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1. Ji SP, Li Q, Dong H: Therapy and prognostic features of primary clear cell carcinoma of the liver. World J Gastroenterol; 2010 Feb 14;16(6):764-9
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Therapy and prognostic features of primary clear cell carcinoma of the liver.
  • AIM: To clarify the therapeutic strategies and prognosis factors of primary clear cell carcinoma of the liver (PCCCL).
  • The patients were divided into two groups to make treatment analysis: curative resection only (n = 40); and curative resection and postoperative chemotherapy with calcium folinate and tegafur (n = 24).
  • Meanwhile, the PCCCL patients were subdivided into two subgroups on the basis of the proportion of clear cells in the tumor for pathological analysis.
  • There were 36 cases in subgroup A for which the proportion of clear cells was more than 70%, and 28 cases in subgroup B for which the proportion was less or equal to 70%, comparing analysis of median survival time of the counterpart groups.
  • The Kaplan-Meier method showed that capsule formation, preoperative liver function, hepatitis C virus infection, large vascular invasion and multiple tumor occurrences were related to disease-free survival.
  • Cox regression analysis showed that the clear cell ratio, capsule formation, preoperative liver function and large vascular invasion were independent risk factors for overall survival.
  • CONCLUSION: Postoperative chemotherapy has no obvious effect on survival of patients with PCCCL.
  • Clear cell ratio, capsule formation, preoperative liver function, and vascular invasion were independent risk factors for prognosis.
  • [MeSH-major] Adenocarcinoma, Clear Cell / drug therapy. Adenocarcinoma, Clear Cell / surgery. Leucovorin / therapeutic use. Liver Neoplasms / drug therapy. Liver Neoplasms / surgery. Tegafur / therapeutic use
  • [MeSH-minor] Adult. Aged. Antimetabolites, Antineoplastic / therapeutic use. Combined Modality Therapy. Female. Hepatectomy. Humans. Kaplan-Meier Estimate. Male. Middle Aged. Prognosis. Retrospective Studies. Treatment Outcome

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  • (PMID = 20135727.001).
  • [ISSN] 2219-2840
  • [Journal-full-title] World journal of gastroenterology
  • [ISO-abbreviation] World J. Gastroenterol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] China
  • [Chemical-registry-number] 0 / Antimetabolites, Antineoplastic; 1548R74NSZ / Tegafur; Q573I9DVLP / Leucovorin
  • [Other-IDs] NLM/ PMC2817067
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2. Lee HY, Lee DG, Chun K, Lee S, Song SY: Clear cell carcinoma of the pancreas--a case report and review of the literature. Cancer Res Treat; 2009 Sep;41(3):175-81
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  • [Title] Clear cell carcinoma of the pancreas--a case report and review of the literature.
  • According to the WHO classification, primary clear cell carcinoma of the pancreas is rare and it is classified as a "miscellaneous" carcinoma.
  • We report here on an unusual case of primary pancreatic clear cell carcinoma, which is the first such reported case in Korea.
  • On the abdominal computed tomography (CT), we detected an abdominal mass involving the pancreas tail and liver, and clear cell carcinoma with rhabdoid feature was seen on the histologic evaluation.
  • The tumor cells showed well defined cell membranes, clear cytoplasm and prominent cell boundaries.
  • She was diagnosed with a primary pancreatic clear cell carcinoma with hepatic metastasis and she received palliative gemcitabine chemotherapy.

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  • (PMID = 19809568.001).
  • [ISSN] 1598-2998
  • [Journal-full-title] Cancer research and treatment : official journal of Korean Cancer Association
  • [ISO-abbreviation] Cancer Res Treat
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Korea (South)
  • [Other-IDs] NLM/ PMC2757667
  • [Keywords] NOTNLM ; Clear cell carcinoma / Pancreas / Rhabdoid tumor
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3. Xiao EH, Li JQ, Huang JF: Effects of p53 on apoptosis and proliferation of hepatocellular carcinoma cells treated with transcatheter arterial chemoembolization. World J Gastroenterol; 2004 Jan 15;10(2):190-4
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  • [Title] Effects of p53 on apoptosis and proliferation of hepatocellular carcinoma cells treated with transcatheter arterial chemoembolization.
  • AIM: To evaluate the effects of p53 on apoptosis and proliferation of hepatocellular carcinoma (HCC) cells treated with transcatheter arterial chemoembolization (TACE).
  • TACE group included 79 patients who had 1-5 courses of TACE before surgery, of them, 11 patients had 1-4 courses of chemotherapy (group A), 33 patients had 1-5 courses of chemotherapy combined with iodized oil (group B), 23 patients had 1-3 courses of chemotherapy, iodized oil and gelatin sponge (group C), 12 patients had 1-3 courses of chemotherapy combined with iodized oil, ethanol and gelatin sponge (group D).
  • RESULTS: P53 protein expressions in trabecular and clear cells in HCC specimens were significantly lower than that in pseudoglandular, solid, poorly differentiated or undifferentiated and sclerosis HCC (P<0.05).
  • Expression of p53 protein in HCC cells increased with the increase of pathological grades (P<0.05), and correlated positively with expressions of Ki-67 and PCNA protein, and negatively with Bcl-2 to Bax protein expression rate and AI (P<0.05).
  • CONCLUSION: Expression of p53 protein can enhance proliferation of HCC cells and suppress apoptosis of HCC cells after TACE.
  • [MeSH-major] Apoptosis / physiology. Carcinoma, Hepatocellular / therapy. Chemoembolization, Therapeutic. Liver Neoplasms / therapy. Tumor Suppressor Protein p53 / metabolism
  • [MeSH-minor] Adult. Aged. Cell Division / physiology. Female. Humans. Immunohistochemistry. In Situ Nick-End Labeling. Ki-67 Antigen / metabolism. Male. Middle Aged. Proliferating Cell Nuclear Antigen / metabolism. Proto-Oncogene Proteins / metabolism. Proto-Oncogene Proteins c-bcl-2 / metabolism. bcl-2-Associated X Protein

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  • (PMID = 14716820.001).
  • [ISSN] 1007-9327
  • [Journal-full-title] World journal of gastroenterology
  • [ISO-abbreviation] World J. Gastroenterol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] China
  • [Chemical-registry-number] 0 / BAX protein, human; 0 / Ki-67 Antigen; 0 / Proliferating Cell Nuclear Antigen; 0 / Proto-Oncogene Proteins; 0 / Proto-Oncogene Proteins c-bcl-2; 0 / Tumor Suppressor Protein p53; 0 / bcl-2-Associated X Protein
  • [Other-IDs] NLM/ PMC4717001
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4. Wu XZ, Zhang L, Shi BZ, Hu P: Inhibitory effects of N-(4-hydrophenyl) retinamide on liver cancer and malignant melanoma cells. World J Gastroenterol; 2005 Oct 7;11(37):5763-9
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  • [Title] Inhibitory effects of N-(4-hydrophenyl) retinamide on liver cancer and malignant melanoma cells.
  • AIM: To investigate the effect of N-(4-hydrophenyl) retinamide (4-HPR), the derivative of retinoic acid, on inhibition of migration, invasion, cell growth, and induction of apoptosis in hepatocellular carcinoma cells (HCCs) and malignant melanoma cells.
  • Cell growth was assayed by MTT chromometry.
  • RESULTS: We observed that the migration of HCC and melanoma cells was significantly suppressed by 4-HPR and the migration cells were reduced to 58+/-5.03 (control 201+/-27.2, P<0.05, n = 4) in SMMC 7721-k3 HCC, and to 254+/-25.04 (control 302+/-30.1, P<0.05, n = 4) in melanoma cells after 6-h incubation with 4-HPR.
  • The invasion through reconstituted basement membrane was also significantly reduced by 4-HPR treatment to 11.2+/-3.3 in SMMC 7721-k3 HCC (control 27+/-13.1), and to 24.3+/-3.2 in melanoma cells (control 67.5+/-10.1, P<0.05, n = 3).
  • Cell growth, especially in melanoma cells, was also significantly inhibited.
  • Furthermore, 3 micromol/L of 4-HPR induced apoptosis in B16 melanoma cells (37.11+/-0.94%) more significantly than all-trans retinoic acid (P<0.05), but it failed to induce apoptosis in SMMC 7721-k3 HCC.
  • The mechanism for 4-HPR-induced apoptosis was not clear, but we observed that 4-HPR could regulate p27(kip1), and overexpression of cerebroside sulfotransferase (CST) diminished the apoptosis induced by 4-HPR in melanoma cells.
  • CONCLUSION: 4-HPR is a potent inhibitor of HCC migration and inducer of melanoma cell apoptosis.
  • [MeSH-major] Antineoplastic Agents / therapeutic use. Carcinoma, Hepatocellular / drug therapy. Fenretinide / therapeutic use. Liver Neoplasms / drug therapy. Melanoma / drug therapy
  • [MeSH-minor] Animals. Apoptosis / drug effects. Cell Cycle / drug effects. Cell Line, Tumor / drug effects. Cell Movement / drug effects. Humans. Mice. Mice, Nude. Sulfotransferases / genetics. Sulfotransferases / metabolism

