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1. Broomfield SA, van der Most RG, Prosser AC, Mahendran S, Tovey MG, Smyth MJ, Robinson BW, Currie AJ: Locally administered TLR7 agonists drive systemic antitumor immune responses that are enhanced by anti-CD40 immunotherapy. J Immunol; 2009 May 1;182(9):5217-24
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  • Topical application of tumors with the TLR7 agonist imiquimod is an effective adjunct treatment for a range of primary dermatological cancers.
  • However, for therapy to be effective against a broad range of solid tumor types, it must promote a strong systemic antitumor response that targets metastases in addition to primary tumor.
  • We therefore investigated the potential of locally delivered imiquimod to stimulate an effective systemic antitumor response in a murine model of malignant mesothelioma (AB1-HA) with primary and distal tumors (dual tumor).
  • This local antitumor immune response required both CD8 T cells and NK cells, but not CD4 T cells, and was reliant on type I IFN induction.
  • In vivo CTL studies and Ly6A/E staining of lymphocytes suggested that local imiquimod treatment had indeed induced a systemic, Ag-specific CD8 response.
  • However, notably this response was not sufficient to retard the growth of an untreated distal tumor.
  • Because local imiquimod treatment did not induce significant CD4 T cell responses, we investigated the efficacy of combining imiquimod with agonistic CD40 Ab (as a surrogate for CD4 T cell help).
  • Combination of locally delivered imiquimod with systemic anti-CD40 immunotherapy not only significantly enhanced the local antitumor response, with 30% complete resolution, but it was also effective at significantly retarding growth of distal tumor.
  • These results demonstrate that antitumor responses induced by locally delivered TLR7 agonists can be harnessed systemically for treating distal tumor.
  • [MeSH-major] Aminoquinolines / administration & dosage. Antibodies, Monoclonal / administration & dosage. Antigens, CD40 / immunology. Membrane Glycoproteins / agonists. Mesothelioma / immunology. Mesothelioma / therapy. Toll-Like Receptor 7 / agonists
  • [MeSH-minor] Adjuvants, Immunologic / administration & dosage. Adjuvants, Immunologic / therapeutic use. Animals. CD8-Positive T-Lymphocytes / immunology. Cell Line, Tumor. Cytotoxicity, Immunologic. Drug Therapy, Combination. Female. Interferon Type I / administration & dosage. Interferon-gamma / administration & dosage. Killer Cells, Natural / immunology. Ligands. Mice. Mice, Inbred BALB C. Mice, Knockout. Mice, Nude. Mice, Transgenic

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  • (PMID = 19380767.001).
  • [ISSN] 1550-6606
  • [Journal-full-title] Journal of immunology (Baltimore, Md. : 1950)
  • [ISO-abbreviation] J. Immunol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Adjuvants, Immunologic; 0 / Aminoquinolines; 0 / Antibodies, Monoclonal; 0 / Antigens, CD40; 0 / Interferon Type I; 0 / Ligands; 0 / Membrane Glycoproteins; 0 / Tlr7 protein, mouse; 0 / Toll-Like Receptor 7; 82115-62-6 / Interferon-gamma; 99011-02-6 / imiquimod
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2. Chua TC, Yao P, Akther J, Young L, Bao S, Samaraweera U, Yan TD, Morris DL: Differential expression of Ki-67 and sex steroid hormone receptors between genders in peritoneal mesothelioma. Pathol Oncol Res; 2009 Dec;15(4):671-8
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  • [Title] Differential expression of Ki-67 and sex steroid hormone receptors between genders in peritoneal mesothelioma.
  • Gender influence on survival in mesothelioma has been observed in several large clinical series.
  • Twenty patients were treated with cytoreductive surgery and hyperthermic intraperitoneal chemotherapy in our peritonectomy unit.
  • The immunostaining was performed using monoclonal mouse anti-human antibodies on an autostainer (Autostainer Plus; Dako, Inc.).
  • For the first time, we demonstrate the presence of sex steroid receptors in peritoneal mesothelioma.
  • Once the exact functional effects of these receptors are understood, the use of established therapeutic options that are clinically available to target the sex steroid pathway may become a reality.
  • [MeSH-major] Ki-67 Antigen / metabolism. Mesothelioma / metabolism. Peritoneal Neoplasms / metabolism. Receptors, Androgen / metabolism. Receptors, Estrogen / metabolism. Receptors, Progesterone / metabolism. Sex Characteristics

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  • (PMID = 19401830.001).
  • [ISSN] 1532-2807
  • [Journal-full-title] Pathology oncology research : POR
  • [ISO-abbreviation] Pathol. Oncol. Res.
  • [Language] eng
  • [Publication-type] Comparative Study; Journal Article
  • [Publication-country] Netherlands
  • [Chemical-registry-number] 0 / Ki-67 Antigen; 0 / Receptors, Androgen; 0 / Receptors, Estrogen; 0 / Receptors, Progesterone
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3. Paik PK, Krug LM: Histone deacetylase inhibitors in malignant pleural mesothelioma: preclinical rationale and clinical trials. J Thorac Oncol; 2010 Feb;5(2):275-9
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  • [Title] Histone deacetylase inhibitors in malignant pleural mesothelioma: preclinical rationale and clinical trials.
  • Malignant pleural mesothelioma (MPM) is a rare and aggressive cancer of the mesothelium with only a limited range of treatment options that are largely ineffective in improving survival.
  • Recent efforts have turned toward the analysis of specific, dysregulated biologic pathways for insight into new treatment targets.
  • An increasing amount of preclinical data highlighting the effectiveness of histone deacetylase inhibition in MPM cell lines and mouse xenograft models has led to a number of early phase clinical trials in patients with MPM.
  • The results of these efforts have led to a multicenter, randomized, placebo-controlled phase III study of the histone deacetylase inhibitor vorinostat in patients with advanced MPM, offering hope for a new and effective therapy in patients with this disease.
  • [MeSH-major] Antineoplastic Agents / pharmacology. Antineoplastic Agents / therapeutic use. Histone Deacetylase Inhibitors / pharmacology. Histone Deacetylase Inhibitors / therapeutic use. Hydroxamic Acids / pharmacology. Hydroxamic Acids / therapeutic use. Mesothelioma / drug therapy. Pleural Neoplasms / drug therapy
  • [MeSH-minor] Animals. Clinical Trials as Topic. Drug Evaluation. Drug Evaluation, Preclinical. Humans. Mice

