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1. Wang C, Yang YG, Wang XL: [Expressions of hTERT, p53, c-erbB-2 and Bcl-2 in colonic adenocarcinoma mouse models with liver metastases: effects of classical traditional Chinese medicine prescriptions for promoting circulation and removing blood stasis]. Di Yi Jun Yi Da Xue Xue Bao; 2004 Jul;24(7):758-60
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  • [Title] [Expressions of hTERT, p53, c-erbB-2 and Bcl-2 in colonic adenocarcinoma mouse models with liver metastases: effects of classical traditional Chinese medicine prescriptions for promoting circulation and removing blood stasis].
  • OBJECTIVE: To observe the effects of classical traditional Chinese medicine prescriptions that function to promote blood circulation and removing blood stasis on the metastatic behavior of malignant tumors, and explore the possible mechanisms of such effects.
  • METHODS: BALB/c mouse models of colonic adenocarcinoma with liver metastases were established by intrasplenic injection of colonic adenocarcinoma cells (CT26) to receive treatment with the three representative classical circulation-promoting and blood stasis-removing prescriptions of traditional Chinese medicine, namely Guizhifuling pills, Didang Tang and Danshenyin, respectively.
  • The expressions of human telomerase reverse transcriptase (hTERT), p53, c-erbB-2 and Bcl-2 were detected in the mouse models with different treatments and in normal control mice.
  • The expressions of hTERT, p53, c-erbB-2 and Bcl-2 in the models receiving treatment with either Didang Tang or Guizhifuling pills differed significantly from those of the untreated model group (P<0.05), whereas between Danshenyin group and the model group, only the expression of hTERT showed significant difference.
  • Such inhibitory effects of the prescriptions on hTERT and the oncogenes might explain their actions to inhibit malignant tumor metastasis, which can be related to performance of the prescriptions in promoting circulation by removing blood stasis.
  • [MeSH-major] Adenocarcinoma / drug therapy. Blood Circulation / drug effects. Colonic Neoplasms / drug therapy. Liver Neoplasms / secondary. Medicine, Chinese Traditional. Proto-Oncogene Proteins c-bcl-2 / analysis. Receptor, ErbB-2 / analysis. Telomerase / analysis. Tumor Suppressor Protein p53 / analysis

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  • (PMID = 15257895.001).
  • [ISSN] 1000-2588
  • [Journal-full-title] Di 1 jun yi da xue xue bao = Academic journal of the first medical college of PLA
  • [ISO-abbreviation] Di Yi Jun Yi Da Xue Xue Bao
  • [Language] chi
  • [Publication-type] English Abstract; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] China
  • [Chemical-registry-number] 0 / DNA-Binding Proteins; 0 / Proto-Oncogene Proteins c-bcl-2; 0 / Tumor Suppressor Protein p53; EC 2.7.10.1 / Receptor, ErbB-2; EC 2.7.7.49 / Telomerase
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2. Zorn CS, Wojno KJ, McCabe MT, Kuefer R, Gschwend JE, Day ML: 5-aza-2'-deoxycytidine delays androgen-independent disease and improves survival in the transgenic adenocarcinoma of the mouse prostate mouse model of prostate cancer. Clin Cancer Res; 2007 Apr 1;13(7):2136-43
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  • [Title] 5-aza-2'-deoxycytidine delays androgen-independent disease and improves survival in the transgenic adenocarcinoma of the mouse prostate mouse model of prostate cancer.
  • PURPOSE: We have previously shown that 5-aza-2'-deoxycytidine (5-aza) is an effective chemopreventive agent capable of preventing early disease progression in the transgenic adenocarcinoma of the mouse prostate (TRAMP) model.
  • One cohort of 22 mice per treatment was euthanized after 10 weeks of treatment, whereas a second cohort of 14 mice per group was followed until death to determine survival.
  • Histologic sections of prostate, pelvic lymph nodes, lung, and liver were blinded and analyzed by a certified genitourinary pathologist (K.J.W.).
  • RESULTS: Combined treatment (castration + 5-aza) provided significant survival benefits over either single treatment (combined versus castration P = 0.029, combined versus 5-aza P = 0.036).
  • At 24 weeks of age, 86% of mice within the PBS cohort exhibited histologic evidence of prostate cancer, whereas only 47% of the combined cohort exhibited malignant disease (P < 0.0001).
  • Additionally, whereas 43% of the PBS treatment group exhibited lymph node metastases, these were only observed in 21% of the combined treatment mice.
  • Based on these preclinical findings, we suggest that 5-aza treatment may prolong the time to an androgen-independent status and thus survival in a hormone-deprived setting in prostate cancer.
  • [MeSH-major] Adenocarcinoma / drug therapy. Antimetabolites, Antineoplastic / therapeutic use. Azacitidine / analogs & derivatives. Neoplasms, Hormone-Dependent / drug therapy. Prostatic Neoplasms / drug therapy
  • [MeSH-minor] Animals. Castration. Combined Modality Therapy. Disease Models, Animal. Male. Mice. Mice, Transgenic

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  • (PMID = 17404097.001).
  • [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 / NIDDK NIH HHS / DK / DK61488; United States / NCI NIH HHS / CA / P50CA69569
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antimetabolites, Antineoplastic; 776B62CQ27 / decitabine; M801H13NRU / Azacitidine
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3. Kobbe G, Schneider P, Rohr U, Fenk R, Neumann F, Aivado M, Dietze L, Kronenwett R, Hünerlitürkoglu A, Haas R: Treatment of severe steroid refractory acute graft-versus-host disease with infliximab, a chimeric human/mouse antiTNFalpha antibody. Bone Marrow Transplant; 2001 Jul;28(1):47-9
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  • [Title] Treatment of severe steroid refractory acute graft-versus-host disease with infliximab, a chimeric human/mouse antiTNFalpha antibody.
  • Patients with severe aGVHD not responding to treatment with steroids have a poor prognosis.
  • We treated four patients with severe aGVHD refractory to steroids with infliximab, a chimeric human/mouse antiTNFalpha antibody.
  • Patients (CML 2, MM 1, AML 1) developed grade III-IV GVHD at a median of 34 days (range 15-76) after myeloablative PBSCT (two), donor lymphocyte infusion for relapsed CML (one) or non-myeloablative PBSCT (one), respectively.
  • All patients had severe intestinal involvement in addition to skin and/or liver disease and had received treatment with high-dose steroids (four) for a median of 11 days (range 5-17) in addition to CsA (four) and MMF (three).
  • In three of four patients a complete resolution of diarrhea and significant improvement of skin and liver disease were observed.
  • At present two patients are alive >200 days after therapy, one with limited cGVHD.
  • Two patients died, one of progressive malignant disease without GVHD and one of refractory GVHD.
  • Infliximab is apparently an active drug for the treatment of aGVHD.
  • [MeSH-major] Antibodies, Monoclonal / administration & dosage. Graft vs Host Disease / drug therapy
  • [MeSH-minor] Acute Disease. Adult. Animals. Anti-Inflammatory Agents / administration & dosage. Female. Hematologic Neoplasms / complications. Hematologic Neoplasms / therapy. Hematopoietic Stem Cell Transplantation / adverse effects. Humans. Infliximab. Male. Mice. Middle Aged. Recombinant Fusion Proteins / administration & dosage. Salvage Therapy. Steroids / therapeutic use. Transplantation, Homologous / adverse effects. Treatment Outcome. Tumor Necrosis Factor-alpha / immunology

