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)

To evaluate the usefulness of contrast material-enhanced ultrasound (US) in detection and treatment of hepatocellular carcinoma (HCC), carbon dioxide was injected as a contrast agent into the hepatic artery in 22 patients with HCC. Plain US had enabled detection of 24 HCC nodules in these patients. Contrast material-enhanced US enabled detection of seven additional nodules, which were confirmed as HCC by means of fine-needle aspiration biopsy performed under guidance with contrast-enhanced US. Six of these seven nodules were detected incidentally during examination of other suspected HCC nodules. Five of the seven nodules were treated with percutaneous ethanol injection (PEI) performed under guidance with contrast-enhanced US; the two other nodules were resected. Contrast-enhanced US made the HCC lesions visible for 15-60 minutes, sufficient time to mark the nodule with an iodized oil-ethanol solution for PEI. Because contrast-enhanced US enabled detection of additional nodules and performance of PEI in lesions not detected with plain US, it may help improve the treatment of HCC.
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PMID:Hepatocellular carcinoma not detected with plain US: treatment with percutaneous ethanol injection under guidance with enhanced US. 132 44

For evaluating hepatic tumors, ultrasonograms using carbon dioxide by arterial injection (CO2US) was performed in 37 patients, including 28 hepatocellular carcinomas, 11 hepatic metastases, and 3 hepatic hemangiomas. Hepatic tumors were enhanced by CO2US and easily identified. CO2US of hepatic tumors were classified into six patients. Generally, on CO2US hepatocellular carcinomas were well enhanced, and hepatic metastases had ring-like enhancement. Hepatic hemangiomas showed peripheral patchy enhancement. In the patients with hepatocellular carcinoma, the primary tumors were better identified on CO2US than conventional sonography. The daughter nodules with hepatocellular carcinoma were also better demonstrated than other examinations. CO2US is helpful in evaluating and differentiating hepatic tumors.
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PMID:[Evaluation of hepatic tumors by contrast ultrasonography with carbon dioxide]. 164 8

Tumor hemodynamics including arterial vascularity (AV) and portal perfusion (PP) were evaluated in histologically confirmed 55 hepatic nodules associated with cirrhosis using ultrasonographic (US) angiography during intraarterial carbon dioxide microbubbles injection and CT during arterial portography. Tumor hemodynamic patterns were classified into 6 types as follows: Type I (n = 10): PP (+), AV (hypo); Type I' (n = 2): PP (+), AV (iso); Type II (n = 5): PP (-), AV (hypo); Type III (n = 8): PP (-), AV (iso); Type IV (n = 25): PP (-), AV (hyper), Type V (n = 5): PP (partially +), AV (vascular spot in hypovascular). Eight nodules of Type I were diagnosed as benign nodules histologically including adenomatous hyperplasia (AH) (n = 6) and regenerative nodule (n = 2). Hundred percent (5/5) of Type II and 88% (7/8) of Type III nodules were well-differentiated HCC, in contrast to 8% (2/25) of Type IV nodules, typical HCCs. Fatty metamorphosis was observed in 75% (6/8) of Type III nodules, in contrast to 16% (4/25) of typical (classical) HCC nodules (Type IV). We concluded that at the malignant transformation from AH to HCC, reduction of portal blood flow in the nodule precedes the initiation of the increase of the arterial tumor vessel. Moreover, early stage HCC could exhibit hypovascular (Type I, II), isovascular (Type III), or vascular spot in hypovascular pattern (Type V) compared with a typical HCC (Type IV). It was also suggested that the more mature as a neoplasms the HCC becomes, the more the arterial tumor vessel in the nodule increases and fatty metamorphosis of well-differentiated HCC is highly related with tumor hemodynamic condition, i.e., hypoperfusion state from both arterial and portal vessel.
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PMID:[Tumor hemodynamics in hepatic nodules associated with liver cirrhosis: relationship between cancer progression and tumor hemodynamic change]. 165 18

The blood supplies of nodular lesions associated with liver cirrhosis were analyzed in vivo with various imaging modalities. The portal blood supply was evaluated with computed tomography (CT) during arterial portography (CTAP); the arterial blood supply was evaluated with hepatic angiography, CT angiography, CT following intraarterial injection of iodized oil, or ultrasound following intraarterial injection of carbon dioxide microbubbles. A total of 84 surgically confirmed hepatocellular carcinomas (HCCs) (less than or equal to 3 cm) and 25 areas of adenomatous hyperplasia (AH) were included in the study. At CTAP, a portal blood supply was seen in 96% of cases of AH and only 6% of HCCs (chi 2, P less than .005). In contrast, an arterial supply greater than that of the surrounding liver was verified in 94% of the HCCs and only 4% of the cases of AH (chi 2, P less than .005). The blood supply of areas of AH with atypical hepatocytes and the blood supply of well-differentiated HCCs (Edmondson grade 1) tended to be intermediate between that of AH without atypia and that of HCC that was Edmondson and Steiner grade 2 or greater. Evaluation of the blood supply of the nodular lesions associated with liver cirrhosis is considered to be useful in the differential diagnosis and treatment of early-stage HCC.
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PMID:Benign and malignant nodules in cirrhotic livers: distinction based on blood supply. 184 40