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  • (PMID = 20035240.001).
  • [ISSN] 1556-1380
  • [Journal-full-title] Journal of thoracic oncology : official publication of the International Association for the Study of Lung Cancer
  • [ISO-abbreviation] J Thorac Oncol
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / T32 CA009207
  • [Publication-type] Journal Article; Review
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / Histone Deacetylase Inhibitors; 0 / Hydroxamic Acids; 58IFB293JI / vorinostat
  • [Number-of-references] 47
  • [Other-IDs] NLM/ NIHMS589324; NLM/ PMC4052955
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4. Spugnini EP, Cardillo I, Verdina A, Crispi S, Saviozzi S, Calogero R, Nebbioso A, Altucci L, Cortese G, Galati R, Chien J, Shridhar V, Vincenzi B, Citro G, Cognetti F, Sacchi A, Baldi A: Piroxicam and cisplatin in a mouse model of peritoneal mesothelioma. Clin Cancer Res; 2006 Oct 15;12(20 Pt 1):6133-43
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  • [Title] Piroxicam and cisplatin in a mouse model of peritoneal mesothelioma.
  • PURPOSE: The aim of the present study was to evaluate the effects of piroxicam, a widely used nonsteroidal anti-inflammatory drug, alone and in combination with cisplatin (CDDP), on cell growth of mesothelioma cells.
  • Moreover, the effects of piroxicam and CDDP on tumor growth and survival of mouse xenograft models of mesothelioma were determined.
  • RESULTS: Piroxicam treatment of MSTO-211H and NCI-H2452 cells resulted in a significant inhibition of proliferation.
  • Last, GeneChip array analysis of MSTO-211H mesothelioma cell line revealed that piroxicam treatment caused up-regulation of metabolic pathway-associated genes and down-regulation of genes related to RNA processing apparatus.
  • Of note, epidermal growth factor receptor, one of the new biological targets of chemotherapy for mesothelioma, was down-regulated and HtrA1, a serine protease recently shown to be an endogenous mediator of CDDP cytotoxicity, was up-regulated following piroxicam treatment both in vitro and in vivo.
  • CONCLUSION: These data suggest that piroxicam sensitizes mesothelioma cells to CDDP-induced cytotoxicity by modulating the expression of several target genes.
  • Therefore, piroxicam in combination with CDDP might potentially be useful in the treatment of patients with mesothelioma.
  • [MeSH-major] Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Cisplatin / therapeutic use. Mesothelioma / drug therapy. Peritoneal Neoplasms / drug therapy. Piroxicam / therapeutic use
  • [MeSH-minor] Animals. Cell Division / drug effects. Cell Line, Tumor. Cell Survival / drug effects. Disease Models, Animal. Female. Humans. Mice. Mice, Nude

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  • (PMID = 17062690.001).
  • [ISSN] 1078-0432
  • [Journal-full-title] Clinical cancer research : an official journal of the American Association for Cancer Research
  • [ISO-abbreviation] Clin. Cancer Res.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 13T4O6VMAM / Piroxicam; Q20Q21Q62J / Cisplatin
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5. Altomare DA, You H, Xiao GH, Ramos-Nino ME, Skele KL, De Rienzo A, Jhanwar SC, Mossman BT, Kane AB, Testa JR: Human and mouse mesotheliomas exhibit elevated AKT/PKB activity, which can be targeted pharmacologically to inhibit tumor cell growth. Oncogene; 2005 Sep 8;24(40):6080-9
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  • [Title] Human and mouse mesotheliomas exhibit elevated AKT/PKB activity, which can be targeted pharmacologically to inhibit tumor cell growth.
  • The phosphatidylinositol 3-kinase (PI3K)/AKT pathway has been implicated in tumor aggressiveness, in part by mediating cell survival and reducing sensitivity to chemotherapy.
  • Treatment of this cell line with the mTOR inhibitor rapamycin resulted in growth arrest in G1 phase.
  • Treatment of MM cells with the PI3K inhibitor LY294002 in combination with cisplatin had greater efficacy in inhibiting cell proliferation and inducing apoptosis than either agent alone.
  • These findings also suggest that mouse models of MM may be useful for future preclinical studies of pharmaceuticals targeting the PI3K/AKT pathway.