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  • (PMID = 11498743.001).
  • [ISSN] 0268-3369
  • [Journal-full-title] Bone marrow transplantation
  • [ISO-abbreviation] Bone Marrow Transplant.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Anti-Inflammatory Agents; 0 / Antibodies, Monoclonal; 0 / Recombinant Fusion Proteins; 0 / Steroids; 0 / Tumor Necrosis Factor-alpha; B72HH48FLU / Infliximab
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4. Kidera Y, Tsubaki M, Yamazoe Y, Shoji K, Nakamura H, Ogaki M, Satou T, Itoh T, Isozaki M, Kaneko J, Tanimori Y, Yanae M, Nishida S: Reduction of lung metastasis, cell invasion, and adhesion in mouse melanoma by statin-induced blockade of the Rho/Rho-associated coiled-coil-containing protein kinase pathway. J Exp Clin Cancer Res; 2010;29:127
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  • [Title] Reduction of lung metastasis, cell invasion, and adhesion in mouse melanoma by statin-induced blockade of the Rho/Rho-associated coiled-coil-containing protein kinase pathway.
  • BACKGROUND: Melanomas are highly malignant and have high metastatic potential; hence, there is a need for new therapeutic strategies to prevent cell metastasis.
  • In the present study, we investigated whether statins inhibit tumor cell migration, invasion, adhesion, and metastasis in the B16BL6 mouse melanoma cell line.
  • Cell adhesion analysis was performed using type I collagen-, type IV collagen-, fibronectin-, and laminin-coated plates.
  • Thus, these findings suggest that statins have potential clinical applications for the treatment of tumor cell metastasis.
  • [MeSH-major] Antineoplastic Agents / pharmacology. Cell Adhesion / drug effects. Cell Movement / drug effects. Hydroxymethylglutaryl-CoA Reductase Inhibitors / pharmacology. Lung Neoplasms / prevention & control. Melanoma, Experimental / drug therapy. Signal Transduction / drug effects. rho GTP-Binding Proteins / metabolism. rho-Associated Kinases / metabolism
  • [MeSH-minor] Administration, Oral. Animals. Blotting, Western. Cell Survival / drug effects. Extracellular Matrix Proteins / metabolism. Fatty Acids, Monounsaturated / pharmacology. Female. Gene Expression Regulation, Enzymologic. Gene Expression Regulation, Neoplastic. Indoles / pharmacology. Integrins / metabolism. Lim Kinases / metabolism. Matrix Metalloproteinases / genetics. Matrix Metalloproteinases / metabolism. Mice. Mice, Inbred C57BL. Myosin Light Chains / metabolism. Neoplasm Invasiveness. Phosphorylation. Protein Kinase Inhibitors / pharmacology. RNA, Messenger / metabolism. Reverse Transcriptase Polymerase Chain Reaction. Simvastatin / pharmacology. Time Factors

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  • (PMID = 20843370.001).
  • [ISSN] 1756-9966
  • [Journal-full-title] Journal of experimental & clinical cancer research : CR
  • [ISO-abbreviation] J. Exp. Clin. Cancer Res.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / Extracellular Matrix Proteins; 0 / Fatty Acids, Monounsaturated; 0 / Hydroxymethylglutaryl-CoA Reductase Inhibitors; 0 / Indoles; 0 / Integrins; 0 / Myosin Light Chains; 0 / Protein Kinase Inhibitors; 0 / RNA, Messenger; 4L066368AS / fluvastatin; AGG2FN16EV / Simvastatin; EC 2.7.11.1 / Lim Kinases; EC 2.7.11.1 / rho-Associated Kinases; EC 3.4.24.- / Matrix Metalloproteinases; EC 3.6.5.2 / rho GTP-Binding Proteins
  • [Other-IDs] NLM/ PMC2949822
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5. Wang L, Shen Y, Song R, Sun Y, Xu J, Xu Q: An anticancer effect of curcumin mediated by down-regulating phosphatase of regenerating liver-3 expression on highly metastatic melanoma cells. Mol Pharmacol; 2009 Dec;76(6):1238-45
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  • [Title] An anticancer effect of curcumin mediated by down-regulating phosphatase of regenerating liver-3 expression on highly metastatic melanoma cells.
  • Phosphatase of regenerating liver-3 (PRL-3) has been suggested as a potential target for anticancer drugs based on its involvement in tumor metastasis.
  • Cells with PRL-3 stably knocked down show less sensitivity to curcumin treatment, which reveals that PRL-3 is the much further upstream target of curcumin.
  • Curcumin treatment also remarkably prevented B16BL6 from invading the draining lymph nodes in the spontaneous metastatic tumor model, which is probably of relevance to PRL-3 down-regulation.
  • Our results reveal a novel capacity of curcumin to down-regulate oncogene PRL-3, raising its possibility in therapeutic regimen against malignant tumor.
  • [MeSH-major] Antineoplastic Agents / pharmacology. Curcumin / pharmacology. Gene Expression Regulation, Neoplastic / drug effects. Immediate-Early Proteins / biosynthesis. Melanoma / enzymology. Protein Tyrosine Phosphatases / biosynthesis
  • [MeSH-minor] Animals. Breast Neoplasms / drug therapy. Breast Neoplasms / enzymology. Cell Line, Tumor. Down-Regulation / drug effects. Female. Humans. Male. Mice. Mice, Inbred C57BL. Neoplasm Metastasis. Neoplasms, Experimental. Prostatic Neoplasms / drug therapy. Prostatic Neoplasms / enzymology. Proto-Oncogene Proteins pp60(c-src) / antagonists & inhibitors. Reverse Transcriptase Polymerase Chain Reaction. STAT3 Transcription Factor / antagonists & inhibitors. Transcription, Genetic / drug effects. Tumor Suppressor Protein p53 / drug effects