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  • (PMID = 16270382.001).
  • [ISSN] 1007-9327
  • [Journal-full-title] World journal of gastroenterology
  • [ISO-abbreviation] World J. Gastroenterol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] China
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 187EJ7QEXL / Fenretinide; EC 2.8.2.- / Sulfotransferases; EC 2.8.2.11 / galactosylceramide sulfotransferase
  • [Other-IDs] NLM/ PMC4479673
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5. Plumlee CR, Lazaro CA, Fausto N, Polyak SJ: Effect of ethanol on innate antiviral pathways and HCV replication in human liver cells. Virol J; 2005 Dec 02;2:89
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  • [Title] Effect of ethanol on innate antiviral pathways and HCV replication in human liver cells.
  • Alcohol abuse reduces response rates to IFN therapy in patients with chronic hepatitis C.
  • To model the molecular mechanisms behind this phenotype, we characterized the effects of ethanol on Jak-Stat and MAPK pathways in Huh7 human hepatoma cells, in HCV replicon cell lines, and in primary human hepatocytes.
  • High physiological concentrations of acute ethanol activated the Jak-Stat and p38 MAPK pathways and inhibited HCV replication in several independent replicon cell lines.
  • With a propensity to progress to chronic infection, approximately 70% of patients with chronic viremia develop histological evidence of chronic liver diseases including chronic hepatitis, cirrhosis, and hepatocellular carcinoma.
  • The situation is even more dire for patients who abuse ethanol, where the risk of developing end stage liver disease is significantly higher as compared to HCV patients who do not drink 12.Recombinant interferon alpha (IFN-alpha) therapy produces sustained responses (ie clearance of viremia) in 8-12% of patients with chronic hepatitis C 3.
  • Significant improvements in response rates can be achieved with IFN plus ribavirin combination 456 and pegylated IFN plus ribavirin 78 therapies.
  • However, over 50% of chronically infected patients still do not clear viremia.
  • Moreover, HCV-infected patients who abuse alcohol have extremely low response rates to IFN therapy 9, but the mechanisms involved have not been clarified.MAPKs play essential roles in regulation of differentiation, cell growth, and responses to cytokines, chemokines and stress.
  • Currently, four MAPK modules have been characterized in mammalian cells: Extracellular Regulated Kinases (ERK1 and 2), Stress activated/c-Jun N terminal kinase (SAPK/JNK), p38 MAP kinases, and ERK5 11.
  • However, information on how ethanol affects MAPKs in the context of innate antiviral pathways such as the Jak-Stat pathway in human cells is extremely limited.
  • In the current report, we postulated that alcohol and HCV proteins modulate MAPK and Jak-Stat pathways in human liver cells.
  • To begin to address these issues, we characterized the interaction of acute ethanol on Jak-Stat and MAPK pathways in Huh7 cells, HCV replicon cells lines, and primary human hepatocytes.

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  • (PMID = 16324217.001).
  • [ISSN] 1743-422X
  • [Journal-full-title] Virology journal
  • [ISO-abbreviation] Virol. J.
  • [Language] ENG
  • [Grant] United States / NIDDK NIH HHS / DK / DK62187; United States / NIAAA NIH HHS / AA / AA13301; United States / NIDDK NIH HHS / DK / R01 DK062187; United States / NIAAA NIH HHS / AA / AA013301-02; United States / NIAAA NIH HHS / AA / R21 AA013301-02; United States / NIAID NIH HHS / AI / AI048214; United States / NIAID NIH HHS / AI / U19 AI048214; United States / NIAAA NIH HHS / AA / R21 AA013301
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / RNA, Viral; 3K9958V90M / Ethanol; EC 2.7.10.1 / Protein-Tyrosine Kinases; EC 2.7.11.24 / p38 Mitogen-Activated Protein Kinases
  • [Other-IDs] NLM/ PMC1318489
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6. Djeha AH, Thomson TA, Leung H, Searle PF, Young LS, Kerr DJ, Harris PA, Mountain A, Wrighton CJ: Combined adenovirus-mediated nitroreductase gene delivery and CB1954 treatment: a well-tolerated therapy for established solid tumors. Mol Ther; 2001 Feb;3(2):233-40
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  • [Title] Combined adenovirus-mediated nitroreductase gene delivery and CB1954 treatment: a well-tolerated therapy for established solid tumors.
  • Gene-directed enzyme prodrug therapy (GDEPT) is a refinement of cancer chemotherapy that generates a potent cell-killing drug specifically in tumor cells by enzymatic activation of an inert prodrug.
  • We describe in vivo studies that evaluate the efficacy and safety of intratumoral (i.t.) injection of an adenovirus vector (CTL102) expressing Escherichia coli nitroreductase (NTR) combined with systemic prodrug (CB1954) treatment.
  • A single i.t. injection of CTL102 (7.5 x 10(9) to -2 x 10(10) particles) followed by CB1954 treatment produced clear anti-tumor effects in subcutaneous (s.c.) xenograft models of four cancers that are likely candidates for GDEPT (i.e., primary liver, head and neck, colorectal and prostate).
  • Virus dose-response studies (s.c. liver model) revealed a steep increase and subsequent rapid plateauing of both NTR gene delivery and anti-tumor efficacy.
  • Preexisting anti-Ad5 neutralizing antibodies may therefore be an advantage rather than an issue in the clinical use of this new therapy.
  • [MeSH-major] Adenoviridae / genetics. Antineoplastic Agents / therapeutic use. Aziridines / therapeutic use. Gene Transfer Techniques. Genetic Therapy / methods. Nitroreductases / genetics. Prodrugs / therapeutic use
  • [MeSH-minor] Animals. Carcinoma, Hepatocellular / therapy. Colorectal Neoplasms / therapy. Dose-Response Relationship, Drug. Escherichia coli / enzymology. Head and Neck Neoplasms / therapy. Humans. Liver Neoplasms / therapy. Luciferases / metabolism. Male. Mice. Mice, Inbred BALB C. Mice, Nude. Neoplasm Transplantation. Prostatic Neoplasms / therapy. Transduction, Genetic. Transfection. Tumor Cells, Cultured

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  • (PMID = 11237680.001).
  • [ISSN] 1525-0016
  • [Journal-full-title] Molecular therapy : the journal of the American Society of Gene Therapy
  • [ISO-abbreviation] Mol. Ther.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / Aziridines; 0 / Prodrugs; 7865D5D01M / tretazicar; EC 1.13.12.- / Luciferases; EC 1.7.- / Nitroreductases
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7. Papoulas M, Theocharis S: Primary liver tumors: origin and target therapy. Expert Opin Ther Targets; 2009 Aug;13(8):957-65
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  • [Title] Primary liver tumors: origin and target therapy.
  • BACKGROUND: The liver is the largest gland and chief metabolic organ of the human body possessing a unique ability to regenerate.
  • The general interest of primary liver tumors is noteworthy because of their increasing worldwide incidence and mortality.
  • OBJECTIVE: To provide a brief and up-to-date review on the cellular origin of primary liver tumors and to examine the use of stem cells in potential future therapeutic attempts.
  • RESULTS: It is clear that hepatic progenitor cells (HPCs) could be the basis of some hepatocellular carcinomas (HCC), cholangiocarcinomas (CHC), hepatocellular adenomas and hepatoblastomas.
  • Cancer stem cell (CSC) theory emphasizes the role of hepatic stem cells in the development and progression of liver tumors.
  • Conventional treatments for HCC do not seem to be beneficial for the majority of patients and new therapeutic approaches such as gene therapy and targeted drug therapy are of great clinical interest.
  • [MeSH-major] Carcinoma, Hepatocellular / pathology. Carcinoma, Hepatocellular / therapy. Cell Transformation, Neoplastic / pathology. Drug Delivery Systems / methods. Hepatocytes / pathology. Liver Neoplasms / pathology. Liver Neoplasms / therapy. Stem Cells / pathology
  • [MeSH-minor] Animals. Biomarkers, Tumor / genetics. Cell Differentiation / genetics. Cell Lineage / genetics. Cholangiocarcinoma / genetics. Cholangiocarcinoma / pathology. Cholangiocarcinoma / therapy. Humans

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  • (PMID = 19606929.001).
  • [ISSN] 1744-7631
  • [Journal-full-title] Expert opinion on therapeutic targets
  • [ISO-abbreviation] Expert Opin. Ther. Targets
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Biomarkers, Tumor
  • [Number-of-references] 84
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8. Zhu Y, Tibensky I, Schmidt J, Ryschich E, Märten A: Interferon-alpha enhances antitumor effect of chemotherapy in an orthotopic mouse model for pancreatic adenocarcinoma. J Immunother; 2008 Sep;31(7):599-606
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  • [Title] Interferon-alpha enhances antitumor effect of chemotherapy in an orthotopic mouse model for pancreatic adenocarcinoma.
  • Data from a phase 2 trial combining chemoradiotherapy with interferon (IFN)-alpha (CapRI scheme) for adjuvant treatment of pancreatic carcinoma are very encouraging.
  • Here, we try to evaluate the effect of IFN-alpha in this combined treatment scheme.
  • Mice were inoculated with syngeneic cells in the pancreas.
  • Tumor growth and immune responses were determined and adoptive cell transfer experiments performed.
  • The impact of IFN-alpha treatment on leukocyte-endothelium interactions was assessed by intravital microscopy.
  • Addition of IFN-alpha to chemotherapy had a significant life-prolonging effect.
  • Regimens including IFN-alpha showed a clear trend toward less metastases than monotherapy.
  • T cells and dendritic cells infiltrated tumors significantly more in 5-FU+IFN-alpha animals and these T cells secreted IFN-gamma tumor specifically.
  • Antitumor response could be transferred by injection of mononuclear cells from 5-FU+IFN-alpha-treated mice into treatment-naive animals.
  • The transferred cells homed to the tumors and proliferated there.
  • IFN-alpha significantly improves chemotherapy.
  • [MeSH-major] Antineoplastic Combined Chemotherapy Protocols / administration & dosage. Interferon-alpha / administration & dosage. Liver Neoplasms / therapy. Pancreatic Neoplasms / therapy. Peritoneal Neoplasms / therapy
  • [MeSH-minor] Adjuvants, Immunologic / administration & dosage. Animals. Cell Adhesion / drug effects. Cell Adhesion / immunology. Cell Line, Tumor. Cell Movement / drug effects. Cell Movement / immunology. Cell Proliferation / drug effects. Cisplatin / administration & dosage. Combined Modality Therapy. Cytokines / drug effects. Cytokines / secretion. Fluorouracil / administration & dosage. Immunotherapy, Adoptive. Mice. Mice, Inbred C57BL. Radiotherapy. Survival Analysis. T-Lymphocytes / drug effects. T-Lymphocytes / immunology. T-Lymphocytes / metabolism. Tumor Burden / drug effects