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  • (PMID = 15897870.001).
  • [ISSN] 0950-9232
  • [Journal-full-title] Oncogene
  • [ISO-abbreviation] Oncogene
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / R01 CA077429; United States / NIEHS NIH HHS / ES / ES-003721; United States / NCI NIH HHS / CA / R01 CA045745; United States / NCI NIH HHS / CA / CA-77429; United States / NCI NIH HHS / CA / CA-45745; United States / NCI NIH HHS / CA / P30 CA006927; United States / NCI NIH HHS / CA / CA-06927
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't; Research Support, U.S. Gov't, P.H.S.
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Proto-Oncogene Proteins; 0 / Tumor Suppressor Proteins; EC 2.7.- / Protein Kinases; EC 2.7.1.- / Phosphatidylinositol 3-Kinases; EC 2.7.1.1 / MTOR protein, human; EC 2.7.1.1 / TOR Serine-Threonine Kinases; EC 2.7.1.1 / mTOR protein, mouse; 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; EC 3.1.3.- / Phosphoric Monoester Hydrolases; EC 3.1.3.48 / PTEN protein, human; EC 3.1.3.67 / PTEN Phosphohydrolase
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6. Beseth BD, Cameron RB, Leland P, You L, Varricchio F, Kreitman RJ, Maki RA, Jablons DM, Husain SR, Puri RK: Interleukin-4 receptor cytotoxin as therapy for human malignant pleural mesothelioma xenografts. Ann Thorac Surg; 2004 Aug;78(2):436-43; discussion 436-43
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  • [Title] Interleukin-4 receptor cytotoxin as therapy for human malignant pleural mesothelioma xenografts.
  • BACKGROUND: Malignant pleural mesothelioma (MPM) is an uncommon but highly fatal neoplasm for which only limited treatment is available.
  • METHODS: Immunohistochemical analysis was used to determine the expression of interleukin-4 receptors (IL-4R) on mesothelioma cell lines and resected mesothelioma tumors.
  • The toxicity of this molecule to mesothelioma cell lines was tested using a protein synthesis inhibition assay.
  • A human mesothelioma xenograft model was then developed to assess the efficacy of this molecule in vivo.
  • Immunohistochemical analysis of resected mesothelioma tumor specimens from 13 patients revealed that all tumors expressed moderate-to-high levels of IL-4R.
  • Coculture of malignant mesothelioma cell lines with IL-4(38-37)-PE38KDEL resulted in a dose-dependent inhibition of tumor cell protein synthesis through an interaction with cell-surface IL-4R.
  • In a nude mouse xenograft model of human MPM, intratumoral administration of IL-4(38-37)-PE38KDEL mediated a dose-dependent decrease in tumor volume and a dose-dependent increase in survival.

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  • (PMID = 15276492.001).
  • [ISSN] 1552-6259
  • [Journal-full-title] The Annals of thoracic surgery
  • [ISO-abbreviation] Ann. Thorac. Surg.
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / CA093708-01A3; United States / NCI NIH HHS / CA / R01 CA093708; United States / NCI NIH HHS / CA / R01 CA093708-01A3
  • [Publication-type] Journal Article
  • [Publication-country] Netherlands
  • [Chemical-registry-number] 0 / Bacterial Toxins; 0 / Exotoxins; 0 / Immunotoxins; 0 / Neoplasm Proteins; 0 / Receptors, Interleukin-4; 0 / Virulence Factors; 0 / interleukin 4 (38-37)-PE38KDEL; 207137-56-2 / Interleukin-4; EC 2.4.2.- / ADP Ribose Transferases; EC 2.4.2.31 / toxA protein, Pseudomonas aeruginosa
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7. Needham DJ, Lee JX, Beilharz MW: Intra-tumoural regulatory T cells: a potential new target in cancer immunotherapy. Biochem Biophys Res Commun; 2006 May 12;343(3):684-91
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  • The AE17 murine mesothelioma model was used for this study.
  • Localised, intra-tumoural depletion of T(reg) cells is a new, clinically relevant treatment option for established tumours.
  • [MeSH-major] Lymphocyte Depletion. Lymphocytes, Tumor-Infiltrating / drug effects. Neoplasms, Experimental / drug therapy. Receptors, Interleukin-2 / antagonists & inhibitors. T-Lymphocytes, Regulatory / drug effects
  • [MeSH-minor] Animals. Antibodies, Monoclonal / therapeutic use. Cell Proliferation. Female. Forkhead Transcription Factors / metabolism. Mesothelioma / drug therapy. Mesothelioma / immunology. Mesothelioma / pathology. Mice. Mice, Inbred C57BL. T-Lymphocyte Subsets / drug effects. T-Lymphocyte Subsets / immunology

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  • (PMID = 16563349.001).
  • [ISSN] 0006-291X
  • [Journal-full-title] Biochemical and biophysical research communications
  • [ISO-abbreviation] Biochem. Biophys. Res. Commun.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antibodies, Monoclonal; 0 / Forkhead Transcription Factors; 0 / Foxp3 protein, mouse; 0 / Receptors, Interleukin-2
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8. Suzuki E, Kapoor V, Cheung HK, Ling LE, DeLong PA, Kaiser LR, Albelda SM: Soluble type II transforming growth factor-beta receptor inhibits established murine malignant mesothelioma tumor growth by augmenting host antitumor immunity. Clin Cancer Res; 2004 Sep 1;10(17):5907-18
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  • [Title] Soluble type II transforming growth factor-beta receptor inhibits established murine malignant mesothelioma tumor growth by augmenting host antitumor immunity.
  • PURPOSE: Transforming growth factor (TGF)-beta blockade has been proposed as an anticancer therapy; however, understanding which tumor patients might benefit most from such therapy is crucial.
  • An ideal target of such inhibitory therapy might be malignant mesothelioma (MM), a highly lethal, treatment-resistant malignancy of mesothelial cells of the pleura and peritoneum that produces large amounts of TGF-beta.
  • The purpose of this study was to explore the possible therapeutic utility of TGF-beta blockade on MM.
  • EXPERIMENTAL DESIGN: To evaluate this hypothesis, we tested the effects of a soluble TGF-beta type II receptor (sTGF-beta R) that specifically inhibits TGF-beta1 and TGF-beta 3 in three different murine MM tumor models, AB12 and AC29 (which produce large amounts of TGF-beta) and AB1 (which does not produce TGF-beta).
  • [MeSH-major] Mesothelioma / therapy. Receptors, Transforming Growth Factor beta / therapeutic use. Transforming Growth Factor beta / antagonists & inhibitors
  • [MeSH-minor] Animals. Antigens, CD95 / metabolism. CD4-Positive T-Lymphocytes / immunology. CD4-Positive T-Lymphocytes / metabolism. CD4-Positive T-Lymphocytes / pathology. CD8-Positive T-Lymphocytes / immunology. CD8-Positive T-Lymphocytes / metabolism. CD8-Positive T-Lymphocytes / pathology. Female. Genes, MHC Class I / physiology. Genes, MHC Class II / physiology. Lymphocyte Depletion. Mice. Mice, Inbred BALB C. Mice, Inbred CBA. Mice, SCID. Protein-Serine-Threonine Kinases. Spleen / immunology. Spleen / metabolism. Spleen / pathology. T-Lymphocytes, Cytotoxic / drug effects. T-Lymphocytes, Cytotoxic / immunology. T-Lymphocytes, Cytotoxic / metabolism. Transforming Growth Factor beta1. Transforming Growth Factor beta3. Tumor Cells, Cultured

