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

A 58-year-old Japanese male visited us with painful lesions on the lower lip, oral mucosa and genital region of an 8-month duration. Histological features of the genital lesion were almost consistent with lichenoid tissue reaction. A few intraepidermal acantholytic keratinocytes were also seen in the suprabasal clefts. Direct immunofluorescence exhibited cell surface immunoglobulin (Ig)G deposition and linear deposition of fibrinogen at the dermoepidermal junction. IgG anti-desmoglein (Dsg)3 antibody, but not anti-Dsg1 antibody, was detected in the patient's serum by enzyme-linked immunosorbent assay. Immunoblotting using normal human epidermal extract detected the 210-kD envoplakin, 190-kD periplakin and 130-kD Dsg3. The diagnosis of paraneoplastic pemphigus (PNP) was made. Subsequent investigation revealed a large space-occupying lesion in the liver. Histological findings from liver biopsy specimen were consistent with hepatocellular carcinoma. The patient has been alive 38 months after the diagnosis of PNP was made, although the liver mass has slowly enlarged. Our case is clinically and histologically similar to erosive mucosal lichen planus. Immunological studies confirmed the diagnosis of PNP. The results of negative Dsg1 and positive Dsg3 were consistent with clinical features showing severe mucosal involvement without cutaneous erosion. In PNP, the association with non-hematological solid tumor is extremely rare.
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PMID:Paraneoplastic pemphigus mimicking erosive mucosal lichen planus associated with primary hepatocellular carcinoma. 1716 86

Phytochemical investigation of Tecoma stans Juss. fruits and flowers resulted in the isolation of a new phenylethanoid, 2-(3,4-dihydroxyphenyl)ethyl-2-O-[6-deoxy-alpha-L-mannopyranosyl-4-(3,4-dihydroxyphenyl)-2-propenoate]-beta-D-glucopyranoside (3), and a novel monoterpene alkaloid, 5-hydroxy-skytanthine hydrochloride (8), along with eleven known compounds; 4-O-E-caffeoyl-alpha-L-rhamnopyranosyl-(1' --> 3)-alpha/beta-D-glucopyranose (1), E/Z-acetoside (2), isoacetoside (4), rutin (5), luteolin 7-O-beta-D-neohespridoside (6), luteolin 7-O-beta-D-glucopyranoside (7) and sucrose (9) were isolated from the fruits, while luteolin 7-O-beta-D-glucuronopyranoside (10), diosmetin 7-O-beta-D-glucuronopyranoside (11), diosmetin 7-O-beta-D-glucopyranoside (12), diosmetin 7-O-beta-D-glucuronopyranoside methyl ester (13) and acetoside (2) were isolated from the flowers. Their chemical structures have been determined on the basis of chemical and spectroscopic evidences. Biological investigations of a T. stans fruits extract and compounds 1, 2, 4, and 8 indicated that the extract, 1, 2, and 4 possessed a strong scavenging activity to DPPH, peroxyl and hydroxyl radicals. Unlike 4, which potentially induced NO generation in bacterial lipopolysaccharide-stimulated raw murine macrophage (RAW 264.7), the extract, 1, 2, and 8 significantly inhibited the NO generation. The extract, 2 and 4 exhibited a cytotoxic effect on human hepatocarcinoma cells (Hep-G2), while the extract, 2 and 8 were potent growth inhibitors of human breast carcinoma cells (MCF-7). 1 and 2 were remarkable growth inducers of human lymphoblastic leukemia cells (1301), whereas the extract, 2, and 8 stimulated the macrophage proliferation rate. Taken together, the novel compound 8 is effective as anti-proliferative agent against MCF-7 cells and as NO inhibitor, whereas 2 exhibited multi-functional properties as antioxidant and anti-proliferative agent against both solid tumor cell lines Hep-G2 and MCF-7 cells.
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PMID:Anti-proliferative and antioxidant constituents from Tecoma stans. 1729 87

Sarcomatous hepatocellular carcinoma is a rare neoplasm of the liver. A 79-year-old man with a liver tumor was admitted to our hospital. Enhanced computed tomography and magnetic resonance imaging revealed a cystlike lesion, whereas abdominal ultrasonography revealed a solid tumor. The patient underwent medial segmentectomy of the liver for the presumptive diagnosis of atypical hepatocellular carcinoma. Microscopically, the tumor was diagnosed as hepatocellular carcinoma with sarcomatous change. Although anticancer therapy is presumed to be a cause of sarcomatous change in hepatocellular carcinoma, some cases in which patients had not previously undergone anticancer therapy have been reported. Here we report a case of sarcomatous hepatocellular carcinoma without previous anticancer therapy and present a review of the literature.
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PMID:Sarcomatous hepatocellular carcinoma without previous anticancer therapy. 1752 Feb 11