Dynamic contrast material-enhanced ultrasonography (US) with intraarterial infusion of carbon dioxide microbubbles was performed for four cases of histologically proved focal nodular hyperplasia (FNH) in four patients and for 167 cases of various hepatic nodules in 144 patients. No complications due to dynamic US were observed in any of the 148 patients. All FNH nodules were less than 3 cm in diameter. Consistent specific findings of FNH were not obtained with US, computed tomography, magnetic resonance imaging, radiocolloid scanning, or angiography in the four cases of FNH. In contrast, the characteristic vascular pattern (ie, early central hypervascular supply with centrifugal filling to the periphery at the arterial phase and a uniform or lobulated dense stain at the capillary phase) was observed in all four cases of FNH with dynamic US. This vascular pattern demonstrated in FNH with dynamic US was not seen in any of the 167 hepatic nodules, including 44 small hepatocellular carcinomas less than 3 cm in diameter. Therefore, the newly developed, dynamic contrast-enhanced US technique seems to be extremely sensitive and specific for diagnosing FNH and is useful in the differentiation of FNH from other hepatic tumors, especially hepatocellular carcinoma.
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PMID:Hepatic focal nodular hyperplasia: specific findings at dynamic contrast-enhanced US with carbon dioxide microbubbles. 184 61

Because the human hepatoma cell line Hep3B produces erythropoietin (Epo) in a regulated fashion, it can be used to investigate the cis-acting regulatory elements of the Epo gene. Comparison of primate and mouse sequences shows strong homology not only in the coding sequence but also within the 5' flanking region, the first intron, and the 3' flanking region. These portions of the Epo gene were inserted 5' and 3' to a reporter gene, human growth hormone (GH). 5A is a 1,192-base pair (bp) HindIII-Xbal fragment that extends from 378 bp 5' to the cap site through the first intron. To obviate the problem of false initiation of translation from the Epo ATG start codon, this site was changed to TAG by site-directed mutagenesis. 3A is a 255-bp Accl-BglII fragment that extends 67 bp upstream from the Epo termination codon and covers most of the 3' noncoding region of homology. The plasmid DNAs were transfected by electroporation into Hep3B cells with RSVCAT as an internal standard to correct for transfection efficiency. One aliquot of cells was exposed to 50 mumol/L CoCl2 or to 1% O2. At the end of the incubations, GH and Epo were measured in the cell media and the cell pellet was assayed for CAT. Production of GH was stimulated 1.7-fold by cobalt or hypoxia. Furthermore, addition of 3A to the GH gene, irrespective of orientation, stimulated GH production 2.6-fold with CoCl2 and 2.3-fold with hypoxia. Stable cell lines were produced by cotransfection of the above constructions, along with the selectable marker pSV-Neo. In two clones, exposure to hypoxia resulted in much more marked (16-fold) induction of GH. Stimulus of both GH and Epo production by hypoxia was partially abrogated by carbon monoxide. These results demonstrate the presence of promoter and enhancer elements within the human Epo gene that are appropriately responsive to hypoxia and cobalt.
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PMID:Regulatory elements of the erythropoietin gene. 198 94

Parallel investigations of the transamination pathways of glutamine oxidation in Ehrlich ascites carcinoma (EAC) and AS 30D hepatoma revealed that hepatoma cells, unlike EAC, produce very little aspartate. This cannot be explained by differences in the activity of glutamine-metabolizing enzymes. Also, the mitochondria from the hepatoma respired at a similar rate to EAC mitochondria with glutamine as sole substrate producing substantial amounts of aspartate. Unlike their isolated mitochondria, intact hepatoma cells showed a very low rate of glutamine oxidation. Compared with EAC, the rate of L-[U-14C]glutamine consumption by AS 30D hepatoma cells was much lower, with insignificant production of 14C-labelled aspartate and CO2. This suggested that the glutamine-transporting system in the hepatoma cell plasma membrane had a very low activity. Isolated hepatoma mitochondria produced 3 times more pyruvate from malate than did EAC mitochondria, indicating a higher activity of NAD(P)-dependent malic enzyme. We postulate that an active malic enzyme may suppress the synthesis of aspartate in hepatoma cells, but further evidence is needed to confirm this assumption.
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PMID:Control and function of the transamination pathways of glutamine oxidation in tumour cells. 199 Oct 25