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  • (PMID = 18600184.001).
  • [ISSN] 1537-4513
  • [Journal-full-title] Journal of immunotherapy (Hagerstown, Md. : 1997)
  • [ISO-abbreviation] J. Immunother.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Adjuvants, Immunologic; 0 / Cytokines; 0 / Interferon-alpha; Q20Q21Q62J / Cisplatin; U3P01618RT / Fluorouracil
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9. Warmann SW, Frank H, Heitmann H, Ruck P, Herberts T, Seitz G, Fuchs J: Bcl-2 gene silencing in pediatric epithelial liver tumors. J Surg Res; 2008 Jan;144(1):43-8
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  • [Title] Bcl-2 gene silencing in pediatric epithelial liver tumors.
  • BACKGROUND: Proteins of the Bcl-2 family prevent cells of various tumor types from undergoing apoptosis and thus contribute to their chemotherapy resistance.
  • The phenotype of multidrug resistance is a major factor for poor treatment results of advanced epithelial liver tumors in children.
  • The purpose of this study was to analyze the influence of Bcl-2 on the chemotherapy resistance of hepatoblastoma (HB) and pediatric hepatocellular carcinoma (HCC).
  • MATERIALS AND METHODS: Bcl-2 expression was analyzed in the HB cell lines HUH6 and HepT1 as well as in the HCC cell line HepG2 before and after treatment with cisplatin, doxorubicin, taxol, and etoposid.
  • Treatment efficiencies of cytotoxic agents were assessed against original and Bcl-2 siRNA transfected tumor cells.
  • RESULTS: The mixed HB cell line HUH6 showed a relevant amount of Bcl-2 expression, which increased after chemotherapy.
  • In these cells Bcl-2 appeared within the nuclei and the cytosol.
  • Treatment with all cytotoxic agents was significantly improved through Bcl-2 siRNA (P < 0.001-0.0054) in this cell line.
  • There was no effect of Bcl-2 siRNA in HepT1 and HepG2 cells.
  • Thus, this gene might serve as target for a gene-directed adjuvant therapy.
  • Further studies seem necessary to clear the susceptibility of pediatric epithelial liver tumors toward the described approach.
  • [MeSH-major] Carcinoma, Hepatocellular / genetics. Drug Resistance, Neoplasm / genetics. Gene Silencing. Liver Neoplasms / genetics. Proto-Oncogene Proteins c-bcl-2 / genetics
  • [MeSH-minor] Antibiotics, Antineoplastic / pharmacology. Antineoplastic Agents, Phytogenic / pharmacology. Antineoplastic Combined Chemotherapy Protocols / pharmacology. Apoptosis / drug effects. Apoptosis / physiology. Blotting, Western. Cell Line, Tumor. Child. Cisplatin / pharmacology. Doxorubicin / pharmacology. Drug Resistance, Multiple / genetics. Epithelium. Etoposide / pharmacology. Genetic Therapy / methods. Humans. Paclitaxel / pharmacology. Transfection

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  • (PMID = 17574594.001).
  • [ISSN] 0022-4804
  • [Journal-full-title] The Journal of surgical research
  • [ISO-abbreviation] J. Surg. Res.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antibiotics, Antineoplastic; 0 / Antineoplastic Agents, Phytogenic; 0 / Proto-Oncogene Proteins c-bcl-2; 6PLQ3CP4P3 / Etoposide; 80168379AG / Doxorubicin; P88XT4IS4D / Paclitaxel; Q20Q21Q62J / Cisplatin
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10. Yip EC, Chan AS, Pang H, Tam YK, Wong YH: Protocatechuic acid induces cell death in HepG2 hepatocellular carcinoma cells through a c-Jun N-terminal kinase-dependent mechanism. Cell Biol Toxicol; 2006 Jul;22(4):293-302
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  • [Title] Protocatechuic acid induces cell death in HepG2 hepatocellular carcinoma cells through a c-Jun N-terminal kinase-dependent mechanism.
  • Cytotoxicity assays showed that PCA, CA and LT (at 100 micromol/L) effectively killed the HepG2 hepatocellular carcinoma cells.
  • Coincidently, PCA-induced cell death was rescued by specific inhibitors for JNK and p38, while the cytotoxicities of CA and LT were partially eliminated by the antioxidant effect of N-acetyl-L-cysteine (NAC).
  • Further investigation demonstrated that the aqueous extract of Lonicera japonica also triggered HepG2 cell death in a JNK-dependent manner, but the amount of PCA alone in this herbal extract was insufficient to contribute the subsequent cytotoxic effect.
  • Collectively, our results suggest that PCA is a naturally occurring compound capable of inducing JNK-dependent hepatocellular carcinoma cell death.
  • [MeSH-major] Antineoplastic Agents / pharmacology. Carcinoma, Hepatocellular / drug therapy. Hydroxybenzoates / pharmacology. JNK Mitogen-Activated Protein Kinases / metabolism. Liver Neoplasms / drug therapy
  • [MeSH-minor] Cell Death. Cell Line, Tumor. Dose-Response Relationship, Drug. Humans. Lonicera / metabolism. MAP Kinase Signaling System. Models, Chemical. Phosphorylation. Plant Extracts / pharmacology. p38 Mitogen-Activated Protein Kinases / metabolism

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  • [ErratumIn] Cell Biol Toxicol. 2007 Mar;23(2):139
  • (PMID = 16835731.001).
  • [ISSN] 0742-2091
  • [Journal-full-title] Cell biology and toxicology
  • [ISO-abbreviation] Cell Biol. Toxicol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Netherlands
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / Hydroxybenzoates; 0 / Plant Extracts; 36R5QJ8L4B / protocatechuic acid; EC 2.7.11.24 / JNK Mitogen-Activated Protein Kinases; EC 2.7.11.24 / p38 Mitogen-Activated Protein Kinases
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11. Hoshida Y, Moriyama M, Otsuka M, Kato N, Taniguchi H, Shiratori Y, Seki N, Omata M: Gene expressions associated with chemosensitivity in human hepatoma cells. Hepatogastroenterology; 2007 Mar;54(74):489-92
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  • [Title] Gene expressions associated with chemosensitivity in human hepatoma cells.
  • BACKGROUND/AIMS: Only limited patients with hepatoma benefit from chemotherapy without a clear explanation.
  • METHODOLOGY: In 8 hepatoma cells (HLE, HLF, Huh7, Hep3B, PLC/PRF/5, SK-Hep1, Huh6, and HepG2) transcriptional profiles were obtained using cDNA microarray including 2300 genes.
  • Chemosensitivities to 8 anticancer drugs (nimustine, mitomycin C, cisplatin, carboplatin, doxorubicin, epirubicin, mitoxantrone, and 5-fluorouracil) were measured by obtaining 50% growth inhibitory concentrations (GI50) using MTT assay.
  • Genes having drug-specific association with chemosensitivity were selected.
  • Drug inactivators reported in non-liver cancers such as multidrug transporters and drug metabolizers showed less diversity of chemosensitivity in hepatoma cells.
  • CONCLUSIONS: To evaluate these gene expressions may be useful to select anticancer drugs, and possibly to consider new therapeutic target to modify drug action.
  • [MeSH-major] Antineoplastic Agents / pharmacology. Carcinoma, Hepatocellular / genetics. Carcinoma, Hepatocellular / pathology. Cell Division / drug effects. Cell Survival / drug effects. Drug Resistance, Neoplasm / genetics. Gene Expression Profiling. Liver Neoplasms / genetics. Liver Neoplasms / pathology
  • [MeSH-minor] Antigens, Neoplasm / genetics. Cell Line, Tumor. DNA Topoisomerases, Type II / genetics. DNA-Binding Proteins / genetics. Dose-Response Relationship, Drug. Gene Expression Regulation, Neoplastic / genetics. Humans. In Vitro Techniques. Membrane Transport Proteins / genetics. Oligonucleotide Array Sequence Analysis. Reverse Transcriptase Polymerase Chain Reaction. Superoxide Dismutase / genetics. Up-Regulation / genetics

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  • (PMID = 17523305.001).
  • [ISSN] 0172-6390
  • [Journal-full-title] Hepato-gastroenterology
  • [ISO-abbreviation] Hepatogastroenterology
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Greece
  • [Chemical-registry-number] 0 / Antigens, Neoplasm; 0 / Antineoplastic Agents; 0 / DNA-Binding Proteins; 0 / Membrane Transport Proteins; 97599-47-8 / peptide permease; EC 1.15.1.1 / Superoxide Dismutase; EC 5.99.1.3 / DNA Topoisomerases, Type II; EC 5.99.1.3 / DNA topoisomerase II alpha
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12. Procopio G, Verzoni E, Gevorgyan A, Mancin M, Pusceddu S, Catena L, Platania M, Guadalupi V, Martinetti A, Bajetta E: Safety and activity of sorafenib in different histotypes of advanced renal cell carcinoma. Oncology; 2007;73(3-4):204-9
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  • [Title] Safety and activity of sorafenib in different histotypes of advanced renal cell carcinoma.
  • BACKGROUND: The aim of our study was to evaluate the efficacy and safety in unresectable or advanced renal carcinoma treated with sorafenib, in a situation closely similar to the everyday medical practice.
  • They were either previously untreated or relapsed after one or more previous treatments with systemic therapy.
  • Most of them had clear cell renal carcinoma (RCC), but other histological types such as papillary, chromophobe, Bellini ducts, sarcomatoid and mixed forms were also represented.
  • Response was observed in the majority of patients with RCC, but also in some patients with non-clear cell RCC.
  • CONCLUSIONS: The results confirm previous ones reported in the literature concerning the efficacy and the safety of sorafenib as second-line treatment in patients with RCC.
  • In addition, they disclose the hypothesis that sorafenib could be effective also in patients who underwent multiple previous treatments and in those with histology different from clear cells.
  • [MeSH-major] Antineoplastic Agents / therapeutic use. Benzenesulfonates / therapeutic use. Carcinoma, Renal Cell / drug therapy. Kidney Neoplasms / drug therapy. Pyridines / therapeutic use
  • [MeSH-minor] Administration, Oral. Adult. Aged. Antineoplastic Combined Chemotherapy Protocols / adverse effects. Bone Neoplasms / drug therapy. Bone Neoplasms / secondary. Carcinoma, Papillary / drug therapy. Carcinoma, Papillary / secondary. Disease Progression. Drug Resistance, Neoplasm. Female. Humans. Liver Neoplasms / drug therapy. Liver Neoplasms / secondary. Lung Neoplasms / drug therapy. Lung Neoplasms / secondary. Male. Middle Aged. Neoplasm Staging. Niacinamide / analogs & derivatives. Phenylurea Compounds. Prognosis. Remission Induction. Salvage Therapy. Survival Rate

