH phenotype in both the primary tumor and the four new cell lines was determined by total activity assay, gel electrophoresis, and histochemistry. By total activity assay, the primary tumor did not possess significant tumor-ALDH activity. In contrast, the four new cell lines expressed tumor-ALDH activity. However, they differed in their basal ALDH activities and in ALDH inducibility by 3-methylcholanthrene, benzo(a)pyrene, and phenobarbital. Additionally, significant decreases in tumor-ALDH activity occurred when cells from each line were passaged in vivo. The four lines have been characterized by light and electron microscopic morphology, tumorigenicity, chromosome number, doubling time, and colony formation efficiency in soft agar.
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PMID:Characteristics and aldehyde dehydrogenase activity of four rat hepatoma cell lines produced by diethylnitrosamine-phenobarbital treatment. 287

We studied the expression of villin, a microfilament-associated, actin-binding protein typical of brush-border microvilli, in a variety of human carcinomas by applying immunofluorescence microscopy to frozen sections and immunoblotting methods to tissue extracts using a rabbit antiserum and a monoclonal antibody specific for villin. All of the 24 primary and metastatic colorectal adenocarcinomas tested were uniformly and strongly positive for villin, with the immunocytochemical labeling concentrated at the luminal cell margin. In poorly differentiated tumor areas, rudimentary tubules were stained. All of the six tubular adenocarcinomas of the stomach studied as well as two adenocarcinomas of the gall bladder and a hepatocellular carcinoma were also villin-positive. Villin was detectable in 12 of 14 adenocarcinomas of the pancreas; in some of these cases, its distribution was heterogeneous. Among 21 renal cell carcinomas investigated, positivity for villin was seen in nine of 13 clear cell tumors (especially those of grade II), and in all four chromophilic cell tumors; however, all four chromophobe cell tumors studied were negative. Four of 11 endometrial but none of nine ovarian carcinomas were (uniformly or focally) villin positive. Of 18 adenocarcinomas of the lung studied, one was uniformly and four focally positive for villin, while the remainder were negative. All of the other epithelial tumors studied, including 12 adenocarcinomas of the breast and seven epithelial or biphasic pleural mesotheliomas, were villin negative. Our results show that the expression of villin in intestinal epithelial cells is consistently maintained in their corresponding carcinomas, even when the organized brush-border structure has been lost. The presence of villin in some endometrial and pulmonary adenocarcinomas--in contrast to its absence in the respective normal epithelia--suggests that this protein is newly expressed during hyperplasia, dysplasia, or carcinogenesis. Determining the presence or absence of villin and its immunocytochemical staining pattern in metastatic adenocarcinomas may be of some help in determining the type and site of the primary tumor.
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PMID:Villin: a cytoskeletal protein and a differentiation marker expressed in some human adenocarcinomas. 289 90

Three patients with symptoms related to metastases from hepatocellular carcinoma are described. The diagnosis of the primary tumor was made at autopsy in two cases and by biopsy in one. The skeletal lesions had a lytic, expansile, and hypervascular appearance. This hypervascularity may lead to bleeding either spontaneously or following biopsy. Hepatocellular carcinoma should be included in the differential diagnosis of osteolytic, expansile, hypervascular metastases, especially when such lesions are encountered in patients with liver cirrhosis.
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PMID:Hepatocellular carcinoma with skeletal metastasis. 298 74

Bone metastasis was observed in 16.1% or in 14 of 87 male autopsy cases of hepatocellular carcinoma. The primary tumor within the liver was located in the right lobe in all but one case. There were six patients who first presented with signs attributable to bone metastasis, and lung metastasis subsequently became evident in five of them. These 6 patients lived significantly longer as compared with 8 other patients with bone metastases and 73 patients without. The possible route by which hepatocellular carcinoma cells were carried to the bone is discussed.
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PMID:Bone metastasis in hepatocellular carcinoma. 298 71

Technetium-99m glucoheptonate (Tc-99m GH) is concentrated in pulmonary and cerebral tumors. The purpose of this study was to assess the uptake of this radionuclide by hepatocellular carcinoma. Its concentration by the primary tumor was compared with that in the non-neoplastic hepatic tissue in 31 patients who showed obvious defects on a colloid scan, and its uptake by pulmonary metastases was examined in six patients with x-ray evidence of this complication. In two patients, the uptake by the tumor was greater than, in six it was equal to, and in ten it was less than that in the non-neoplastic hepatic tissue. In the remaining 13 patients, there was no concentration at all in the tumor. In none of the six patients with multiple pulmonary metastases could uptake of Tc-99m GH by the metastases be demonstrated. It is concluded that Tc-99m GH is of limited value in the diagnosis of primary or metastatic hepatocellular carcinoma.
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PMID:Technetium-99m glucoheptonate as a scanning agent in hepatocellular carcinoma. 299 36