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  • (PMID = 15355924.001).
  • [ISSN] 1078-0432
  • [Journal-full-title] Clinical cancer research : an official journal of the American Association for Cancer Research
  • [ISO-abbreviation] Clin. Cancer Res.
  • [Language] eng
  • [Grant] United States / PHS HHS / / P01 66726
  • [Publication-type] Journal Article; Research Support, U.S. Gov't, P.H.S.
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antigens, CD95; 0 / Receptors, Transforming Growth Factor beta; 0 / Tgfb1 protein, mouse; 0 / Tgfb3 protein, mouse; 0 / Transforming Growth Factor beta; 0 / Transforming Growth Factor beta1; 0 / Transforming Growth Factor beta3; EC 2.7.11.1 / Protein-Serine-Threonine Kinases; EC 2.7.11.30 / transforming growth factor-beta type II receptor
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9. Yanagihara K, Tsumuraya M, Takigahira M, Mihara K, Kubo T, Ohuchi K, Seyama T: An orthotopic implantation mouse model of human malignant pleural mesothelioma for in vivo photon counting analysis and evaluation of the effect of S-1 therapy. Int J Cancer; 2010 Jun 15;126(12):2835-46
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  • [Title] An orthotopic implantation mouse model of human malignant pleural mesothelioma for in vivo photon counting analysis and evaluation of the effect of S-1 therapy.
  • Human malignant pleural mesothelioma (HMPM) is an aggressive neoplasm that is highly resistant to conventional therapies.
  • We established 3 HMPM cell lines (TCC-MESO-1, TCC-MESO-2 and TCC-MESO-3) from Japanese patients; the first 2 from the primary and metastatic tumors of a patient with the epithelioid type of HMPM, and the third from a patient with biphasic characteristics of the tumor (epithelioid and sarcomatous phenotypes).
  • Oral administration of S-1, an anticancer agent, suppressed the proliferation of the luciferase gene-expressing Me1Tu subline in the mouse models in vivo, with a treated-to-control ratio of the mean tumor volume of 0.2.
  • The orthotopic implantation mouse model proved to be useful for quantitative evaluation of the efficacy of novel anticancer drugs and also for studying the biology of HMPMs in vivo.
  • [MeSH-major] Antimetabolites, Antineoplastic / administration & dosage. Disease Models, Animal. Mesothelioma / drug therapy. Oxonic Acid / administration & dosage. Photons. Pleural Neoplasms / drug therapy. Tegafur / administration & dosage
  • [MeSH-minor] Administration, Oral. Animals. Cell Line, Transformed. Cell Proliferation / drug effects. Cell Survival. Cytokines / metabolism. Drug Combinations. Humans. Immunoenzyme Techniques. Luciferases / metabolism. Male. Mice. Mice, Inbred BALB C. Mice, Nude. Mice, SCID. Middle Aged. Neoplasm Proteins / metabolism. Tumor Cells, Cultured. Tumor Suppressor Protein p53 / genetics. Xenograft Model Antitumor Assays


10. Chua TC, Yao P, Akther J, Morris DL: Impact of tumor angiogenesis in peritoneal mesothelioma after radical cytoreduction and hyperthermic intraperitoneal chemotherapy. Pathol Oncol Res; 2010 Jun;16(2):217-22
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  • [Title] Impact of tumor angiogenesis in peritoneal mesothelioma after radical cytoreduction and hyperthermic intraperitoneal chemotherapy.
  • Peritoneal mesothelioma is one of the peritoneal surface malignancies where long-term survival is a reality after cytoreductive surgery (CRS) and hyperthermic intraperitoneal chemotherapy (HIPEC).
  • Tumor angiogenesis has been shown to be of prognostic significance on survival in mesothelioma.
  • We investigated the impact of survival of patients with peritoneal mesothelioma following CRS and HIPEC to determine the impact of tumor angiogenesis on survival after this radical surgical treatment.
  • The immunostaining was performed using monoclonal mouse anti-human antibodies (VEGF-C and CD31) on an autostainer (Autostainer Plus; Dako, Inc.).
  • After CRS and HIPEC, our results demonstrate that the prognostic significance of tumor angiogenesis is negated, highlighting the potential importance of other co-contributory mechanisms in mesotheliomagenesis and undergoing radial treatment.
  • [MeSH-major] Antineoplastic Combined Chemotherapy Protocols / administration & dosage. Hyperthermia, Induced. Mesothelioma / pathology. Neovascularization, Pathologic / pathology. Peritoneal Neoplasms / pathology
  • [MeSH-minor] Adult. Aged. Antigens, CD31 / metabolism. Cisplatin / administration & dosage. Combined Modality Therapy. Doxorubicin / administration & dosage. Female. Humans. Image Processing, Computer-Assisted. Immunohistochemistry. Infusions, Intralesional. Kaplan-Meier Estimate. Male. Middle Aged. Prognosis. Vascular Endothelial Growth Factor A / metabolism