The present study was undertaken to investigate the mechanism by which dimethylsulfoxide (DMSO) exerts its protective action on cytochrome P450-dependent activities and differentiation in cultured rat hepatocytes. Loss of cytochrome P450 is associated with a shortage of heme and reduced activity of delta-aminolaevulinic acid dehydratase: the addition of DMSO, which induces this enzyme in human hepatoma cells, is not able to affect it in hepatocytes in primary culture. DMSO is a strong scavenger of hydroxyl radicals and may destroy the reactive oxygen species formed under conventional culture conditions (i.e., 95% air and 5% CO2). In fact other powerful scavengers of oxygen radicals like dimethylthiourea, desferal, and catalase itself maintain higher levels of cytochrome P450 and higher activities of 7-ethoxycoumarin O-deethylase during 3 days of culture. DMSO and the other scavengers are also able to retain features of the morphological and biochemical differentiation of hepatocytes such as the ability to induce tyrosine aminotransferase activity in response to glucocorticoids.
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PMID:Mechanism of maintenance of liver-specific functions by DMSO in cultured rat hepatocytes. 201 49

To investigate the effects of iron supplementation on hepatoma cell growth, cells from a human hepatoma cell line, PLC/PRF/5, were grown in RPMI 1640 supplemented with 0, 10 and 20 micrograms/ml of FeSO4 and harvested weekly. At the end of 6 wk culture, cell mass measured 9.6, 14.7 and 13.2 gm, respectively. Amounts of ferritin from these cell masses were 0 (undetectable), 0.89 and 2.27 micrograms/gm of cells. To study the effects of iron deprivation of hepatoma cells, three human hepatoma cell lines (PLC/PRF/5, Hep G2 and Hep 3B) were incubated in tissue culture medium mixed with graded amounts of an iron-chelating agent, desferoxamine, for 48 to 96 hr at 37 degrees C with 5% CO2. Over 50% cell death in PLC/PRF/5 cells and 30% to 50% cell death in Hep G2 and Hep 3B cells were observed 48 to 72 hr after exposure to desferoxamine. Addition of ferric citrate partially reversed the cytotoxic effect of desferoxamine. On the other hand, viability of control cells, human diploid cell line (WI 38), was not affected by desferoxamine. Even after 96 hr exposure to desferoxamine, cell death was only 2% to 4%. These results suggest that (a) iron enhances tumor cell growth, (b) iron induces increased ferritin synthesis by tumor cells in vitro and (c) iron depletion causes tumor cell death but has little effect on normal human diploid cells. These findings should be considered when designing treatment of patients with hepatoma. Iron oversupply in patients with cancer might enhance tumor growth and adversely affect cancer therapy. Iron chelation with desferoxamine might have a place in the treatment of patients with hepatoma in conjunction with other anticancer agents.
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PMID:Effect of iron and desferoxamine on cell growth and in vitro ferritin synthesis in human hepatoma cell lines. 215 79

Metabolism of arabinose 5-P, ribose 5-P and glucose 6-P in permeabilized and resealed Morris hepatoma 5123TC cells was investigated by measuring the contribution of these compounds to nucleic acid biosynthesis. The level of [14C]-arabinose (non-phosphorylated) incorporation into nucleic acids was slight, presumably due to the low activity of the transport system or the absence or low activity of a specific 'kinase' enzyme. The permeabilizing procedure involved the brief treatment of Morris hepatoma 5123TC cells with lysolecithin and resulted in a cell population which was permeable to charged compounds i.e. sugar phosphates and nucleotides, that otherwise could not cross the plasma membrane. The permeabilized (and resealed cells) retained normal cellular morphology and intactness of specific organelles as judged by the maintenance of functional properties. Following permeabilization, these cells resealed when transferred back to normal growth medium, and continued to divide and increase at the same rates as control non-permeabilized cell cultures. The permeabilized cells incorporated deoxyribonucleotides ([methyl -3H]-TTP) into DNA at a linear rate of 0.047 nmol per 10(7) cells min-1, representing 90-100 per cent of the DNA synthesis rate in vivo. The permeabilization technique, when coupled with procedures to establish cell synchrony, permitted the comparative estimate of the contributions of [14C]-labelled arabinose 5-P, ribose 5-P and glucose 6-P to RNA, DNA, amino acids, CO2, lactate and sugar mono- and bisphosphates. The percentage of [14C]-isotope incorporated into total nucleic acids by these three labelled sugar phosphates were 2.3, 4.9 and 6.3 respectively. Possible reasons for the lower incorporation of 14C from arabinose 5-P are given. The results are consistent with the proposal that arabinose 5-P, an intermediate of the L-type pentose pathway activity of 5123TC cells, was incorporated into nucleic acids by its interconversion with ribulose 5-P and ribose 5-P and thus into PRPP. This study represents the first report of sugar phosphate as opposed to free sugar metabolism by tumour cells in culture.
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PMID:Introduction and metabolism of pentose and hexose phosphates in permeabilized Morris hepatoma 5123TC cells. 244


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