Primary liver sarcoma is rare and especially its coexistence with hepatocellular carcinoma is extremely rare. We have collected eight cases of their coexistence in the literatures. The patient was a 62-year-old male complaining of right hypochondralgia and general malaise for about one month. CT scanning revealed the liver tumor and right hepatic lobectomy was performed. The tumor was sized in 14 by 9 by 9 cm and composed of hepatocellular carcinoma and rhabdomyosarcoma, which were were collided. Apparent striations in the rhabdomyosarcoma cells was observed under light-microscope. Alphafetoprotein, of which serum level was extraordinarily high, was detected only in hepatocellular carcinoma by special stains. He discharged one month after operation. He was readmitted due to recurrence and received trans-arterial embolisation therapy and systemic chemotherapy. Though transient effect was obtained. He died forty-five days after operation. Autopsy revealed that recurrent liver tumors consisted of only hepatocellular carcinoma and that no other tumorous lesion was found in the other parts of the body. Rhabdomyosarcoma was proved to be primary tumor the liver.
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PMID:[A resected case of collision tumor of hepatocellular carcinoma and primary liver rhabdomyosarcoma]. 301 14

Forty-six patients who had been evaluated because of skeletal metastases of unknown origin, were reviewed. Twenty-six of the patients were referred to an orthopedic surgeon before confirmation of the metastases by biopsy; 20 others were referred to an oncology clinic after a diagnosis of bone metastases had been established. A simple diagnostic sequence consisting of a medical history, physical examination, routine laboratory studies, chest roentgenogram, technetium 99m phosphonate bone scintigram, and intravenous pyelogram identified the site of the primary tumor in 14 patients; 7 of the primaries were lung carcinomas, 4 were hypernephromas, 2 were breast carcinomas, and 1 was a prostate carcinoma. In two other patients, the histologic findings from the biopsy study were diagnostic; one had a thyroid carcinoma and one, a prostate carcinoma. Further extensive diagnostic workups revealed the site of origin in only four additional patients; two had hypernephromas which were discovered by computed axial tomography of the abdomen; one had an ovarian carcinoma and one had a hepatoma, both of which were found at laparotomy. On the basis of this study, a simple diagnostic strategy is recommended for patients with histopathologically confirmed skeletal metastases of unknown origin: medical history, physical examination, routine laboratory studies, chest radiograph, and technetium 99m phosphonate bone scintigram, followed by computed axial tomographic examination of the abdomen and pelvis. In female patients, it may be judicious to use mammography. If this regimen fails to reveal the primary site, it is unlikely that it will be identified with further extensive diagnostic procedures.
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PMID:The search for the primary tumor in patients with skeletal metastases of unknown origin. 301 75

This clinical study was undertaken in order to evaluate the effect of CDDP on 43 patients with far-advanced or recurrent carcinoma of the gastrointestinal tract. For all these patients, CDDP at 100 mg/m2 had been administered by continuous intravenous infusion for 24 hours and repeated one to seven times at an interval of 3 to 4 weeks. The effect of this therapy was assessed according to the criteria of clinical evaluation of chemotherapy for solid cancers by Koyama and Saito. The response rate for both complete and partial response was 27.9% among all 43 patients, including 47.1% (8/17) for gastric cancer, 33.3% (1/3) for esophageal cancer, 25.0% (1/4) for hepatocellular carcinoma, 25.0% (1/4) for carcinoma of the gallbladder or bile duct, 20.0% (1/5) for pancreatic cancer and none (0/10) for colorectal cancer. In particular, a good response rate of 37.5% (3/8) was obtained for patients with recurrent tumor and one of 33.3% (6/18) for those with palliative resection of the primary tumor, which was much higher that the rate of 17.6% (3/17) for those without resection. As for the side effects of CDDP therapy, gastrointestinal symptoms were most frequently found in 78.3% of patients followed by bone marrow suppression in 15.2%, and abnormalities of hepatic and renal function in 4.3% and 4.3%, respectively. Consequently, 24-hour continuous intravenous infusion of CDDP was considered to be effective for far-advanced or recurrent carcinoma, especially in cases of gastric cancer.
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PMID:[Clinical study on the effect of 24-hour continuous intravenous infusion of CDDP in far-advanced and recurrent carcinoma of the gastrointestinal tract]. 303 10

C3H/He mice hyperimmune against syngeneic MH134 hepatoma were prepared by intradermal (id) inoculation of viable tumor cells followed by surgical resection of the tumor and by repeated id challenges with viable tumor cells. Winn assays performed utilizing spleen cells from these mice have revealed that both Lyt-2+ and L3T4+ T cell subsets from MH134-hyperimmune mice produced complete tumor protection. The in vivo tumor-neutralizing activity was also found in spleen cells from tumor-bearing mice at various times after id implantation of MH134 tumor cells. However, in contrast to comparable tumor-neutralization by Lyt-2+ and L3T4+ T subsets from hyperimmune mice, only the Lyt-2+ T cell subset from tumor-bearing mice was capable of mediating the in vivo protective immunity. L3T4+ T cell-mediated immunity was not detectable in the tumor-bearing state irrespective of the length of the sensitization period with a primary growing tumor, but emerged in the mice which resisted the first tumor challenge after the resection of the primary tumor. These results indicate that the emergence of L3T4+ T cell-mediated anti-tumor immunity is stage-dependent and the Lyt-2+ T cells represent the main functional subset in the tumor-bearing state, although both subsets of T cells are potentially capable of effecting anti-tumor in vivo immunity. The results are discussed in relation to the selective suppression of the L3T4+ but not of Lyt-2+ T cell function in the tumor-bearing state.
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PMID:Selective suppression of the generation of anti-tumor L3T4+ but not of Lyt-2+ T cell-mediated immunity in the tumor-bearing state. 313 99


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