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  • (PMID = 19789996.001).
  • [ISSN] 1532-2807
  • [Journal-full-title] Pathology oncology research : POR
  • [ISO-abbreviation] Pathol. Oncol. Res.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Netherlands
  • [Chemical-registry-number] 0 / Antigens, CD31; 0 / Vascular Endothelial Growth Factor A; 80168379AG / Doxorubicin; Q20Q21Q62J / Cisplatin
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11. Catassi A, Paleari L, Servent D, Sessa F, Dominioni L, Ognio E, Cilli M, Vacca P, Mingari M, Gaudino G, Bertino P, Paolucci M, Calcaterra A, Cesario A, Granone P, Costa R, Ciarlo M, Alama A, Russo P: Targeting alpha7-nicotinic receptor for the treatment of pleural mesothelioma. Eur J Cancer; 2008 Oct;44(15):2296-311
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  • [Title] Targeting alpha7-nicotinic receptor for the treatment of pleural mesothelioma.
  • Human malignant pleural mesothelioma (MPM) is a dreadful disease and there is still no standard therapy available for a consistent therapeutic approach.
  • This research is aimed at the evaluation of the potential therapeutic effect of a specific nicotinic receptor (nAChR) antagonist, namely alpha-Cobratoxin (alpha-CbT).
  • Its effectiveness was tested in mesothelioma cell lines and in primary mesothelioma cells in vitro, as well as in vivo, in orthotopically xenotransplanted NOD/SCID mice.
  • Non-immunogenic derivatives of the alpha-CbT molecule need to be developed for possible human use.
  • [MeSH-major] Antineoplastic Agents / therapeutic use. Cobra Neurotoxin Proteins / therapeutic use. Mesothelioma / drug therapy. Nicotinic Antagonists / therapeutic use. Pleural Neoplasms / drug therapy. Receptors, Nicotinic / metabolism
  • [MeSH-minor] Animals. Apoptosis / drug effects. Dose-Response Relationship, Drug. Drug Evaluation, Preclinical / methods. Humans. Mice. Mice, Inbred NOD. Mice, SCID. Neoplasm Proteins / metabolism. Neoplasm Transplantation. Reverse Transcriptase Polymerase Chain Reaction / methods. Transplantation, Heterologous. Tumor Cells, Cultured. alpha7 Nicotinic Acetylcholine Receptor

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  • (PMID = 18722110.001).
  • [ISSN] 1879-0852
  • [Journal-full-title] European journal of cancer (Oxford, England : 1990)
  • [ISO-abbreviation] Eur. J. Cancer
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / Chrna7 protein, human; 0 / Chrna7 protein, mouse; 0 / Cobra Neurotoxin Proteins; 0 / Neoplasm Proteins; 0 / Nicotinic Antagonists; 0 / Receptors, Nicotinic; 0 / alpha7 Nicotinic Acetylcholine Receptor; 69344-74-7 / alpha-cobratoxin
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12. Kim S, Buchlis G, Fridlender ZG, Sun J, Kapoor V, Cheng G, Haas A, Cheung HK, Zhang X, Corbley M, Kaiser LR, Ling L, Albelda SM: Systemic blockade of transforming growth factor-beta signaling augments the efficacy of immunogene therapy. Cancer Res; 2008 Dec 15;68(24):10247-56
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  • [Title] Systemic blockade of transforming growth factor-beta signaling augments the efficacy of immunogene therapy.
  • This article explores the potential for increased efficacy when combining immunotherapies with TGF-beta suppression using the TGF-beta type I receptor kinase inhibitor SM16.
  • AB12 (mesothelioma) and LKR (lung cancer) tumors or intratracheally in a Kras orthotopic lung tumor model.
  • Tumor growth was assessed and cytokine expression and cell populations were measured in tumors and spleens by real-time PCR and flow cytometry.
  • Blockade of the TGF-beta signaling pathway augments the antitumor effects of Ad.IFN-beta immune-activating or Ad.E7 vaccination therapy.

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  • (PMID = 19074893.001).
  • [ISSN] 1538-7445
  • [Journal-full-title] Cancer research
  • [ISO-abbreviation] Cancer Res.
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / P01 CA066726; United States / NCI NIH HHS / CA / P01 CA066726-12; United States / NCI NIH HHS / CA / CA066726-120002; United States / NCI NIH HHS / CA / P01 CA 66726; United States / NIEHS NIH HHS / ES / ES013508-02; United States / NIEHS NIH HHS / ES / P30 ES013508; United States / NCI NIH HHS / CA / CA066726-12; United States / NIEHS NIH HHS / ES / P30 ES013508-02; United States / NCI NIH HHS / CA / P01 CA066726-120002
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Azabicyclo Compounds; 0 / Cancer Vaccines; 0 / Cytokines; 0 / Epitopes, T-Lymphocyte; 0 / Icam1 protein, mouse; 0 / Oncogene Proteins, Viral; 0 / RNA, Messenger; 0 / SM16 compound; 0 / Transforming Growth Factor beta; 126547-89-5 / Intercellular Adhesion Molecule-1; 77238-31-4 / Interferon-beta
  • [Other-IDs] NLM/ NIHMS78784; NLM/ PMC2637471
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13. van der Most RG, Currie AJ, Mahendran S, Prosser A, Darabi A, Robinson BW, Nowak AK, Lake RA: Tumor eradication after cyclophosphamide depends on concurrent depletion of regulatory T cells: a role for cycling TNFR2-expressing effector-suppressor T cells in limiting effective chemotherapy. Cancer Immunol Immunother; 2009 Aug;58(8):1219-28
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  • [Title] Tumor eradication after cyclophosphamide depends on concurrent depletion of regulatory T cells: a role for cycling TNFR2-expressing effector-suppressor T cells in limiting effective chemotherapy.
  • However, the efficacy of anti-tumor chemotherapy may be limited by tumor-driven immunosuppression, e.g., through CD25+ regulatory T cells.
  • We addressed this question in a mouse model of mesothelioma by depleting or reconstituting CD25+ regulatory T cells in combination with two different chemotherapeutic drugs.
  • Analysis of post-chemotherapy regulatory T cell populations revealed that cyclophosphamide depleted cycling (Ki-67(hi)) T cells, including foxp3+ regulatory CD4+ T cells.
  • Our data suggest that regulatory T cell depletion could be used to improve the efficacy of anti-cancer chemotherapy regimens.
  • Indeed, we observed that the drug gemcitabine, which does not deplete cycling regulatory T cells, eradicates established tumors in mice only when CD25+ CD4+ T cells are concurrently depleted.
  • Cyclophosphamide could be used to achieve regulatory T cell depletion in combination with chemotherapy.
  • [MeSH-major] CD8-Positive T-Lymphocytes / immunology. Cyclophosphamide / therapeutic use. Immunosuppressive Agents / therapeutic use. Lymphocyte Depletion. Mesothelioma / drug therapy. Receptors, Tumor Necrosis Factor, Type II / immunology. T-Lymphocytes, Regulatory / drug effects
  • [MeSH-minor] Adoptive Transfer. Animals. Antigens, Differentiation, T-Lymphocyte / immunology. Antigens, Differentiation, T-Lymphocyte / metabolism. Deoxycytidine / analogs & derivatives. Deoxycytidine / therapeutic use. Inducible T-Cell Co-Stimulator Protein. Kaplan-Meier Estimate. Ki-67 Antigen / immunology. Ki-67 Antigen / metabolism. L-Selectin / immunology. L-Selectin / metabolism. Mice. Mice, Inbred BALB C. Mice, Nude