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  • [Copyright] (c) 2008 S. Karger AG, Basel
  • (PMID = 18418013.001).
  • [ISSN] 1423-0232
  • [Journal-full-title] Oncology
  • [ISO-abbreviation] Oncology
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Switzerland
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / Benzenesulfonates; 0 / Phenylurea Compounds; 0 / Pyridines; 25X51I8RD4 / Niacinamide; 9ZOQ3TZI87 / sorafenib
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13. Thompson JA, Kuzel T, Bukowski R, Masciari F, Schmalbach T: Phase Ib trial of a targeted TLR9 CpG immunomodulator (CPG 7909) in advanced renal cell carcinoma (RCC). J Clin Oncol; 2004 Jul 15;22(14_suppl):4644

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  • [Title] Phase Ib trial of a targeted TLR9 CpG immunomodulator (CPG 7909) in advanced renal cell carcinoma (RCC).
  • CPG 7909, one of a new class of oligodeoxynucleotide immunomodulators, binds Toll-like receptor 9 on dendritic cells, with induction of cytokines including IFNα, activation of NK cells, and modulation of a Th1 CTL environment.
  • Based upon the medical need and the novel mechanism of action, the current trial evaluates CPG 7909 in the treatment of metastatic RCC.
  • Patients had prior nephrectomy but no systemic therapy for clear-cell RCC, ECOG performance ≤1, with measurable soft tissue metastases (bone, liver, brain excluded).
  • The primary endpoint is safety, with secondary endpoints including pharmacokinetic and pharmacodynamic parameters, responses by RECIST, duration of response, time to progression, and survival.
  • Twenty-seven patients are off-study prior to, or at 24 weeks of treatment.
  • Four patients continue on therapy.
  • Median time to progression is 112 days.
  • No drug-related serious adverse events have been reported, with good tolerability up to 0.54 mg/kg.

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  • (PMID = 28015762.001).
  • [ISSN] 1527-7755
  • [Journal-full-title] Journal of clinical oncology : official journal of the American Society of Clinical Oncology
  • [ISO-abbreviation] J. Clin. Oncol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
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14. Yan J, Gong Y, Wang G, Gong Y, Burczynski FJ: Regulation of liver fatty acid binding protein expression by clofibrate in hepatoma cells. Biochem Cell Biol; 2010 Dec;88(6):957-67
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  • [Title] Regulation of liver fatty acid binding protein expression by clofibrate in hepatoma cells.
  • Peroxisome proliferator-activated receptor (PPAR) agonists such as clofibrate are known to affect liver fatty acid binding protein (L-FABP) levels, which in turn influence hepatocellular oxidant status.
  • The mechanism of clofibrate's modulation of L-FABP levels is not clear.
  • In this study we used clofibrate (PPARα agonist), MK886 (PPARα antagonist), and GW9662 (PPARγ antagonist) in determining the regulating mechanism of L-FABP expression and its antioxidant activity in CRL-1548 hepatoma cells.
  • RT-PCR and mRNA stability assay showed that clofibrate treatment enhanced L-FABP mRNA stability, which resulted in increased L-FABP levels.
  • A nuclear run-off assay and RT-PCR measurements of L-FABP mRNA revealed that clofibrate increased the L-FABP gene transcription rate.
  • Levels of superoxide dismutase, glutathione peroxidase, and catalase were not affected by clofibrate treatment.
  • [MeSH-minor] Anilides / pharmacology. Animals. Carcinoma, Hepatocellular / drug therapy. Carcinoma, Hepatocellular / enzymology. Catalase / analysis. Catalase / metabolism. Cell Line, Tumor. Fluoresceins / analysis. Gene Expression Regulation, Neoplastic / drug effects. Glutathione Peroxidase / analysis. Glutathione Peroxidase / metabolism. Hepatocytes / drug effects. Hepatocytes / enzymology. Humans. Hydrogen Peroxide / administration & dosage. Indoles / pharmacology. Liver Neoplasms / drug therapy. Liver Neoplasms / enzymology. Oxidative Stress. RNA Stability / drug effects. RNA, Messenger / metabolism. Rats. Superoxide Dismutase / analysis. Superoxide Dismutase / metabolism

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  • (PMID = 21102658.001).
  • [ISSN] 1208-6002
  • [Journal-full-title] Biochemistry and cell biology = Biochimie et biologie cellulaire
  • [ISO-abbreviation] Biochem. Cell Biol.
  • [Language] eng
  • [Grant] Canada / Canadian Institutes of Health Research / /
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Canada
  • [Chemical-registry-number] 0 / 2-chloro-5-nitrobenzanilide; 0 / Anilides; 0 / Fatty Acid-Binding Proteins; 0 / Fluoresceins; 0 / Indoles; 0 / PPAR alpha; 0 / RNA, Messenger; 118414-82-7 / L 663536; 76-54-0 / 2',7'-dichlorofluorescein; BBX060AN9V / Hydrogen Peroxide; EC 1.11.1.6 / Catalase; EC 1.11.1.9 / Glutathione Peroxidase; EC 1.15.1.1 / Superoxide Dismutase; HPN91K7FU3 / Clofibrate
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15. Sharma A, Upadhyay AK, Bhat MK: Inhibition of Hsp27 and Hsp40 potentiates 5-fluorouracil and carboplatin mediated cell killing in hepatoma cells. Cancer Biol Ther; 2009 Nov;8(22):2106-13
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  • [Title] Inhibition of Hsp27 and Hsp40 potentiates 5-fluorouracil and carboplatin mediated cell killing in hepatoma cells.
  • Heat shock proteins (Hsps) modulate several cellular functions and are ubiquitously present in cell.
  • Moreover, effect of quercetin (Qctn), an inhibitor of Hsps, on chemotherapeutic drugs treatment in hepatoma cells Hep3B and HepG2 was investigated.
  • We for the first time report that 5-fluorouracil (5-FU) and carboplatin specifically induce expression of Hsp40 in addition to Hsp27 in Hep3B and HepG2 cells.
  • Induction of Hsps following exposure to sub lethal dose of drugs is a cellular challenge to survival.
  • However, under lethal environmental conditions with reduced cell viability, cells fail to sustain the induction of survival proteins, Hsp27 and Hsp40.
  • Though Qctn itself, to certain extent is cytotoxic to cells, it potentiates the pro-apoptotic action of 5-FU and carboplatin, by inhibiting expression of Hsps.
  • The increased cell killing correlates with decreased levels of procaspase-3.
  • Furthermore, siRNA mediated knockdown of Hsp27 and Hsp40 diminishes survival of drugs exposed cells.
  • Altogether, our data provides clear evidence that Hsp27 and 40 promote cell survival and inhibition of their expression does not allow cells to adapt to drug exposure and survive.
  • Collectively, our novel findings on compelling action of 5-FU or carboplatin following knockdown of Hsp40 and that of Hsp27 highlights their strategic implications towards an effective therapy against HCC.
  • [MeSH-major] Antimetabolites, Antineoplastic / pharmacology. Antineoplastic Agents, Alkylating / pharmacology. Apoptosis / drug effects. Carboplatin / pharmacology. Carcinoma, Hepatocellular / pathology. Fluorouracil / pharmacology. HSP27 Heat-Shock Proteins / physiology. HSP40 Heat-Shock Proteins / physiology. Liver Neoplasms / pathology. Neoplasm Proteins / physiology. Quercetin / pharmacology
  • [MeSH-minor] Cell Line, Tumor / cytology. Cell Line, Tumor / drug effects. Drug Resistance, Neoplasm. Drug Synergism. Gene Expression Regulation, Neoplastic / drug effects. Humans. RNA Interference. RNA, Small Interfering / pharmacology. Transfection