Hypoxia is a prominent feature of solid tumor development and is known to stimulate mitochondrial ROS (mROS), which, in turn, can activate hypoxia-inducible transcription factor-1alpha and nuclear factor-kappaB (NF-kappaB). Because NF-kappaB plays a central role in carcinogenesis, we examined the mechanism of mROS-mediated NF-kappaB activation and the fate of cancer cells during hypoxia after mitochondrial reduced glutathione (mGSH) depletion. Hypoxia generated mROS in hepatoma (HepG2, H35), neuroblastoma (SH-SY5Y), and colon carcinoma (DLD-1) cells, leading to hypoxia-inducible transcription factor-1alpha-dependent gene expression and c-Src activation that was prevented in cells expressing a redox-insensitive c-Src mutant (C487A). c-Src stimulation activated NF-kappaB without IkappaB-alpha degradation due to IkappaB-alpha tyrosine phosphorylation that was inhibited by rotenone/TTFA or c-Src antagonism. The c-Src-NF-kappaB signaling contributed to the survival of cells during hypoxia as c-Src inhibition or p65 down-regulation by small interfering RNA-sensitized HepG2 cells to hypoxia-induced cell death. Moreover, selective mGSH depletion resulted in an accelerated and enhanced mROS generation by hypoxia that killed SH-SY5Y and DLD-1 cells without disabling the c-Src-NF-kappaB pathway. Thus, although mROS promote cell survival by NF-kappaB activation via c-Src, mROS overgeneration may be exploited to sensitize cancer cells to hypoxia.
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PMID:Dual role of mitochondrial reactive oxygen species in hypoxia signaling: activation of nuclear factor-{kappa}B via c-SRC and oxidant-dependent cell death. 1767 Dec 7

In the following study, we prepared a double-chain miniprotein with each chain containing three linear repeats of the self-peptide gonadotropin-releasing hormone (GnRH(3)), the hinge region of human IgG1 (hinge), and a T-helper epitope from the measles virus protein (MVP). The di-GnRH(3)-hinge-MVP miniprotein was conjugated to purified recombinant heat shock protein 65 (Hsp65) of Mycobacterium bovis and used to immunize BALB/c mice primed with subcutaneous injection of Bacillus Calmette-Gurerin (BCG) in the absence of adjuvants. After anti-GnRH antibodies were successfully produced, mice were inoculated with H22 cells as a solid tumor. The results showed that after GnRH was inhibited by anti-GnRH antibodies the testosterone levels in sera markedly decreased (P<0.01) and the testicle weights reduced as well (P<0.05) in GnRH(3)-hinge-MVP-Hsp65-immunized mice. The average weight of tumors in mice treated with GnRH(3)-hinge-MVP-Hsp65 was significantly lower than in mice treated with saline only (neutral control, P<0.001), or less than in mice treated with Hsp65 (negative control, P<0.005). The data reported here demonstrated that GnRH(3)-hinge-MVP-Hsp65 could significantly attenuate the progression of liver tumor in mice transplanted with H22 cells, and might develop to be palliative treatment of hepatocellular carcinoma (HCC) patients in the future.
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PMID:Inhibition effects on liver tumors of BALB/c mice bearing H22 cells by immunization with a recombinant immunogen of GnRH linked to heat shock protein 65. 1772 21

Tyroserleutide (YSL), extracted from spleen of pigs, is a tripeptide that has shown therapeutic efficacy in an experimental BEL-7402 human hepatocarcinoma model. The hollow fiber assay (HFA) is a solid tumor model for large-scale screening of potential anticancer compounds that minimizes expenditures of materials, time, and money. Tumor cells are cultivated within biocompatible, semipermeable hollow fibers, which are implanted in immunosuppressed mice. In this study, the HFA was used to investigate the therapeutic efficacy of YSL for human hepatocarcinoma. In vitro effects of YSL on human hepatocarcinoma cell lines BEL-7402, SMMC-7721, Hep3B, HepG2, and SK-HEP-1 were assayed by the MTS method. In vivo effects of YSL on the five human hepatocarcinoma cell lines were assayed by HFA. Mice implanted with tumor cells in hollow fibers were treated with YSL, and the effects of YSL on tumor cell populations were assessed by MTT assay. YSL significantly inhibited the proliferation of the five human hepatocarcinoma, both in vitro and in vivo (P < 0.05). The HFA is a rapid, accurate, and economical method for evaluating the inhibitory effects of drugs on different tumor cells in vivo. These results support the clinical application of YSL for treatment of human hepatocarcinoma.
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PMID:Evaluation of the therapeutic efficacy of tripeptide tyroserleutide (YSL) for human hepatocarcinoma by in vivo hollow fiber assay. 1826 78