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  • (PMID = 19779032.001).
  • [ISSN] 1521-0111
  • [Journal-full-title] Molecular pharmacology
  • [ISO-abbreviation] Mol. Pharmacol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / Immediate-Early Proteins; 0 / Ptp4a3 protein, mouse; 0 / STAT3 Transcription Factor; 0 / Tumor Suppressor Protein p53; EC 2.7.10.2 / Proto-Oncogene Proteins pp60(c-src); EC 3.1.3.48 / Protein Tyrosine Phosphatases; IT942ZTH98 / Curcumin
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6. Suwa D, Konno H, Tanaka T, Urano T: Intraperitoneal infusion of recombinant plasminogen activator inhibitor type 2 induced apoptosis in implanted human colon cancer and inhibited its growth and liver metastasis. Anticancer Res; 2008 Mar-Apr;28(2A):693-8
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  • [Title] Intraperitoneal infusion of recombinant plasminogen activator inhibitor type 2 induced apoptosis in implanted human colon cancer and inhibited its growth and liver metastasis.
  • Antitumor effects of plasminogen activator (PA) inhibitors (PAls) were analyzed in a mouse model of human colon cancer xenografts.
  • Liver metastasis was less frequent in the rPAI-1 (5/19) and rPAI-2-treated groups (1/16) than in the control group (14/15).
  • This may indicate the therapeutic potential of these PAls in malignant patients.
  • [MeSH-major] Apoptosis / drug effects. Colonic Neoplasms / drug therapy. Liver Neoplasms / secondary. Plasminogen Activator Inhibitor 2 / pharmacology
  • [MeSH-minor] Animals. Drug Evaluation. Humans. Infusions, Parenteral. Mice. Mice, Inbred BALB C. Mice, Nude. Recombinant Proteins / pharmacology. Xenograft Model Antitumor Assays

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  • (PMID = 18507009.001).
  • [ISSN] 0250-7005
  • [Journal-full-title] Anticancer research
  • [ISO-abbreviation] Anticancer Res.
  • [Language] eng
  • [Publication-type] Comparative Study; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Greece
  • [Chemical-registry-number] 0 / Plasminogen Activator Inhibitor 2; 0 / Recombinant Proteins
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7. Kizaka-Kondoh S, Itasaka S, Zeng L, Tanaka S, Zhao T, Takahashi Y, Shibuya K, Hirota K, Semenza GL, Hiraoka M: Selective killing of hypoxia-inducible factor-1-active cells improves survival in a mouse model of invasive and metastatic pancreatic cancer. Clin Cancer Res; 2009 May 15;15(10):3433-41
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  • [Title] Selective killing of hypoxia-inducible factor-1-active cells improves survival in a mouse model of invasive and metastatic pancreatic cancer.
  • However, the behavior of the cells having HIF-1 activity during the malignant progression in pancreatic cancer has not been tested.
  • RESULTS: In vivo optical imaging showed that HIF-1 activity proceeded along with local invasion, the peritoneal dissemination, and the liver metastasis.
  • Moreover, selective killing of HIF-1-active hypoxic cells significantly suppressed malignant progression, resulting in a significant improvement in survival rate.
  • CONCLUSIONS: These results show that HIF-1-active cells constitute a large proportion of invading and metastatic cells and suggest that eradication of these cells may improve the outcome in advanced pancreatic cancer, a condition for which no effective therapy currently exists.
  • [MeSH-major] Hypoxia-Inducible Factor 1 / metabolism. Liver Neoplasms / drug therapy. Pancreatic Neoplasms / drug therapy. Recombinant Fusion Proteins / pharmacology
  • [MeSH-minor] Abdominal Cavity / pathology. Amino Acid Sequence. Animals. Caspase 3 / metabolism. Cell Line, Tumor. Disease Progression. Green Fluorescent Proteins / genetics. Green Fluorescent Proteins / metabolism. Humans. Luciferases / genetics. Luciferases / metabolism. Luminescent Measurements / methods. Male. Mice. Mice, Inbred BALB C. Mice, Nude. Molecular Sequence Data. Neoplasm Invasiveness. Oxygen / metabolism. Peritoneum / drug effects. Peritoneum / metabolism. Peritoneum / pathology. Survival Analysis. Transfection. Xenograft Model Antitumor Assays

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  • (PMID = 19417024.001).
  • [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 / Hypoxia-Inducible Factor 1; 0 / Recombinant Fusion Proteins; 0 / TOP3 fusion protein; 147336-22-9 / Green Fluorescent Proteins; EC 1.13.12.- / Luciferases; EC 3.4.22.- / Caspase 3; S88TT14065 / Oxygen
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8. Taper HS, Roberfroid MB: Nontoxic potentiation of cancer chemotherapy by dietary oligofructose or inulin. Nutr Cancer; 2000;38(1):1-5
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  • [Title] Nontoxic potentiation of cancer chemotherapy by dietary oligofructose or inulin.
  • Our previously published results indicated that dietary treatment with oligofructose or inulin inhibited malignant tumor growth in experimental animals.
  • Thus it appeared to be interesting to investigate whether the same treatment could have a positive influence on tumor chemotherapy.
  • The chemotherapy-potentiating effect of 15% oligofructose or inulin incorporated into the basal diet for experimental animals was investigated on a transplantable mouse liver tumor.
  • This dietary adjuvant therapy was started seven days before intraperitoneal transplantation of transplantable liver tumor and was continued until the end of experiments.
  • A single, subtherapeutic dose of six different cytotoxic drugs commonly utilized in treatment of human cancer was intraperitoneally injected 48 hours after tumor transplantation.
  • In all experiments, dietary oligofructose or inulin significantly potentiated the therapeutic effects of six different cytotoxic drugs.
  • Such dietary treatment potentiating cancer chemotherapy could be introduced into classical protocols of human cancer treatment as a new, nontoxic, and easily applicable adjuvant cancer therapy without any supplementary risk for patients.
  • [MeSH-major] Antineoplastic Agents / therapeutic use. Food-Drug Interactions. Inulin / therapeutic use. Liver Neoplasms, Experimental / diet therapy. Liver Neoplasms, Experimental / drug therapy. Oligosaccharides / therapeutic use
  • [MeSH-minor] Animal Feed. Animals. Dietary Supplements. Injections, Intraperitoneal. Male. Mice. Mice, Inbred Strains. Neoplasm Transplantation. Treatment Outcome