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  • (PMID = 19901540.001).
  • [ISSN] 1555-8576
  • [Journal-full-title] Cancer biology & therapy
  • [ISO-abbreviation] Cancer Biol. Ther.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antimetabolites, Antineoplastic; 0 / Antineoplastic Agents, Alkylating; 0 / DNAJB1 protein, human; 0 / HSP27 Heat-Shock Proteins; 0 / HSP40 Heat-Shock Proteins; 0 / HSPB1 protein, human; 0 / Neoplasm Proteins; 0 / RNA, Small Interfering; 9IKM0I5T1E / Quercetin; BG3F62OND5 / Carboplatin; U3P01618RT / Fluorouracil
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16. Altomonte J, Marozin S, Schmid RM, Ebert O: Engineered newcastle disease virus as an improved oncolytic agent against hepatocellular carcinoma. Mol Ther; 2010 Feb;18(2):275-84
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  • [Title] Engineered newcastle disease virus as an improved oncolytic agent against hepatocellular carcinoma.
  • Several clinical trials have reported NDV to be a safe and effective agent for cancer therapy; however, there remains a clear need for improvement in therapeutic outcome.
  • The endogenous NDV fusion (F) protein directs membrane fusion, which is required for virus entry and cell-cell fusion.
  • Here, we report a novel NDV vector harboring an L289A mutation within the F gene, which resulted in enhanced fusion and cytotoxicity of hepatocellular carcinoma (HCC) cells in vitro, as compared with the rNDV/F3aa control virus.
  • In vivo administration of the recombinant vector, termed rNDV/F3aa(L289A), via hepatic arterial infusion in immune-competent Buffalo rats bearing multifocal, orthotopic liver tumors resulted in tumor-specific syncytia formation and necrosis, with no evidence of toxicity to the neighboring hepatic parenchyma.
  • Taken together, rNDV/F(L289A) represents a safe, yet more effective vector than wild-type NDV for the treatment of HCC, making it an ideal candidate for clinical application in HCC patients.
  • [MeSH-major] Carcinoma, Hepatocellular / therapy. Liver Neoplasms / therapy. Newcastle disease virus / physiology. Oncolytic Virotherapy / methods
  • [MeSH-minor] Animals. Cell Line. Cell Line, Tumor. Chickens. Genetic Vectors / drug effects. Genetic Vectors / genetics. Genetic Vectors / physiology. Humans. Interferon Type I / pharmacology. Male. Rats

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  • (PMID = 19809404.001).
  • [ISSN] 1525-0024
  • [Journal-full-title] Molecular therapy : the journal of the American Society of Gene Therapy
  • [ISO-abbreviation] Mol. Ther.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Interferon Type I
  • [Other-IDs] NLM/ PMC2839313
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17. Qin X, Liu C, Zhou Y, Wang G: Cisplatin induces programmed death-1-ligand 1(PD-L1) over-expression in hepatoma H22 cells via Erk /MAPK signaling pathway. Cell Mol Biol (Noisy-le-grand); 2010;56 Suppl:OL1366-72
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  • [Title] Cisplatin induces programmed death-1-ligand 1(PD-L1) over-expression in hepatoma H22 cells via Erk /MAPK signaling pathway.
  • Cisplatin has been widely used in cancer treatment.
  • However, the prognosis of the cancer patients following chemotherapy has not been substantially improved and several different mechanisms could be involved.
  • Clinically alternative strategies such as immunotherapy and their combinations with chemotherapy have being used.
  • Cancer immunoresistance and immune escape are major obstacles in chemotherapy.
  • However, the effects of cisplatin on the immune responses of cancer cells are not clear.
  • In the present studies, we investigate the expression of immunoresistance moleculor PD-L1 (the negative regulator programmed death-1-ligand 1) on cisplatin-induced hepatoma H22 cells, which can interact with PD-1 on T cells to mediate cancer immunoresistance.
  • Hepatoma H22 cells were treated with cisplatin in vivo or in vitro to analysis the expression of PD-L1 by flow cytometry (FACS).
  • We demonstrated that cisplatin was able to induce H22 cell apoptosis and when the concentration less than IC50 cisplatin could up-regulate PD-L1 expression in hepatoma H22 cells.
  • Meanwhile, cisplatin could induce the phosphorylation of Erk1/2.The lack of effect during treatment with a specific MAPK pathway inhibitor PD98059, demonstrated that cisplatin-induced PD-L1 expression is dependent of Erk1/2 phosphorylation.
  • Our studies reveal a potential link between chemotherapy and cancer immunoresistance.
  • PD-L1 and its signaling pathway appear to be a potential therapeutic target for the cisplatin treatment of hepatoma.
  • [MeSH-minor] Animals. Antigens, CD274. Apoptosis. Carcinoma, Hepatocellular / metabolism. Cell Line, Tumor. Flavonoids / pharmacology. Liver Neoplasms / metabolism. Mice. Phosphorylation. Signal Transduction

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  • (PMID = 20937224.001).
  • [ISSN] 1165-158X
  • [Journal-full-title] Cellular and molecular biology (Noisy-le-Grand, France)
  • [ISO-abbreviation] Cell. Mol. Biol. (Noisy-le-grand)
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] France
  • [Chemical-registry-number] 0 / 2-(2-amino-3-methoxyphenyl)-4H-1-benzopyran-4-one; 0 / Antigens, CD274; 0 / Antigens, CD80; 0 / Antineoplastic Agents; 0 / Cd274 protein, mouse; 0 / Flavonoids; 0 / Membrane Glycoproteins; 0 / Peptides; EC 2.7.11.24 / Extracellular Signal-Regulated MAP Kinases; EC 2.7.11.24 / Mitogen-Activated Protein Kinase 1; EC 2.7.11.24 / Mitogen-Activated Protein Kinase 3; Q20Q21Q62J / Cisplatin
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18. Dokmak S, Cabral C, Couvelard A, Aussilhou B, Belghiti J, Sauvanet A: Pancreatic metastasis from nephroblastoma: an unusual entity. JOP; 2009;10(4):396-9
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  • CONTEXT: Pancreatic metastasis from renal cell carcinoma is a well-known entity.
  • When metastatic disease is limited to the pancreas, pancreatic resection is the optimal treatment.
  • A metastatic nephroblastoma mainly affects the lung and the liver.
  • CASE REPORT: We report an extremely rare case of pancreatic metastases in a 20-year-old man who had a right nephroblastoma resected at 9 years of age and liver metastases treated by right hepatectomy at 18 years of age.
  • Imaging studies revealed no other localization except a 1.5 cm liver nodule.
  • Surgical resection was performed without preoperative chemotherapy because the patient was symptomatic and had already received numerous chemotherapy protocols.
  • The patient underwent pancreaticoduodenectomy and limited liver resection with an uneventful postoperative course.
  • Pathological examination confirmed pancreatic and liver metastases from a nephroblastoma composed of blastematous cells mixed with embryonic tubular structures without lymph node metastases.
  • After resection, the patient received adjuvant high dose chemotherapy with autologous hematopoietic stem-cell support.
  • After a 21-month follow-up, the patient was in good general condition but had liver recurrence without intra-pancreatic recurrence.
  • A nephroblastoma, like clear cell renal carcinoma, can be considered a possible etiology of pancreatic metastasis from a primary renal tumor.
  • [MeSH-minor] Combined Modality Therapy. Drug Therapy / methods. Humans. Male. Pancreaticoduodenectomy / methods. Treatment Outcome. Young Adult

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  • (PMID = 19581742.001).
  • [ISSN] 1590-8577
  • [Journal-full-title] JOP : Journal of the pancreas
  • [ISO-abbreviation] JOP
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] Italy
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19. Lin HL, Liu TY, Chau GY, Lui WY, Chi CW: Comparison of 2-methoxyestradiol-induced, docetaxel-induced, and paclitaxel-induced apoptosis in hepatoma cells and its correlation with reactive oxygen species. Cancer; 2000 Sep 1;89(5):983-94
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  • [Title] Comparison of 2-methoxyestradiol-induced, docetaxel-induced, and paclitaxel-induced apoptosis in hepatoma cells and its correlation with reactive oxygen species.
  • BACKGROUND: Previously, the authors observed that paclitaxel treatment of hepatoma cells resulted in differential cytotoxicity.
  • Whether other antimicrotubule agents (docetaxel and 2-methoxyestradiol) are more effective than paclitaxel is not clear.
  • Moreover, whether the modulation of reactive oxygen species (ROS) is involved in the drug-induced growth inhibition of hepatoma cells is not known.
  • METHODS: The authors examined the effects of 2-methoxyestradiol, paclitaxel, and docetaxel on HepG2, Hep3B, HA22T/VGH, and Hepa1-6 hepatoma cell lines.
  • The parameters examined included cell viability, cell membrane permeability, cell cycle distribution, DNA fragmentation, and ROS generation.
  • RESULTS: Docetaxel and paclitaxel inhibited the growth of hepatoma cells at submicromolar concentrations, whereas that of 2-methoxyestradiol was within a micromolar range.
  • This drug-induced growth inhibition was cell cycle dependent.
  • 2-Methoxyestradiol-treated (10-50 microM) cells resulted in G2/M block prior to apoptosis.
  • High dose (0.1 microM) docetaxel- and paclitaxel-treated cells resulted in a G2/M arrest followed by generation of polyploidy or apoptosis; however, low dose (0.01 microM) treatment induced apoptosis without G2/M arrest.
  • The low dose effect was more significant in docetaxel-treated cells than in paclitaxel-treated cells.
  • Although these antimicrotubule agents increased the formation of ROS, antioxidant treatment did not block drug-induced cell cycle and growth inhibition effects.
  • CONCLUSIONS: The current results suggest that the growth inhibition of hepatoma cells induced by 2-methoxyestradiol, paclitaxel, and docetaxel was mediated through G2/M-phase arrest, caspase activation, and DNA fragmentation.
  • The drug-induced apoptosis was independent of ROS formation.
  • Docetaxel was more effective than paclitaxel in killing hepatoma cells.
  • The potential of using 2-methoxyestradiol and docetaxel for the treatment of patients with hepatoma is worthy of further study.
  • [MeSH-major] Apoptosis. Carcinoma, Hepatocellular / drug therapy. Estradiol / analogs & derivatives. Estradiol / pharmacology. Liver Neoplasms / drug therapy. Paclitaxel / analogs & derivatives. Paclitaxel / pharmacology. Reactive Oxygen Species / metabolism. Taxoids
  • [MeSH-minor] Antineoplastic Agents, Phytogenic / pharmacology. Cell Cycle / drug effects. Cell Survival / drug effects. DNA Fragmentation. Flow Cytometry. Humans. Microtubules / drug effects. Tumor Cells, Cultured