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  • (PMID = 19052741.001).
  • [ISSN] 1432-0851
  • [Journal-full-title] Cancer immunology, immunotherapy : CII
  • [ISO-abbreviation] Cancer Immunol. Immunother.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Germany
  • [Chemical-registry-number] 0 / Antigens, Differentiation, T-Lymphocyte; 0 / Icos protein, mouse; 0 / Immunosuppressive Agents; 0 / Inducible T-Cell Co-Stimulator Protein; 0 / Ki-67 Antigen; 0 / Mki67 protein, mouse; 0 / Receptors, Tumor Necrosis Factor, Type II; 0W860991D6 / Deoxycytidine; 126880-86-2 / L-Selectin; 8N3DW7272P / Cyclophosphamide; B76N6SBZ8R / gemcitabine
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14. Tabata C, Tabata R, Hirayama N, Yasumitsu A, Yamada S, Murakami A, Iida S, Tamura K, Terada T, Kuribayashi K, Fukuoka K, Nakano T: All-trans-retinoic acid inhibits tumour growth of malignant pleural mesothelioma in mice. Eur Respir J; 2009 Nov;34(5):1159-67
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  • [Title] All-trans-retinoic acid inhibits tumour growth of malignant pleural mesothelioma in mice.
  • Malignant pleural mesothelioma (MPM) is an aggressive malignant tumour of mesothelial origin associated with asbestos exposure.
  • Because MPM has limited response to conventional chemotherapy and radiotherapy, the prognosis is very poor.
  • We investigated whether ATRA had an inhibitory effect on the cell growth of MPM, the origin of which was mesenchymal cells similar to lung fibroblasts, using a subcutaneous xenograft mouse model.
  • These data may provide a rationale to explore the clinical use of ATRA for the treatment of MPM.
  • [MeSH-major] Mesothelioma / drug therapy. Pleural Neoplasms / drug therapy. Tretinoin / pharmacology

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  • (PMID = 19443527.001).
  • [ISSN] 1399-3003
  • [Journal-full-title] The European respiratory journal
  • [ISO-abbreviation] Eur. Respir. J.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Switzerland
  • [Chemical-registry-number] 0 / Interleukin-6; 0 / Platelet-Derived Growth Factor; 0 / Proto-Oncogene Proteins c-sis; 0 / RNA, Messenger; 0 / Transforming Growth Factor beta1; 0 / platelet-derived growth factor BB; 1332-21-4 / Asbestos; 5688UTC01R / Tretinoin; EC 2.7.10.1 / Receptor, Platelet-Derived Growth Factor beta
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15. Hassan R, Ebel W, Routhier EL, Patel R, Kline JB, Zhang J, Chao Q, Jacob S, Turchin H, Gibbs L, Phillips MD, Mudali S, Iacobuzio-Donahue C, Jaffee EM, Moreno M, Pastan I, Sass PM, Nicolaides NC, Grasso L: Preclinical evaluation of MORAb-009, a chimeric antibody targeting tumor-associated mesothelin. Cancer Immun; 2007;7:20
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  • Novel therapeutic agents that are safe and effective are needed for the treatment of pancreatic, ovarian, lung adenocarcinomas and mesotheliomas.
  • Mesothelin is a glycosyl-phosphatidyl inositol (GPI)-linked membrane protein of 40 kDa over-expressed in all pancreatic adenocarcinoma and mesothelioma, in >70% of ovarian adenocarcinoma, and in non-small cell lung and colorectal cancers.
  • We have recently developed MORAb-009, a mouse-human chimeric IgG1kappa monoclonal antibody with an affinity of 1.5 nM for human mesothelin.
  • Treatment that included MORAb-009 in combination with chemotherapy led to a marked reduction in tumor growth of mesothelin-expressing tumors in nude mice compared to chemotherapy or MORAb-009 treatment alone.
  • We have in fact initiated a Phase I clinical study enrolling patients with mesothelin-positive pancreatic, mesothelioma, non-small cell lung and ovarian cancers.
  • [MeSH-major] Antibodies, Monoclonal / immunology. Antibodies, Monoclonal / therapeutic use. Antibodies, Neoplasm / immunology. Antibodies, Neoplasm / therapeutic use. Membrane Glycoproteins / antagonists & inhibitors. Membrane Glycoproteins / immunology. Neoplasms / drug therapy
  • [MeSH-minor] Animals. Antibody-Dependent Cell Cytotoxicity / drug effects. Antineoplastic Agents / pharmacology. Cell Adhesion / drug effects. Cell Line, Tumor. Drug Evaluation, Preclinical. Drug-Related Side Effects and Adverse Reactions. Endocytosis / drug effects. GPI-Linked Proteins. Humans. Mice. Mice, Nude