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  • (PMID = 11341034.001).
  • [ISSN] 0163-5581
  • [Journal-full-title] Nutrition and cancer
  • [ISO-abbreviation] Nutr Cancer
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / Oligosaccharides; 0 / oligofructose; 9005-80-5 / Inulin
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9. Jansen B, Wacheck V, Heere-Ress E, Schlagbauer-Wadl H, Hoeller C, Lucas T, Hoermann M, Hollenstein U, Wolff K, Pehamberger H: Chemosensitisation of malignant melanoma by BCL2 antisense therapy. Lancet; 2000 Nov 18;356(9243):1728-33
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  • [Title] Chemosensitisation of malignant melanoma by BCL2 antisense therapy.
  • BACKGROUND: Chemoresistance of malignant melanoma has been linked to expression of the proto-oncogene BCL2.
  • Antisense oligonucleotides (ASO) targeted against BCL2 mRNA decreased BCL2 protein concentrations, increased tumour-cell apoptosis, and led to tumour responses in a mouse xenotransplantation model when combined with systemic dacarbazine.
  • This phase I-II clinical study investigated the combination of BCL2 ASO (augmerosen, Genasense, G3139) and dacarbazine in patients with advanced malignant melanoma expressing BCL2.
  • METHODS: In a within-patient dose-escalation protocol, 14 patients with advanced malignant melanoma were given augmerosen intravenously or subcutaneously in daily doses of 0.6-6.5 mg/kg plus standard dacarbazine treatment (total doses up to 1000 mg/m2 per cycle).
  • Four patients had liver-function abnormalities that resolved within 1 week.
  • By day 5, daily doses of 1.7 mg/kg and higher led to a median 40% decrease in BCL2 protein in melanoma samples compared with baseline, concomitantly with increased tumour-cell apoptosis, which was greatly increased after dacarbazine treatment.
  • Such downregulation of BCL2, combined with standard anticancer therapy, offers a new approach to the treatment of patients with resistant neoplasms.
  • [MeSH-major] DNA, Antisense / therapeutic use. Melanoma / drug therapy. Proto-Oncogene Proteins c-bcl-2 / antagonists & inhibitors
  • [MeSH-minor] Adult. Aged. Aged, 80 and over. Antineoplastic Agents, Alkylating / adverse effects. Antineoplastic Agents, Alkylating / therapeutic use. Dacarbazine / adverse effects. Dacarbazine / therapeutic use. Dose-Response Relationship, Drug. Drug Therapy, Combination. Female. Fever / chemically induced. Follow-Up Studies. Hematologic Diseases / chemically induced. Humans. Male. Middle Aged. Skin / drug effects. Skin / pathology. Skin Neoplasms / prevention & control. Skin Neoplasms / secondary. Survival Analysis. Treatment Outcome

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  • (PMID = 11095261.001).
  • [ISSN] 0140-6736
  • [Journal-full-title] Lancet (London, England)
  • [ISO-abbreviation] Lancet
  • [Language] eng
  • [Publication-type] Clinical Trial; Clinical Trial, Phase I; Clinical Trial, Phase II; Controlled Clinical Trial; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] ENGLAND
  • [Chemical-registry-number] 0 / Antineoplastic Agents, Alkylating; 0 / DNA, Antisense; 0 / Proto-Oncogene Proteins c-bcl-2; 7GR28W0FJI / Dacarbazine
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10. Kasuya T, Jung J, Kadoya H, Matsuzaki T, Tatematsu K, Okajima T, Miyoshi E, Tanizawa K, Kuroda S: In vivo delivery of bionanocapsules displaying Phaseolus vulgaris agglutinin-L4 isolectin to malignant tumors overexpressing N-acetylglucosaminyltransferase V. Hum Gene Ther; 2008 Sep;19(9):887-95
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  • [Title] In vivo delivery of bionanocapsules displaying Phaseolus vulgaris agglutinin-L4 isolectin to malignant tumors overexpressing N-acetylglucosaminyltransferase V.
  • Metastasis is a key aspect of tumor malignancy, and several malignant tumors show expression of various mature N-type glycans.
  • Bionanocapsules (BNCs), hollow particles with a diameter of approximately 80 nm and composed of hepatitis B surface antigen (HBsAg) and a lipid bilayer, have been developed as human liver-specific nanocapsules for in vivo drug delivery system.
  • In this study, we have generated L(4)-PHA-displaying BNCs (PHA-BNCs) and examined whether L(4)-PHA could retarget the BNCs to malignant tumors as a "biosensor" distinguishing tumor metastaticity.
  • Fluorescence-labeled PHA-BNCs injected systemically into a mouse xenograft model were found to accumulate in beta1-6 GlcNAc-expressing malignant tumors.
  • The PHA-BNCs were able to deliver DNA to the malignant cancer cells.
  • These results open up the possibility of using L(4)-PHA lectin as a targeting molecule in a drug delivery system, and of using PHA-BNCs as a novel nanodevice for malignant tumor-specific bioimaging and drug delivery.
  • [MeSH-major] Neoplasms / diagnosis. Neoplasms / drug therapy. Phytohemagglutinins / administration & dosage
  • [MeSH-minor] Animals. Cell Line, Tumor. DNA, Recombinant / administration & dosage. DNA, Recombinant / genetics. Drug Delivery Systems. Genetic Therapy / methods. Humans. Liver Neoplasms, Experimental / diagnosis. Liver Neoplasms, Experimental / drug therapy. Liver Neoplasms, Experimental / secondary. Male. Mice. Mice, Nude. N-Acetylglucosaminyltransferases / metabolism. Nanocapsules. Neoplasm Transplantation. Phaseolus. Phytotherapy. Transplantation, Heterologous