Dynamic contrast-enhanced ultrasonography (DCE-US) using the contrast agent Sonovue and vascular recognition imaging software is a novel technique that enables the detection of microvessels and quantitative assessment of solid tumor perfusion using raw linear data. Clinical trials have shown that DCE-US can be used to assess the anticancer efficacy of antiangiogenic treatment, for which conventional efficacy criteria based on size are unsuitable. Reduction in tumor vascularization can easily be detected in responders after 1-2 weeks and is correlated with progression-free survival and overall survival. DCE-US is supported by the French Cancer National Institut. This program is currently studying the technique in metastatic breast cancer, melanoma, colon cancer, gastrointestinal stromal tumor, and renal cell carcinoma, as well as in primary hepatocellular carcinoma, to establish the optimal perfusion parameters and timing for quantitative anticancer efficacy assessments.
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PMID:Dynamic contrast-enhanced ultrasonography (DCE-US) with quantification of tumor perfusion: a new diagnostic tool to evaluate the early effects of antiangiogenic treatment. 1837 62

Hepatocellular carcinoma (HCC) is currently the fifth most common solid tumor worldwide and the third leading cause of cancer-related death. Eighty percent of new cases occur in developing countries, but the incidence is rising in economically developed regions including Japan, Western Europe, and the United States. More than 80% of patients present with advanced or unresectable disease, and for those patients who do undergo resection, the recurrence rates can be as high as 50% at 2 years. Thus, a large number of patients will seek systemic therapy. Systemic cytotoxic chemotherapy is largely ineffective and can have significant toxicity in patients with underlying liver dysfunction. Newer biologic agents that target molecular abnormalities common to HCC may improve the clinical outcome in patients with HCC.
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PMID:Systemic therapy for hepatocellular carcinoma. 1839 18

Liver cancer is the sixth most common cancer, killing 600,000 people each year worldwide. Hepatocellular carcinoma (HCC) is the most common form of liver cancer. HCC has several specific features. In particular, the risk factors and causes are well known, thereby permitting - in theory - primary prevention and early detection surveillance programs. Also, HCC is a vascular solid tumor with a high degree of drug resistance (the so-called angiogenic and MDR phenotype). These features should be targeted primarily, if not exclusively, by future biological therapies. In this review, the authors report the most recent therapeutic developments, including emerging targeted strategies.
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PMID:[Therapeutic advances in hepatocellular carcinoma]. 1866 79

Cytotoxin III (CTX III), a basic polypeptide with 60 amino acid residues isolated from Naja naja atra venom, have potential therapeutic activity in tumor therapy. However, the therapeutic effect in solid tumor treatment with CTX III are still largely unknown. In the present study, we investigated whether CTX III affects cell growth and cell cycle progression of hepatocellular carcinoma cell (HepG2). We found that the proliferation of HepG2 cell was inhibited by CTX III, to some extent, in a time- and dose-dependent manner (IC50 2.58microg/ml at 24h). Flow cytometric analysis and annexin V labeling also demonstrated that CTX III increased the percentage of apoptotic cells being associated with cell cycle arrest at S-phase. Semi-quantitative reverse transcription-polymerase chain reaction (RT-PCR) and Western blot revealed that cyclin D1, cyclin A and cyclin E, which involved in cell apopotosis and cell cycle progression, were down regulated both at transcription and translation levels. CTX III-induced caspase-8, -9 and caspase-3 activation, generation of truncated Bid, releasing of cytochrome c and the change of Bcl-2/Bax ratio on protein and mRNA levels. These findings demonstrated that cyclin D1, cyclin B and cyclin A down-regulation, change of Bcl-2/Bax ratio and caspase-8 and -9 activation contribute to CTX III-induced HepG2 cell apoptosis.
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PMID:Apoptosis of human hepatocellular carcinoma cell (HepG2) induced by cardiotoxin III through S-phase arrest. 1898 2


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