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  • (PMID = 18088084.001).
  • [ISSN] 1424-9634
  • [Journal-full-title] Cancer immunity
  • [ISO-abbreviation] Cancer Immun.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antibodies, Monoclonal; 0 / Antibodies, Neoplasm; 0 / Antineoplastic Agents; 0 / GPI-Linked Proteins; 0 / MORAb-009 monoclonal antibody; 0 / Membrane Glycoproteins; 0 / mesothelin
  • [Other-IDs] NLM/ PMC2935758
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16. Vandermeers F, Hubert P, Delvenne P, Mascaux C, Grigoriu B, Burny A, Scherpereel A, Willems L: Valproate, in combination with pemetrexed and cisplatin, provides additional efficacy to the treatment of malignant mesothelioma. Clin Cancer Res; 2009 Apr 15;15(8):2818-28
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  • [Title] Valproate, in combination with pemetrexed and cisplatin, provides additional efficacy to the treatment of malignant mesothelioma.
  • PURPOSE: Present chemotherapeutic regimens are marginally efficient in tumor cells being particularly resistant to radiotherapy and/or chemotherapy.
  • We hypothesized that unresponsiveness of tumors to conventional therapeutic agents might be due to inappropriate gene expression resulting from epigenetic modifications and leading to transcriptional silencing.
  • The goal of this study was to evaluate the anticancer effect of a histone deacetylase inhibitor, valproate, on mesothelioma cells in combination with pemetrexed and cisplatin, the usual first-line regimen of chemotherapy for this tumor.
  • EXPERIMENTAL DESIGN AND RESULTS: We show that valproate augments apoptosis induced by pemetrexed and cisplatin in mesothelioma cell lines and in tumor cells from patient's biopsies.
  • Finally, valproate when combined with pemetrexed and cisplatin prevents tumor growth in mouse models of epithelioid mesothelioma.
  • CONCLUSIONS: These observations support the potential additional efficacy of valproate in combination with pemetrexed and cisplatin for treatment of malignant mesothelioma.
  • [MeSH-major] Antineoplastic Agents / therapeutic use. Cisplatin / therapeutic use. Enzyme Inhibitors / therapeutic use. Glutamates / therapeutic use. Guanine / analogs & derivatives. Mesothelioma / drug therapy. Valproic Acid / therapeutic use
  • [MeSH-minor] Animals. Antineoplastic Combined Chemotherapy Protocols. Apoptosis / drug effects. Apoptosis / physiology. BH3 Interacting Domain Death Agonist Protein / drug effects. BH3 Interacting Domain Death Agonist Protein / metabolism. Caspase 8 / metabolism. Cell Line, Tumor. Cell Survival / drug effects. Cell Survival / physiology. Cyclin-Dependent Kinase Inhibitor p21 / agonists. Cyclin-Dependent Kinase Inhibitor p21 / metabolism. Cytochromes c / drug effects. Cytochromes c / metabolism. Drug Synergism. Histones / drug effects. Histones / metabolism. Humans. Mice. Mice, Inbred BALB C. Mice, SCID. Mitochondria / drug effects. Mitochondria / metabolism. Pemetrexed. Reactive Oxygen Species / metabolism

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  • (PMID = 19351772.001).
  • [ISSN] 1078-0432
  • [Journal-full-title] Clinical cancer research : an official journal of the American Association for Cancer Research
  • [ISO-abbreviation] Clin. Cancer Res.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / BH3 Interacting Domain Death Agonist Protein; 0 / BID protein, human; 0 / CDKN1A protein, human; 0 / Cyclin-Dependent Kinase Inhibitor p21; 0 / Enzyme Inhibitors; 0 / Glutamates; 0 / Histones; 0 / Reactive Oxygen Species; 04Q9AIZ7NO / Pemetrexed; 5Z93L87A1R / Guanine; 614OI1Z5WI / Valproic Acid; 9007-43-6 / Cytochromes c; EC 3.4.22.- / Caspase 8; Q20Q21Q62J / Cisplatin
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17. Capiaux GM, Budak-Alpdogan T, Alpdogan O, Bornmann W, Takebe N, Banerjee D, Maley F, Bertino JR: Protection of hematopoietic stem cells from pemetrexed toxicity by retroviral gene transfer with a mutant dihydrofolate reductase-mutant thymidylate synthase fusion gene. Cancer Gene Ther; 2004 Dec;11(12):767-73
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  • Myelosuppression is one of the major side effects of most anticancer drugs.
  • To confer myeloprotection, our laboratory generated drug-resistant mutants of select target human enzymes for gene transfer to the bone marrow.
  • In this study, we examined the sensitivity of the DHFR F/S-TS G52S fusion protein to the multitargeted antifolate, pemetrexed (LY231514, Alimta), which targets both DHFR and TS and is currently in phase III trials for the treatment of solid tumors and in combination with cisplatin has been shown to be an advance in the treatment of mesothelioma.
  • Similarly, expression of the DHFR F/S-TS G52S fusion gene in retrovirally transduced mouse marrow cells resulted in an increased survival of CFU-GM colonies when compared to cells transduced with either of the mutants alone.
  • This construct may be useful for conferring myeloprotection to patients receiving this drug.
  • [MeSH-major] Cytoprotection / genetics. Gene Expression Regulation. Genetic Therapy / methods. Glutamates / toxicity. Guanine / analogs & derivatives. Guanine / toxicity. Hematopoietic Stem Cells / drug effects. Tetrahydrofolate Dehydrogenase / genetics. Thymidylate Synthase / genetics