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  • (PMID = 18717644.001).
  • [ISSN] 1557-7422
  • [Journal-full-title] Human gene therapy
  • [ISO-abbreviation] Hum. Gene Ther.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / DNA, Recombinant; 0 / Nanocapsules; 0 / Phytohemagglutinins; EC 2.4.1.- / N-Acetylglucosaminyltransferases; EC 2.4.1.155 / alpha-1,6-mannosylglycoprotein beta 1,6-N-acetylglucosaminyltransferase
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11. Yoshiji H, Kuriyama S, Hicklin DJ, Huber J, Yoshii J, Ikenaka Y, Noguchi R, Nakatani T, Tsujinoue H, Fukui H: The vascular endothelial growth factor receptor KDR/Flk-1 is a major regulator of malignant ascites formation in the mouse hepatocellular carcinoma model. Hepatology; 2001 Apr;33(4):841-7
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  • [Title] The vascular endothelial growth factor receptor KDR/Flk-1 is a major regulator of malignant ascites formation in the mouse hepatocellular carcinoma model.
  • The vascular endothelial growth factor-A (VEGF-A), also known as the vascular permeability factor (VPF), has been shown to play an important role in malignant ascites formation.
  • The effects of VEGF-A are mediated through flt-1 and kinase insert domain-containing receptor/fetal liver kinase (KDR/Flk-1) receptors.
  • In this study, we examined the role of KDR/Flk-1 in the murine MH134 hepatic malignant ascites formation by means of VEGF-A- and KDR/Flk-1-specific neutralizing antibodies (VEGF-A nAb and KDR/Flk-1 nAb, respectively).
  • The mean volume of ascites, number of tumor cells in ascites, and the peritoneal capillary permeability were significantly suppressed by VEGF-A nAb and KDR/Flk-1 nAb treatment.
  • The autophosphorylation of KDR/ Flk-1 in the peritoneal wall was almost completely abolished by KDR/ Flk-1 nAb, whereas a certain level of activation was still shown by VEGF-A nAb treatment.
  • Furthermore, in the therapeutic experiment, although both VEGF-A nAb and KDR/Flk-1 nAb prolonged the survival rate of ascites-bearing mice, the latter showed a more significant impact on the survival of animals.
  • These results suggest that KDR/Flk-1 is a major regulator of malignant hepatic ascites formation, and that in addition to VEGF-A, VEGF-C may also be involved in the malignant ascites formation via KDR/ Flk-1 activation.
  • [MeSH-major] Ascites / etiology. Carcinoma, Hepatocellular / complications. Liver Neoplasms / complications. Receptor Protein-Tyrosine Kinases / physiology. Receptors, Growth Factor / physiology
  • [MeSH-minor] Animals. Antibodies / pharmacology. Antibodies / therapeutic use. Capillary Permeability / drug effects. Cell Division / drug effects. Endothelial Growth Factors / immunology. Endothelial Growth Factors / metabolism. Mice. Mice, Inbred C3H. Peritoneum / blood supply. Peritonitis / drug therapy. Peritonitis / etiology. Receptors, Vascular Endothelial Growth Factor. Tumor Cells, Cultured. Vascular Endothelial Growth Factor A. Vascular Endothelial Growth Factor C

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  • (PMID = 11283848.001).
  • [ISSN] 0270-9139
  • [Journal-full-title] Hepatology (Baltimore, Md.)
  • [ISO-abbreviation] Hepatology
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antibodies; 0 / Endothelial Growth Factors; 0 / Receptors, Growth Factor; 0 / Vascular Endothelial Growth Factor A; 0 / Vascular Endothelial Growth Factor C; EC 2.7.10.1 / Receptor Protein-Tyrosine Kinases; EC 2.7.10.1 / Receptors, Vascular Endothelial Growth Factor
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12. Speicher T, Foehrenbacher A, Pochic I, Weiland T, Wendel A: Malignant but not naïve hepatocytes of human and rodent origin are killed by TNF after metabolic depletion of ATP by fructose. J Hepatol; 2010 Nov;53(5):896-902
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  • [Title] Malignant but not naïve hepatocytes of human and rodent origin are killed by TNF after metabolic depletion of ATP by fructose.
  • BACKGROUND & AIMS: TNF was the first cytokine employed for cancer therapy, but its use was limited due to its insufficient selectivity towards malignant cells.
  • Fructose induces transient hepatic ATP depletion in humans and rodents due to the liver-specific fructose metabolism via fructokinase, while other cells e.g.
  • Our aim was to identify metabolic differences between normal and malignant liver cells that can be exploited for selective immunotherapy.
  • RESULTS: Primary mouse, rat and human hepatocytes depleted of ATP by fructose were fully protected against TNF-induced cytotoxicity.
  • CONCLUSION: Increased expression of HKII in malignant cells of hepatic origin shifts the fructose metabolism from liver- to muscle-type, thereby preventing ATP depletion and subsequent cytoprotection of the target cells.
  • Therefore, healthy liver cells are transiently protected from TNF-mediated cell death by fructose-induced ATP depletion, while malignant cells can be selectively eliminated through TNF-induced apoptosis.
  • [MeSH-major] Adenosine Triphosphate / metabolism. Fructose / pharmacology. Hepatocytes / drug effects. Liver Neoplasms / pathology. Tumor Necrosis Factor-alpha / pharmacology
  • [MeSH-minor] Animals. Apoptosis / drug effects. Cells, Cultured. Cytoprotection. Fructokinases / physiology. Fructose-Bisphosphate Aldolase / physiology. Hexokinase / genetics. Humans. Hypoxia-Inducible Factor 1, alpha Subunit / physiology. Mice. Rats

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  • [Copyright] Copyright © 2010. Published by Elsevier B.V.
  • (PMID = 20800309.001).
  • [ISSN] 1600-0641
  • [Journal-full-title] Journal of hepatology
  • [ISO-abbreviation] J. Hepatol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / HIF1A protein, human; 0 / Hypoxia-Inducible Factor 1, alpha Subunit; 0 / Tumor Necrosis Factor-alpha; 30237-26-4 / Fructose; 8L70Q75FXE / Adenosine Triphosphate; EC 2.7.1.- / Fructokinases; EC 2.7.1.1 / Hexokinase; EC 2.7.1.4 / fructokinase; EC 4.1.2.13 / Fructose-Bisphosphate Aldolase
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13. Trosko JE, Chang CC: Mechanism of up-regulated gap junctional intercellular communication during chemoprevention and chemotherapy of cancer. Mutat Res; 2001 Sep 1;480-481:219-29
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Mechanism of up-regulated gap junctional intercellular communication during chemoprevention and chemotherapy of cancer.
  • Antitumor promoters (retinoids, carotenoids, green tea components) and antioncogene drugs (i.e. lovastatin) can up-regulate GJIC.
  • Recently, a specific connexin knockout mouse was shown to have a higher frequency of spontaneous and induced liver cancers.
  • Multiple mechanisms of up- or down-regulation of GJIC exist, as well as multiple types of pre-malignant and malignant tumor cells that are unable able to have functional GJIC.
  • Alteration of gene expression at the transcriptional, translational or post-translational levels would require specific dietary prevention or treatment of cancer.
  • In conclusion, if dietary prevention or treatment of cancer is to occur, it must ameliorate the growth-stimulatory effects, above threshold levels, of chemicals, growth factors or hormones, that trigger various mitogenic/antiapoptotic signal transducing systems that block GJIC.
  • [MeSH-major] Cell Communication. Gap Junctions / metabolism. Neoplasms / drug therapy. Neoplasms / prevention & control. Up-Regulation
  • [MeSH-minor] Animals. Anticarcinogenic Agents / therapeutic use. Antineoplastic Agents / therapeutic use. Cell Lineage / genetics. Cell Transformation, Neoplastic / genetics. Chemoprevention. Homeostasis. Humans. Stem Cells / cytology. Stem Cells / pathology