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  • (PMID = 10964328.001).
  • [ISSN] 0008-543X
  • [Journal-full-title] Cancer
  • [ISO-abbreviation] Cancer
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] UNITED STATES
  • [Chemical-registry-number] 0 / Antineoplastic Agents, Phytogenic; 0 / Reactive Oxygen Species; 0 / Taxoids; 15H5577CQD / docetaxel; 4TI98Z838E / Estradiol; 6I2QW73SR5 / 2-methoxyestradiol; P88XT4IS4D / Paclitaxel
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20. Basile J, Caldwell S, Nolan N, Hammerle C: Clear cell hepatocellular carcinoma arising 25 years after the successful treatment of an infantile hepatoblastoma. Ann Hepatol; 2010 Oct-Dec;9(4):465-7
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  • [Title] Clear cell hepatocellular carcinoma arising 25 years after the successful treatment of an infantile hepatoblastoma.
  • Primary liver tumors in children are rare with hepatoblastoma (HB) being the most common malignancy.
  • Clear cell carcinoma, a variant of hepatocellular carcinoma (HCC), is another rare tumor of the liver that tends to affect adults.
  • We describe the diagnosis and management of the only known documented case of a primary clear cell HCC arising twenty-five years after the patient was successfully treated with chemotherapy and surgical resection for a malignant HB as an infant.
  • While some evidence has shown a genetic link between HB and various types of HCC, other research has shown distinct chromosomal alterations and molecular mechanisms unique to both.
  • Further knowledge of liver tumorigenesis will help elucidate the complicated genetic, molecular, and environmental factors involved in the development of these two rare hepatic malignancies.
  • [MeSH-major] Carcinoma, Hepatocellular / diagnosis. Hepatoblastoma / drug therapy. Hepatoblastoma / surgery. Liver Neoplasms / diagnosis
  • [MeSH-minor] Adult. Biopsy. Combined Modality Therapy. Genetic Predisposition to Disease / genetics. Humans. Magnetic Resonance Imaging. Male. Time Factors. Treatment Outcome

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  • (PMID = 21057168.001).
  • [ISSN] 1665-2681
  • [Journal-full-title] Annals of hepatology
  • [ISO-abbreviation] Ann Hepatol
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] Mexico
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21. Gao Y, Lin LP, Zhu CH, Chen Y, Hou YT, Ding J: Growth arrest induced by C75, A fatty acid synthase inhibitor, was partially modulated by p38 MAPK but not by p53 in human hepatocellular carcinoma. Cancer Biol Ther; 2006 Aug;5(8):978-85
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  • [Title] Growth arrest induced by C75, A fatty acid synthase inhibitor, was partially modulated by p38 MAPK but not by p53 in human hepatocellular carcinoma.
  • In this study, we reveal that C75 is a cell cycle arrest inducer and explore the potential mechanisms for this effect in hepatocellular carcinoma (HCC) cell lines with abundant FAS expression: HepG2 and SMMC7721 cells with wt-p53, and Hep3B cells with null p53.
  • The results showed FAS protein expression and basal activity levels were higher in HepG2 cells than in the other two HCC cell lines.
  • Treatment with C75 inhibited FAS activity within 30 min of administration and induced G(2) phase arrest accompanied by p53 overexpression in HepG2 and SMMC7721 cells.
  • By contrast, C75 triggered G(1) phase arrest in Hep3B cells, and RNA interference targeting p53 did not attenuate C75-induced G(2) arrest in HepG2 cells.
  • Similarly, p53 overexpression via p53 plasmid transfection did not affect C75-induced G(1) phase arrest in Hep3B cells.
  • However, we observed a clear correlation between p38 MAPK activation triggered by C75 and the induction of cell cycle arrest in all three HCC cells.
  • Furthermore, treatment with the p38 MAPK inhibitor SB203580 reduced p38 MAPK activity and cell cycle arrest, and also partially restored cyclin A, cyclin B1, cyclin D1 and p21 protein levels.
  • Collectively, it was p38 MAPK but not p53 involved in C75-mediated tumor cell growth arrest in HCC cells.
  • [MeSH-major] 4-Butyrolactone / analogs & derivatives. Carcinoma, Hepatocellular / metabolism. Fatty Acid Synthases / antagonists & inhibitors. G2 Phase / drug effects. Liver Neoplasms / metabolism. Tumor Suppressor Protein p53 / metabolism. p38 Mitogen-Activated Protein Kinases / metabolism
  • [MeSH-minor] Antigens, CD95 / metabolism. Blotting, Western. Cell Proliferation. Cyclin A / metabolism. Cyclin B / metabolism. Cyclin B1. Cyclin D1 / metabolism. Cyclin-Dependent Kinase Inhibitor p21 / metabolism. Flow Cytometry. Humans. Immunoprecipitation. Plasmids / genetics. RNA, Small Interfering / pharmacology. Tumor Cells, Cultured

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  • [CommentIn] Cancer Biol Ther. 2006 Aug;5(8):986-7 [16998303.001]
  • (PMID = 16855382.001).
  • [ISSN] 1538-4047
  • [Journal-full-title] Cancer biology & therapy
  • [ISO-abbreviation] Cancer Biol. Ther.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / 4-methylene-2-octyl-5-oxofuran-3-carboxylic acid; 0 / Antigens, CD95; 0 / CCNB1 protein, human; 0 / Cyclin A; 0 / Cyclin B; 0 / Cyclin B1; 0 / Cyclin-Dependent Kinase Inhibitor p21; 0 / RNA, Small Interfering; 0 / Tumor Suppressor Protein p53; 136601-57-5 / Cyclin D1; EC 2.3.1.85 / Fatty Acid Synthases; EC 2.7.11.24 / p38 Mitogen-Activated Protein Kinases; OL659KIY4X / 4-Butyrolactone
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22. Koizumi N, Hatano E, Nitta T, Tada M, Harada N, Taura K, Ikai I, Shimahara Y: Blocking of PI3K/Akt pathway enhances apoptosis induced by SN-38, an active form of CPT-11, in human hepatoma cells. Int J Oncol; 2005 May;26(5):1301-6
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  • [Title] Blocking of PI3K/Akt pathway enhances apoptosis induced by SN-38, an active form of CPT-11, in human hepatoma cells.
  • Hepatocellular carcinoma (HCC) is a common malignancy and often resistant to chemotherapy.
  • Many chemotherapy regimens have been tried to control advanced HCC, but have produced a low response rate and no clear impact.
  • CPT-11, a derivative of camptothecin, works as type-I DNA topoisomerase inhibitor and showed a major objective response rate in patients with metastatic colorectal cancer.
  • Hep3B was the most resistant to SN-38 among three hepatoma cell lines.
  • [MeSH-major] Antineoplastic Agents, Phytogenic / pharmacology. Apoptosis. Camptothecin / analogs & derivatives. Camptothecin / pharmacology. Carcinoma, Hepatocellular / pathology. Liver Neoplasms / pathology. Phosphatidylinositol 3-Kinases / metabolism. Protein-Serine-Threonine Kinases / metabolism. Proto-Oncogene Proteins / metabolism
  • [MeSH-minor] Drug Resistance, Neoplasm. Humans. NF-kappa B / metabolism. Proto-Oncogene Proteins c-akt. Tumor Cells, Cultured

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  • (PMID = 15809721.001).
  • [ISSN] 1019-6439
  • [Journal-full-title] International journal of oncology
  • [ISO-abbreviation] Int. J. Oncol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Greece
  • [Chemical-registry-number] 0 / Antineoplastic Agents, Phytogenic; 0 / NF-kappa B; 0 / Proto-Oncogene Proteins; 7673326042 / irinotecan; EC 2.7.1.- / Phosphatidylinositol 3-Kinases; EC 2.7.11.1 / AKT1 protein, human; EC 2.7.11.1 / Protein-Serine-Threonine Kinases; EC 2.7.11.1 / Proto-Oncogene Proteins c-akt; XT3Z54Z28A / Camptothecin
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23. Durantel D, Carrouée-Durantel S, Branza-Nichita N, Dwek RA, Zitzmann N: Effects of interferon, ribavirin, and iminosugar derivatives on cells persistently infected with noncytopathic bovine viral diarrhea virus. Antimicrob Agents Chemother; 2004 Feb;48(2):497-504
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  • [Title] Effects of interferon, ribavirin, and iminosugar derivatives on cells persistently infected with noncytopathic bovine viral diarrhea virus.
  • In chronic carriers, the viral infection induces liver damage that predisposes the patient for cirrhosis and can lead to hepatocellular carcinoma.
  • In addition to its limited efficacy, this treatment is frequently poorly tolerated because of its side effects.
  • The urgently needed development of new drugs is made difficult by the lack of an in vitro or in vivo infectivity model, and no cell line has been found so far to reliably and reproducibly support HCV infection.
  • In this study we used an MDBK cell line persistently infected with noncytopathic BVDV to assess the antiviral effect of IFN-alpha and RBV, the two drugs currently in clinical use against HCV.
  • The same system was then used to evaluate the potential of two classes of iminosugar derivates to clear noncytopathic BVDV infection from MDBK cells.
  • We show that treatment with long-alkyl-chain deoxynojirimycin derivatives, which are inhibitors of the endoplasmic reticulum (ER)-resident alpha-glucosidases, can greatly reduce the amount of secreted enveloped viral RNA.
  • [MeSH-major] Antiviral Agents / pharmacology. Bovine Virus Diarrhea-Mucosal Disease / drug therapy. Bovine Virus Diarrhea-Mucosal Disease / virology. Diarrhea Viruses, Bovine Viral / drug effects. Diarrhea Viruses, Bovine Viral / pathogenicity. Interferon Type I / pharmacology. Ribavirin / pharmacology
  • [MeSH-minor] Animals. Cattle. Cell Line. Cytopathogenic Effect, Viral / drug effects. Fluorescent Antibody Technique. Imino Acids / chemistry. RNA, Viral / biosynthesis. RNA, Viral / genetics. Recombinant Proteins. Reverse Transcriptase Polymerase Chain Reaction. Viral Plaque Assay. Virus Replication / drug effects