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  • (PMID = 15359285.001).
  • [ISSN] 0929-1903
  • [Journal-full-title] Cancer gene therapy
  • [ISO-abbreviation] Cancer Gene Ther.
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / P01 CA59350; United States / NCI NIH HHS / CA / R01 CA-08010; United States / NCI NIH HHS / CA / R01-CA 44355
  • [Publication-type] Comparative Study; Journal Article; Research Support, U.S. Gov't, P.H.S.
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Glutamates; 0 / Recombinant Fusion Proteins; 04Q9AIZ7NO / Pemetrexed; 5Z93L87A1R / Guanine; EC 1.5.1.3 / Tetrahydrofolate Dehydrogenase; EC 2.1.1.45 / Thymidylate Synthase
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18. van der Most RG, Currie AJ, Cleaver AL, Salmons J, Nowak AK, Mahendran S, Larma I, Prosser A, Robinson BW, Smyth MJ, Scalzo AA, Degli-Esposti MA, Lake RA: Cyclophosphamide chemotherapy sensitizes tumor cells to TRAIL-dependent CD8 T cell-mediated immune attack resulting in suppression of tumor growth. PLoS One; 2009;4(9):e6982
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  • [Title] Cyclophosphamide chemotherapy sensitizes tumor cells to TRAIL-dependent CD8 T cell-mediated immune attack resulting in suppression of tumor growth.
  • BACKGROUND: Anti-cancer chemotherapy can be simultaneously lymphodepleting and immunostimulatory.
  • Pre-clinical models clearly demonstrate that chemotherapy can synergize with immunotherapy, raising the question how the immune system can be mobilized to generate anti-tumor immune responses in the context of chemotherapy.
  • METHODS AND FINDINGS: We used a mouse model of malignant mesothelioma, AB1-HA, to investigate T cell-dependent tumor resolution after chemotherapy.
  • This treatment was associated with an IFN-alpha/beta response and a profound negative impact on the anti-tumor and total CD8 T cell responses.
  • CONCLUSION: The data support a model in which chemotherapy sensitizes tumor cells for T cell-, and possibly NK cell-, mediated apoptosis.
  • [MeSH-major] Antineoplastic Agents / pharmacology. CD8-Positive T-Lymphocytes / immunology. Cyclophosphamide / pharmacology. Neoplasms / therapy. TNF-Related Apoptosis-Inducing Ligand / metabolism

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  • (PMID = 19746156.001).
  • [ISSN] 1932-6203
  • [Journal-full-title] PloS one
  • [ISO-abbreviation] PLoS ONE
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / TNF-Related Apoptosis-Inducing Ligand; 0 / TNFSF10 protein, human; 82115-62-6 / Interferon-gamma; 8N3DW7272P / Cyclophosphamide
  • [Other-IDs] NLM/ PMC2734989
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19. Gabrielson EW, Pinn ML, Testa JR, Kuhajda FP: Increased fatty acid synthase is a therapeutic target in mesothelioma. Clin Cancer Res; 2001 Jan;7(1):153-7
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  • [Title] Increased fatty acid synthase is a therapeutic target in mesothelioma.
  • Many common human cancer tissues express high levels of fatty acid synthase (FAS), the primary enzyme for the synthesis of fatty acids, and the differential expression of FAS between normal and neoplastic tissues has led to the consideration of FAS as a target for anticancer therapy.
  • To investigate the potential of targeting FAS for the treatment of pleural mesothelioma, we first determined whether FAS is overexpressed in human mesothelioma.
  • By immunohistochemistry, we found 22 of 30 human mesothelioma tissue samples tested to express significantly increased levels of FAS compared with normal tissues, including mesothelium.
  • To further explore FAS as a therapeutic target in mesothelioma, we established a nude mouse xenograft model for human mesothelioma using the H-Meso cell line.
  • The i.p. xenografts of this cell line have high levels of FAS expression and fatty acid synthesis pathway activity and grow along mesothelial surfaces in a manner similar to the growth pattern of human mesothelioma.
  • These results suggest that FAS may be an effective target for pharmacological therapy in a high proportion of human mesotheliomas.
  • [MeSH-major] 4-Butyrolactone / analogs & derivatives. 4-Butyrolactone / therapeutic use. Antineoplastic Agents / therapeutic use. Fatty Acid Synthases / antagonists & inhibitors. Mesothelioma / drug therapy. Neoplasms, Mesothelial / drug therapy
  • [MeSH-minor] Animals. Antifungal Agents / pharmacology. Cerulenin / pharmacology. Disease Models, Animal. Humans. Immunoenzyme Techniques. Mice. Mice, Nude. Neoplasm Transplantation. Paraffin Embedding. Prognosis. Tumor Cells, Cultured / cytology. Tumor Cells, Cultured / drug effects

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  • (PMID = 11205903.001).
  • [ISSN] 1078-0432
  • [Journal-full-title] Clinical cancer research : an official journal of the American Association for Cancer Research
  • [ISO-abbreviation] Clin. Cancer Res.
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / CA-06927; United States / NCI NIH HHS / CA / CA-45745
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't; Research Support, U.S. Gov't, Non-P.H.S.; Research Support, U.S. Gov't, P.H.S.
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / 4-methylene-2-octyl-5-oxofuran-3-carboxylic acid; 0 / Antifungal Agents; 0 / Antineoplastic Agents; 17397-89-6 / Cerulenin; EC 2.3.1.85 / Fatty Acid Synthases; OL659KIY4X / 4-Butyrolactone
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