14. Ripoll GV, Garona J, Hermo GA, Gomez DE, Alonso DF: Effects of the synthetic vasopressin analog desmopressin in a mouse model of colon cancer. Anticancer Res; 2010 Dec;30(12):5049-54

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Effects of the synthetic vasopressin analog desmopressin in a mouse model of colon cancer.
  • Here we explored the antitumor effects of DDAVP in cultured colon carcinoma cells and in a syngeneic Balb/c mouse model.
  • Both human Colo-205 and mouse CT-26 colon carcinoma cell lines expressed the V2 receptor, as revealed by immunofluorescence.
  • Perioperative administration of DDAVP significantly inhibited tumor progression in animals surgically implanted in the spleen with CT-26 cells, and caused some reduction in liver metastasis.
  • Although DDAVP and 5-fluorouracil demonstrated additive cytostatic effects in vitro, no antitumor effects were observed in this study in mice receiving a single cycle of chemotherapy (25 mg/kg) in combination with the peptide.
  • Our data suggest that DDAVP may be potentially used to minimize spread or survival of residual malignant cells during surgical procedures for colon and other gastrointestinal tumors.
  • [MeSH-major] Colonic Neoplasms / drug therapy. Deamino Arginine Vasopressin / pharmacology

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  • (PMID = 21187489.001).
  • [ISSN] 1791-7530
  • [Journal-full-title] Anticancer research
  • [ISO-abbreviation] Anticancer Res.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Greece
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / Receptors, Vasopressin; ENR1LLB0FP / Deamino Arginine Vasopressin
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15. Sebastian M, Kiewe P, Schuette W, Brust D, Peschel C, Schneller F, Rühle KH, Nilius G, Ewert R, Lodziewski S, Passlick B, Sienel W, Wiewrodt R, Jäger M, Lindhofer H, Friccius-Quecke H, Schmittel A: Treatment of malignant pleural effusion with the trifunctional antibody catumaxomab (Removab) (anti-EpCAM x Anti-CD3): results of a phase 1/2 study. J Immunother; 2009 Feb-Mar;32(2):195-202
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  • [Title] Treatment of malignant pleural effusion with the trifunctional antibody catumaxomab (Removab) (anti-EpCAM x Anti-CD3): results of a phase 1/2 study.
  • Catumaxomab is a trifunctional monoclonal antibody consisting of a mouse immunoglobulin G2a part and a rat immunoglobulin G2b part with 2 different antigen binding sites binding the epithelial cell adhesion molecule antigen on tumor cells and CD3 on T lymphocytes.
  • As catumaxomab demonstrated efficacy in patients with malignant ascites, we performed this phase 1/2 trial in patients with malignant pleural effusion (MPE).
  • Most frequent adverse events were pyrexia, elevated liver enzymes, nausea, and decreased lymphocytes.
  • Five patients with breast cancer out of 7 evaluable patients had a response to treatment.
  • Intrapleural administration of catumaxomab is feasible although the substantial number of drop-outs and deaths in short proximity to study treatment raise questions whether MPE is the right indication for catumaxomab or whether the patient population should be defined different.
  • [MeSH-major] Antibodies, Bispecific / therapeutic use. Pleural Effusion, Malignant / therapy
  • [MeSH-minor] Adult. Aged. Animals. Cell Proliferation / drug effects. Cytokines / drug effects. Cytokines / immunology. Female. Humans. Male. Mice. Middle Aged. Neoplasms / complications. Rats. Treatment Outcome

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  • (PMID = 19238019.001).
  • [ISSN] 1537-4513
  • [Journal-full-title] Journal of immunotherapy (Hagerstown, Md. : 1997)
  • [ISO-abbreviation] J. Immunother.
  • [Language] eng
  • [Publication-type] Clinical Trial, Phase I; Clinical Trial, Phase II; Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antibodies, Bispecific; 0 / Cytokines; 0 / catumaxomab
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16. Nanni P, Nicoletti G, Landuzzi L, Croci S, Murgo A, Palladini A, Antognoli A, Ianzano ML, Stivani V, Grosso V, Maira SM, García-Echeverría C, Scotlandi K, De Giovanni C, Lollini PL: High metastatic efficiency of human sarcoma cells in Rag2/gammac double knockout mice provides a powerful test system for antimetastatic targeted therapy. Eur J Cancer; 2010 Feb;46(3):659-68
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] High metastatic efficiency of human sarcoma cells in Rag2/gammac double knockout mice provides a powerful test system for antimetastatic targeted therapy.
  • We studied whether a genetically modified mouse host lacking T, B and NK immunity allowed an improved expression of the metastatic phenotype of malignant human tumours.
  • Rag2(-/-);gammac(-/-) mice receiving intravenous (i.v.) or subcutaneous (s.c.) human sarcoma cell lines developed extensive multiorgan metastases.
  • Most human sarcomas metastasised in the liver of Rag2(-/-);gammac(-/-) mice, a kind of organ preference undetectable in nude mice and specific of sarcomas, as several carcinoma cell lines failed to colonise the liver of Rag2(-/-);gammac(-/-) mice, independently of their metastatic spread to other sites.
  • In vitro analysis of the molecular mechanisms of liver metastasis of sarcomas implicated liver-produced growth and motility factors, in particular the insulin-like growth factor (IGF) axis.
  • NVP-BEZ235, a specific inhibitor of downstream signal transduction targeting PI3K and mTOR, strongly inhibited liver metastasis of human sarcoma cells.
  • In conclusion, the Rag2(-/-);gammac(-/-) mouse model allowed the expression of human metastatic phenotypes inapparent in conventional immunodeficient mice and the preclinical testing of appropriate targeted therapies.
  • [MeSH-minor] Animals. Antineoplastic Agents / therapeutic use. Chemotaxis / immunology. Culture Media, Conditioned. Enzyme Inhibitors / therapeutic use. Female. Humans. Imidazoles / therapeutic use. Immune Tolerance. Liver Neoplasms / drug therapy. Liver Neoplasms / immunology. Liver Neoplasms / pathology. Liver Neoplasms / secondary. Lung Neoplasms / immunology. Lung Neoplasms / pathology. Lung Neoplasms / secondary. Mice. Mice, Knockout. Neoplasm Transplantation. Phosphatidylinositol 3-Kinases / antagonists & inhibitors. Quinolines / therapeutic use. Transplantation, Heterologous. Treatment Outcome. Tumor Cells, Cultured. Xenograft Model Antitumor Assays / methods