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  • (PMID = 14742201.001).
  • [ISSN] 0066-4804
  • [Journal-full-title] Antimicrobial agents and chemotherapy
  • [ISO-abbreviation] Antimicrob. Agents Chemother.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antiviral Agents; 0 / Imino Acids; 0 / Interferon Type I; 0 / RNA, Viral; 0 / Recombinant Proteins; 49717AWG6K / Ribavirin
  • [Other-IDs] NLM/ PMC321564
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24. Yang JC, Hughes M, Kammula U, Royal R, Sherry RM, Topalian SL, Suri KB, Levy C, Allen T, Mavroukakis S, Lowy I, White DE, Rosenberg SA: Ipilimumab (anti-CTLA4 antibody) causes regression of metastatic renal cell cancer associated with enteritis and hypophysitis. J Immunother; 2007 Nov-Dec;30(8):825-30
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  • [Title] Ipilimumab (anti-CTLA4 antibody) causes regression of metastatic renal cell cancer associated with enteritis and hypophysitis.
  • The inhibitory receptor CTLA4 has a key role in peripheral tolerance of T cells for both normal and tumor-associated antigens.
  • Therefore, a phase II study of ipilimumab was conducted in patients with metastatic renal cell cancer with a primary end point of response by Response Evaluation Criteria in Solid Tumors (RECIST) criteria.
  • CTLA4 blockade with ipilimumab induces cancer regression in some patients with metastatic clear cell renal cancer, even if they have not responded to other immunotherapies.
  • [MeSH-major] Antibodies, Monoclonal / therapeutic use. Carcinoma, Renal Cell / drug therapy. Enteritis / chemically induced. Kidney Neoplasms / drug therapy. Pituitary Diseases / chemically induced
  • [MeSH-minor] Adrenal Insufficiency / chemically induced. Adult. Aged. Antineoplastic Agents / administration & dosage. Antineoplastic Agents / adverse effects. Antineoplastic Agents / therapeutic use. Bone Neoplasms / drug therapy. Bone Neoplasms / immunology. Bone Neoplasms / secondary. Colitis / chemically induced. Duodenitis / chemically induced. Female. Humans. Hypopituitarism / chemically induced. Liver Neoplasms / drug therapy. Liver Neoplasms / immunology. Liver Neoplasms / secondary. Lung Neoplasms / drug therapy. Lung Neoplasms / immunology. Lung Neoplasms / secondary. Male. Meningitis, Aseptic / chemically induced. Middle Aged. Treatment Outcome

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  • (PMID = 18049334.001).
  • [ISSN] 1524-9557
  • [Journal-full-title] Journal of immunotherapy (Hagerstown, Md. : 1997)
  • [ISO-abbreviation] J. Immunother.
  • [Language] eng
  • [Grant] United States / Intramural NIH HHS / / Z01 SC003811-32
  • [Publication-type] Clinical Trial, Phase II; Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antibodies, Monoclonal; 0 / Antineoplastic Agents; 0 / ipilimumab
  • [Other-IDs] NLM/ NIHMS35214; NLM/ PMC2134980
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25. Torresi J, Bharadwaj M, Jackson DC, Gowans EJ: Neutralising antibody, CTL and dendritic cell responses to hepatitis C virus: a preventative vaccine strategy. Curr Drug Targets; 2004 Jan;5(1):41-56
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Neutralising antibody, CTL and dendritic cell responses to hepatitis C virus: a preventative vaccine strategy.
  • Hepatitis C virus (HCV) accounts for the majority of cases of transfusion acquired hepatitis and hepatitis transmitted by injecting drug use.
  • The patients who do not clear the infection become chronic carriers of HCV and form a reservoir of infection within human populations.
  • Furthermore, these carriers are at serious risk of developing cirrhosis of the liver and hepatocellular carcinoma.
  • The disease is of major concern in developing as well as in developed countries and yet there are no vaccines against HCV, treatment is confined to the use of chemotherapy which is expensive and not always effective.
  • The major obstacle in vaccine development is a limited understanding of the type of immune response that is necessary for viral clearance and the occurrence of various genotypes and quasispecies of HCV.
  • [MeSH-major] Dendritic Cells / immunology. Hepacivirus / immunology. Hepatitis C Antibodies / immunology. Hepatitis C, Chronic / prevention & control. T-Lymphocytes, Cytotoxic / immunology. Viral Hepatitis Vaccines / immunology

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  • (PMID = 14738217.001).
  • [ISSN] 1389-4501
  • [Journal-full-title] Current drug targets
  • [ISO-abbreviation] Curr Drug Targets
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] Netherlands
  • [Chemical-registry-number] 0 / Hepatitis C Antibodies; 0 / Viral Hepatitis Vaccines
  • [Number-of-references] 168
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26. Frese M, Schwärzle V, Barth K, Krieger N, Lohmann V, Mihm S, Haller O, Bartenschlager R: Interferon-gamma inhibits replication of subgenomic and genomic hepatitis C virus RNAs. Hepatology; 2002 Mar;35(3):694-703
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  • Persistent infection with hepatitis C virus (HCV) is a major cause of chronic hepatitis, liver cirrhosis, and hepatocellular carcinoma.
  • All treatments known so far rely on the antiviral activity of interferon alfa (IFN-alpha) that is given alone or in combination with ribavirin.
  • Unfortunately, only a fraction of the patients clear the virus during therapy and for those who do not respond there is currently no alternative treatment.
  • In conclusion, our results suggest that cytotoxic T cells and natural killer cells may contribute to HCV clearance not only by cell killing but also by producing IFN-gamma, thereby enhancing the intracellular inhibition of viral replication.
  • [MeSH-major] Hepacivirus / drug effects. Interferon-gamma / pharmacology. RNA, Viral / biosynthesis. Virus Replication / drug effects
  • [MeSH-minor] Humans. Interferon Type I / biosynthesis. Nitric Oxide / biosynthesis. Nitric Oxide Synthase / physiology. Nitric Oxide Synthase Type II. Replicon / drug effects. Tryptophan / metabolism. Tumor Cells, Cultured. Viral Nonstructural Proteins / metabolism

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  • (PMID = 11870386.001).
  • [ISSN] 0270-9139
  • [Journal-full-title] Hepatology (Baltimore, Md.)
  • [ISO-abbreviation] Hepatology
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Interferon Type I; 0 / NS-5 protein, hepatitis C virus; 0 / NS3 protein, hepatitis C virus; 0 / RNA, Viral; 0 / Viral Nonstructural Proteins; 31C4KY9ESH / Nitric Oxide; 82115-62-6 / Interferon-gamma; 8DUH1N11BX / Tryptophan; EC 1.14.13.39 / NOS2 protein, human; EC 1.14.13.39 / Nitric Oxide Synthase; EC 1.14.13.39 / Nitric Oxide Synthase Type II
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27. Selvendiran K, Koga H, Ueno T, Yoshida T, Maeyama M, Torimura T, Yano H, Kojiro M, Sata M: Luteolin promotes degradation in signal transducer and activator of transcription 3 in human hepatoma cells: an implication for the antitumor potential of flavonoids. Cancer Res; 2006 May 1;66(9):4826-34
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  • [Title] Luteolin promotes degradation in signal transducer and activator of transcription 3 in human hepatoma cells: an implication for the antitumor potential of flavonoids.
  • In this study, we have investigated the underlying molecular mechanism for the potent proapoptotic effect of luteolin on human hepatoma cells both in vitro and in vivo, focusing on the signal transducer and activator of transcription 3 (STAT3)/Fas signaling.
  • A clear apoptosis was found in the luteolin-treated HLF hepatoma cells in a time- and dosage-dependent manner.
  • Consistent with the increased Fas/CD95 expression, a drastic decrease in the Tyr(705) phosphorylation of STAT3, a known negative regulator of Fas/CD95 transcription, was found within 20 minutes in the luteolin-treated cells, leading to down-regulation in the target gene products of STAT3, such as cyclin D1, survivin, Bcl-xL, and vascular endothelial growth factor.
  • The expression level of Ser(727)-phosphorylated STAT3 was gradually decreased by the luteolin treatment, followed by a fast and clear down-regulation in the active forms of CDK5, which can phosphorylate STAT3 at Ser(727).
  • In nude mice with xenografted tumors using HAK-1B hepatoma cells, luteolin significantly inhibited the growth of the tumors in a dosage-dependent manner.
  • [MeSH-major] Carcinoma, Hepatocellular / drug therapy. Liver Neoplasms / drug therapy. Luteolin / pharmacology. STAT3 Transcription Factor / metabolism
  • [MeSH-minor] Animals. Antigens, CD95 / biosynthesis. Antineoplastic Agents / pharmacology. Apoptosis / drug effects. Apoptosis / physiology. Cell Growth Processes / drug effects. Cell Line, Tumor. Down-Regulation. Humans. Male. Mice. Mice, Inbred BALB C. Mice, Nude. Phosphorylation / drug effects. Receptors, Tumor Necrosis Factor, Type I / biosynthesis. Ubiquitin / metabolism. Xenograft Model Antitumor Assays