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  • [Copyright] Copyright (c) 2009 Elsevier Ltd. All rights reserved.
  • (PMID = 20031388.001).
  • [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 / Culture Media, Conditioned; 0 / DNA-Binding Proteins; 0 / Enzyme Inhibitors; 0 / Imidazoles; 0 / Quinolines; 0 / Rag2 protein, mouse; EC 2.7.1.- / Phosphatidylinositol 3-Kinases; RUJ6Z9Y0DT / dactolisib
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17. Wang CH, Shen YC, Hsieh JJ, Yeh KY, Chang JW: Clodronate alleviates cachexia and prolongs survival in nude mice xenografted with an anaplastic thyroid carcinoma cell line. J Endocrinol; 2006 Aug;190(2):415-23
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  • Cancer cachexia is one of the most common manifestations of advanced malignant disease and is frequently associated with decreased survival.
  • Previously, we reported the establishment of a new anaplastic thyroid carcinoma cell line, Thena, and its mouse xenograft, Thena-Nu, which induced cachexia in athymic nude mice.
  • Subsequent studies showed that the addition of clodronate to Thena-Nu cultures reduced cell proliferation as well as cytokine production in a dose- and time-dependent manner.
  • Liver necrosis, observed in tumor-bearing mice, was also improved following clodronate treatment.
  • Discontinuation of clodronate treatment, however, resulted in progressive tumor growth and weight loss.
  • Our results demonstrated that clodronate could exert therapeutic efficacy on amelioration of cancer cachexia in the hosts.
  • Nevertheless, this study also points out that a longer period of treatment is required to maintain these effects.
  • [MeSH-major] Cachexia / drug therapy. Carcinoma / drug therapy. Clodronic Acid / therapeutic use. Diphosphonates / therapeutic use. Thyroid Neoplasms / drug therapy
  • [MeSH-minor] Animals. Apoptosis. Cell Line, Tumor. Cell Proliferation / drug effects. Enzyme-Linked Immunosorbent Assay / methods. Granulocyte Colony-Stimulating Factor / analysis. Interleukin-6 / analysis. Leukemia Inhibitory Factor. Liver / pathology. Mice. Mice, Inbred BALB C. Mice, Nude. Necrosis. Neoplasm Transplantation. Transplantation, Heterologous. Tumor Necrosis Factor-alpha / analysis

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  • (PMID = 16899574.001).
  • [ISSN] 0022-0795
  • [Journal-full-title] The Journal of endocrinology
  • [ISO-abbreviation] J. Endocrinol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Diphosphonates; 0 / Interleukin-6; 0 / Leukemia Inhibitory Factor; 0 / Lif protein, mouse; 0 / Tumor Necrosis Factor-alpha; 0813BZ6866 / Clodronic Acid; 143011-72-7 / Granulocyte Colony-Stimulating Factor
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18. Hall WA, Vallera DA: Efficacy of antiangiogenic targeted toxins against glioblastoma multiforme. Neurosurg Focus; 2006;20(4):E23
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • OBJECT: Because the prognosis for patients with glioblastoma multiforme (GBM) remains poor, investigators have focused on developing new and more effective treatment modalities.
  • Targeted toxins represent a new class of compounds composed of a potent protein toxin and a carrier ligand that will recognize cell surface antigens located on target tissue.
  • This diptheria toxin-uPA fusion protein (DTAT) has the advantage over other fusion proteins of targeting malignant glioma cells and the endothelial cells of the neovasculature that express the urokinase-type plasminogen activator receptor (uPAR).
  • Tumor volume was assessed over time and analyzed using the Student t-test.
  • Both DTAT and DTAT13 had little effect on histological findings in the liver, kidney, spleen, and lungs.
  • Serum analysis did not demonstrate an effect on blood urea nitrogen levels, but liver alanine aminotransferase levels rose to statistically significant (p = 0.046) but not life-threatening levels.
  • [MeSH-major] Angiogenesis Inhibitors / therapeutic use. Antineoplastic Agents / therapeutic use. Brain Neoplasms / drug therapy. Cytotoxins / therapeutic use. Glioblastoma / drug therapy. Neovascularization, Pathologic / drug therapy. Oncogene Proteins, Fusion / therapeutic use. Recombinant Fusion Proteins / pharmacology. Recombinant Fusion Proteins / therapeutic use
  • [MeSH-minor] Animals. Bacterial Toxins / pharmacology. Bacterial Toxins / therapeutic use. Cell Line, Tumor. Cell Proliferation / drug effects. Disease Models, Animal. Female. Humans. Interleukin-13 Receptor alpha1 Subunit. Liver / drug effects. Liver / enzymology. Mice. Mice, Inbred C57BL. Mice, Nude. Molecular Weight. Receptors, Cell Surface / drug effects. Receptors, Cell Surface / metabolism. Receptors, Interleukin / drug effects. Receptors, Interleukin / metabolism. Receptors, Interleukin-13. Receptors, Urokinase Plasminogen Activator. Treatment Outcome. Urokinase-Type Plasminogen Activator / chemistry

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  • (PMID = 16709029.001).
  • [ISSN] 1092-0684
  • [Journal-full-title] Neurosurgical focus
  • [ISO-abbreviation] Neurosurg Focus
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Angiogenesis Inhibitors; 0 / Antineoplastic Agents; 0 / Bacterial Toxins; 0 / Cytotoxins; 0 / DTAT13 protein; 0 / IL13RA1 protein, human; 0 / Il13ra1 protein, mouse; 0 / Interleukin-13 Receptor alpha1 Subunit; 0 / Oncogene Proteins, Fusion; 0 / PLAUR protein, human; 0 / Plaur protein, mouse; 0 / Receptors, Cell Surface; 0 / Receptors, Interleukin; 0 / Receptors, Interleukin-13; 0 / Receptors, Urokinase Plasminogen Activator; 0 / Recombinant Fusion Proteins; 0 / diphtheria toxin-urokinase fusion protein, human; EC 3.4.21.73 / Urokinase-Type Plasminogen Activator
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19. Jia L, Wang S, Zhou H, Cao J, Hu Y, Zhang J: Caveolin-1 up-regulates CD147 glycosylation and the invasive capability of murine hepatocarcinoma cell lines. Int J Biochem Cell Biol; 2006;38(9):1584-93

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • CD147 which is a regulator of matrix metalloproteinase (MMP) production on the surface of many malignant tumor cells, shows a highly specific association with caveolin-1 (Cav-1).
  • This study investigated the possible role of Cav-1 in CD147 glycosylation in the HcaF, HcaP and Hepa1-6 mouse hepatocarcinoma cell lines, which have high, low and no metastatic potential in the lymph nodes, respectively, and in the normal mouse liver cell line IAR-20.
  • Cav-1 is therefore proposed to act as both an oncogene and a tumor suppressor gene, and could represent a new potential target for gene therapy.
  • [MeSH-minor] Animals. Cell Line, Tumor. Glycosylation / drug effects. Liver Neoplasms, Experimental. Matrix Metalloproteinase 11. Metalloendopeptidases / biosynthesis. Mice. Up-Regulation