28. Krotkiewski M, Przybyszewska M, Janik P: Cytostatic and cytotoxic effects of alkylglycerols (Ecomer). Med Sci Monit; 2003 Nov;9(11):PI131-5
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  • BACKGROUND: Shark liver oil, with a standardized concentration of alkylglycerols and their methoxyderivates, has been widely used in Scandinavian countries as complementary medicine in the treatment of different forms of cancer.
  • The aim of our study was to verify the hypothesized antiproliferative effect of alkylglycerols in different human cancer cell lines.
  • MATERIAL/METHODS: The plating efficiency method was used to assay the effect of alkylglycerols on the plating efficiency of human ovarian carcinoma (OVP-10), mammary carcinoma (MCF-7), and prostate cancer (DU-145, PC-3 and PCa-2b) cell lines.
  • Tumor colonies containing more than 20 cells were scored as positive.
  • Flow cytometry was applied to identify necrotic vs. apoptotic mode of cell death.
  • The cells were exposed to Ecomer shark liver oil containing 20% alkylglycerols and 3% methoxyderivates in a dose of 0.1 mg/ml, up to a concentration corresponding to LD-50.
  • Apoptotic and necrotic cells were stained with Anexin V and propidium iodine respectively.
  • RESULTS: The prostate cells from DU-145, PC-3 and PCa-2B showed a dramatic reduction in the colony number even after relatively small doses of 0.5 and 0.1 mg/ml medium.
  • Flow cytomery showed an increased percentage of apoptotic cells of ovarian and prostate carcinoma, while mammary carcinoma cells showed predominantly necrotic cells after exposure to Ecomer.
  • CONCLUSIONS: The alkylglycerols and their methoxyderivates present in Ecomer shark liver oil showed a clear apoptotic/necrotic effect on human prostate and mammary carcinoma cell lines.
  • [MeSH-major] Alkanes / chemistry. Alkanes / therapeutic use. Glycerol / chemistry. Glycerol / therapeutic use
  • [MeSH-minor] Annexin A5 / pharmacology. Apoptosis. Breast Neoplasms / drug therapy. Cell Division / drug effects. Cell Line, Tumor. Coloring Agents / pharmacology. Female. Humans. Male. Necrosis. Propidium / pharmacology. Prostatic Neoplasms / drug therapy

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  • (PMID = 14586289.001).
  • [ISSN] 1234-1010
  • [Journal-full-title] Medical science monitor : international medical journal of experimental and clinical research
  • [ISO-abbreviation] Med. Sci. Monit.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Poland
  • [Chemical-registry-number] 0 / Alkanes; 0 / Annexin A5; 0 / Coloring Agents; 36015-30-2 / Propidium; PDC6A3C0OX / Glycerol
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29. [Tuberculosis in compromised hosts]. Kekkaku; 2003 Nov;78(11):717-22
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  • Many new findings and useful reports for practical medical treatment are submitted; why these compromised hosts are predisposed to tuberculosis, tuberculosis diagnostic and remedial notes of those compromised hosts etc.
  • It is reported that serum level of these cytokines and their production by peripheral blood mononuclear cells (PBMC) are reduced in tuberculosis patients with DM, and this is supposed to be involved in the high incidence of tuberculosis in DM.
  • In 1980, Saiki and co-workers reported that host defense and delayed-type hypersensitivity response to M. tuberculosis was hampered in a mouse DM model established by injecting streptozotocin (Infect Immun.
  • Interestingly, levels of IFN-gamma and IL-12 in serum, lung, liver and spleen after infection were significantly reduced in DM mice when compared with those in control mice.
  • Thus, it is not likely that the increased level of glucose directly suppresses the cell-mediated immune responses.
  • Further investigations are needed to make these points clear.
  • Gastrectomy was done due to carcinoma of the stomach in 31 cases, gastric and/or duodenal ulcer in 21 cases, adenomatous polyp in two cases, and accidental injury in one case.
  • No one had recurrence of carcinoma of the stomach.
  • I calculated the odds of tuberculosis among gastrectomy patients to be 3.8 times that of appropriate controls.
  • The cell immunity has decreased, and tuberculosis attacks.
  • Due to the decrease in the cell immunity, cavities are not formed easily.
  • It is easy to stay in the leaching lesion so that anti-tuberculosis drugs are much effective, and the patients recover easily.
  • However, if the treatment is delayed, it is fatally because hematogenous metastasis are easy to occur and become miliary tuberculosis.
  • With AIDS patients with tuberculosis, there are the following problems on the treatment. (1) The adverse reactions by antituberculosis drugs tend to occur in AIDS patients.
  • Eleven of 33 AIDS patients with tuberculosis had the adverse reactions (skin rash, fever, liver dysfunction) considered to be due to antituberculosis drugs.
  • It is a very large burden for the HIV infected persons to take simultaneously antituberculosis drugs, medicines for opportunistic infections, and anti-HIV medicines.
  • Since many medicines are taken, it is difficult to determine which drug is the cause once an adverse reaction occurs and all medicines should be often stopped. (2) The combined use with rifampicin (RFP) is difficult for the protease inhibitors and nonnuclear acid reverse transcriptase inhibitors.
  • RFP induces cytochrome P-450 in liver, accelerates the metabolism of some concomitant drug agents, and reduces blood concentration them remarkably.
  • When starting the two above-mentioned medicines during tuberculosis treatment, RFP should be changed to rifabutin (RFB) which has less induction of P-450 than RFP.
  • So, the treatment with EFV and RFP is recently chosen.
  • However, the monitor of the blood concentration of EFV is required, and the dose of EFV should be increased if it is a low value. (3) When a highly active antiretroviral therapy (HAART) is given to AIDS patients with tuberculosis, transient worsening of tuberculosis may develop after about two weeks. (ABSTRACT TRUNCATED)

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  • (PMID = 14672050.001).
  • [ISSN] 0022-9776
  • [Journal-full-title] Kekkaku : [Tuberculosis]
  • [ISO-abbreviation] Kekkaku
  • [Language] jpn
  • [Publication-type] English Abstract; Journal Article
  • [Publication-country] Japan
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30. Jung KH, Lee KH, Paik JY, Ko BH, Bae JS, Lee BC, Sung HJ, Kim DH, Choe YS, Chi DY: Favorable biokinetic and tumor-targeting properties of 99mTc-labeled glucosamino RGD and effect of paclitaxel therapy. J Nucl Med; 2006 Dec;47(12):2000-7
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  • [Title] Favorable biokinetic and tumor-targeting properties of 99mTc-labeled glucosamino RGD and effect of paclitaxel therapy.
  • Cell-binding characteristics were tested on human endothelial cells.
  • Mice bearing RR1022 fibrosarcoma and Lewis lung carcinoma (LLC) tumors were used for in vivo biodistribution and blocking experiments and for imaging studies.
  • Separate LLC-bearing mice underwent antiangiogenic therapy with 0, 20, or 40 mg of paclitaxel per kilogram of body weight every 2 d.
  • RESULTS: Glucosamino (99m)Tc-d-c(RGDfK) binding to endothelial cells was dose-dependently inhibited by excess RGD.
  • Biodistribution in mice showed rapid blood clearance of glucosamino (99m)Tc-d-c(RGDfK), with substantially lower liver uptake and higher tumor uptake compared with (125)I-c(RGD(I)yV).
  • Excess RGD blocked uptake by 76.5% and 70.2% for the respective tumors. gamma-Camera imaging allowed clear tumor visualization, with an increase of sarcoma-to-thigh count ratios from 5.5 +/- 0.7 at 1 h to 10.1 +/- 2.2 at 4 h and sustained carcinoma-to-thigh count ratios from 4 to 17 h.
  • Paclitaxel therapy in LLC tumor-bearing mice significantly retarded tumor growth.
  • CONCLUSION: Glucosamino (99m)Tc-d-c(RGDfK) has favorable in vivo biokinetics and tumor-imaging properties and may be useful for noninvasive evaluation of tumor integrin expression and response to antiangiogenic therapeutics.
  • [MeSH-minor] Animals. Antineoplastic Agents, Phytogenic / administration & dosage. Cell Line, Tumor. Cell Proliferation / drug effects. Drug Delivery Systems / methods. Humans. Kinetics. Male. Metabolic Clearance Rate / drug effects. Mice. Mice, Inbred BALB C. Mice, Nude. Organ Specificity / drug effects. Radiopharmaceuticals / pharmacokinetics. Rats. Tissue Distribution / drug effects. Treatment Outcome

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  • (PMID = 17138743.001).
  • [ISSN] 0161-5505
  • [Journal-full-title] Journal of nuclear medicine : official publication, Society of Nuclear Medicine
  • [ISO-abbreviation] J. Nucl. Med.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antineoplastic Agents, Phytogenic; 0 / Oligopeptides; 0 / Radiopharmaceuticals; 7440-26-8 / Technetium; 99896-85-2 / arginyl-glycyl-aspartic acid; P88XT4IS4D / Paclitaxel
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31. Chen Y, Cheng G, Mahato RI: RNAi for treating hepatitis B viral infection. Pharm Res; 2008 Jan;25(1):72-86
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  • Chronic hepatitis B virus (HBV) infection is one of the leading causes of liver cirrhosis and hepatocellular carcinoma (HCC).
  • Current treatment strategies of HBV infection including the use of interferon (IFN)-alpha and nucleotide analogues such as lamivudine and adefovir have met with only partial success.
  • Therefore, it is necessary to develop more effective antiviral therapies that can clear HBV infection with fewer side effects.
  • The successful use of chemically synthesized siRNA, endogenous expression of small hairpin RNA (shRNA) or microRNA (miRNA) to silence the target gene make this technology towards a potentially rational therapeutics for HBV infection.
  • In this review, we discuss several strategies for improving the anti-HBV therapeutic efficacy of siRNAs, while avoiding their off-target effects and immunostimulation.
  • There is an in-depth discussion on the (1) mechanisms of RNAi, (2) methods for siRNA/shRNA production, (3) barriers to RNAi-based therapies, and (4) delivery strategies of siRNA for treating HBV infection.

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  • (PMID = 18074201.001).
  • [ISSN] 0724-8741
  • [Journal-full-title] Pharmaceutical research
  • [ISO-abbreviation] Pharm. Res.
  • [Language] ENG
  • [Grant] United States / NIDDK NIH HHS / DK / R01 DK069968; United States / NIDDK NIH HHS / DK / R01 DK 064633; United States / NIDDK NIH HHS / DK / R01 DK 069968
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't; Review
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antiviral Agents; 0 / Excipients; 0 / RNA, Small Interfering
  • [Number-of-references] 126
  • [Other-IDs] NLM/ PMC2217617
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