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  • (PMID = 16702020.001).
  • [ISSN] 1357-2725
  • [Journal-full-title] The international journal of biochemistry & cell biology
  • [ISO-abbreviation] Int. J. Biochem. Cell Biol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Caveolin 1; 136894-56-9 / Antigens, CD147; EC 3.4.24.- / Matrix Metalloproteinase 11; EC 3.4.24.- / Metalloendopeptidases
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20. Cambien B, Karimdjee BF, Richard-Fiardo P, Bziouech H, Barthel R, Millet MA, Martini V, Birnbaum D, Scoazec JY, Abello J, Al Saati T, Johnson MG, Sullivan TJ, Medina JC, Collins TL, Schmid-Alliana A, Schmid-Antomarchi H: Organ-specific inhibition of metastatic colon carcinoma by CXCR3 antagonism. Br J Cancer; 2009 Jun 2;100(11):1755-64

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • Liver and lung metastases are the predominant cause of colorectal cancer (CRC)-related mortality.
  • Recent research has indicated that CXCR3/chemokines interactions that orchestrate haematopoetic cell movement are implicated in the metastatic process of malignant tumours, including that of CRC cells to lymph nodes.
  • To date, however, the contribution of CXCR3 to liver and lung metastasis in CRC has not been addressed.
  • To determine whether CXCR3 receptors regulate malignancy-related properties of CRC cells, we have used CXCR3-expressing CRC cell lines of human (HT29 cells) and murine (C26 cells) origins that enable the development of liver and lung metastases when injected into immunodeficient and immunocompetent mice, respectively, and assessed the effect of CXCR3 blockade using AMG487, a small molecular weight antagonist.
  • In vitro, activation of CXCR3 on human and mouse CRC cells by its cognate ligands induced migratory and growth responses, both activities being abrogated by AMG487.
  • In vivo, systemic CXCR3 antagonism by preventive or curative treatments with AMG487 markedly inhibited the implantation and the growth of human and mouse CRC cells within lung without affecting that in the liver.
  • In addition, we measured increased levels of CXCR3 and ligands expression within lung nodules compared with liver tumours.
  • Altogether, our findings indicate that activation of CXCR3 receptors by its cognate ligands facilitates the implantation and the progression of CRC cells within lung tissues and that inhibition of this axis decreases pulmonary metastasis of CRC in two murine tumour models.
  • [MeSH-major] Colonic Neoplasms / metabolism. Colonic Neoplasms / pathology. Receptors, CXCR3 / antagonists & inhibitors
  • [MeSH-minor] Animals. Antineoplastic Agents / therapeutic use. Cell Line, Tumor. Cell Movement. Humans. Ligands. Liver Neoplasms / drug therapy. Liver Neoplasms / metabolism. Liver Neoplasms / secondary. Lung Neoplasms / drug therapy. Lung Neoplasms / metabolism. Lung Neoplasms / secondary. Mice. Neoplasm Transplantation. Organ Specificity. Survival Rate

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  • (PMID = 19436305.001).
  • [ISSN] 1532-1827
  • [Journal-full-title] British journal of cancer
  • [ISO-abbreviation] Br. 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 / Ligands; 0 / Receptors, CXCR3
  • [Other-IDs] NLM/ PMC2695685
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21. Soloman R, Gabizon AA: Clinical pharmacology of liposomal anthracyclines: focus on pegylated liposomal Doxorubicin. Clin Lymphoma Myeloma; 2008 Feb;8(1):21-32
Hazardous Substances Data Bank. DOXORUBICIN .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • Pegylated liposomal doxorubicin (PLD) is a liposomal formulation with a distinct pharmacokinetic profile characterized by an extended circulation time and a reduced volume of distribution.
  • Biodistribution animal studies indicate preferential accumulation of PLD into various implanted mouse-human tumors, with an enhancement of liposomal drug tumor levels compared with free drugs.
  • The extended circulation time of pegylated liposomes and their ability to extravasate through the leaky vasculature of tumors results in the enhanced delivery of liposomal drug and/or radiotracers to the tumor site in patients with cancer.
  • In malignant effusions, Kaposi sarcoma skin lesions, and a variety of solid tumors there is evidence of selective tumor uptake detected by various methods.
  • [MeSH-major] Doxorubicin / analogs & derivatives. Neoplasms / drug therapy. Polyethylene Glycols / therapeutic use
  • [MeSH-minor] Animals. Capillary Permeability / drug effects. Heart / drug effects. Humans. Liver / drug effects. Mononuclear Phagocyte System / metabolism. Mucositis / chemically induced. Protein Binding. Skin / drug effects

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  • (PMID = 18501085.001).
  • [ISSN] 1557-9190
  • [Journal-full-title] Clinical lymphoma & myeloma
  • [ISO-abbreviation] Clin Lymphoma Myeloma
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / liposomal doxorubicin; 30IQX730WE / Polyethylene Glycols; 80168379AG / Doxorubicin
  • [Number-of-references] 95
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22. Katz MH, Bouvet M, Takimoto S, Spivack D, Moossa AR, Hoffman RM: Selective antimetastatic activity of cytosine analog CS-682 in a red fluorescent protein orthotopic model of pancreatic cancer. Cancer Res; 2003 Sep 1;63(17):5521-5
The Lens. Cited by Patents in .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • -administered cytosine analogue, CS-682, to effectively prolong survival and inhibit metastatic growth in an imageable orthotopic mouse model of pancreatic cancer.
  • Tumor RFP fluorescence facilitated real-time, sequential imaging, and quantification of primary and metastatic growth and dissemination in vivo.
  • Mice were treated with various p.o. doses of CS-682 on a five times per week schedule until death.
  • CS-682 also decreased the development of malignant ascites and the formation of metastases, which were reduced significantly in number in the diaphragm, lymph nodes, liver, and kidney.
  • Selective RFP tumor fluorescence enabled noninvasive real-time comparison between groups during treatment and facilitated identification of micrometastases in solid organs at autopsy.
  • [MeSH-major] Arabinonucleosides / pharmacology. Cytosine / analogs & derivatives. Cytosine / pharmacology. Luminescent Proteins / metabolism. Pancreatic Neoplasms / drug therapy
  • [MeSH-minor] Animals. Cell Division / drug effects. Cell Division / physiology. Humans. Male. Mice. Mice, Nude. Microscopy, Fluorescence. Neoplasm Metastasis. Transduction, Genetic. Tumor Cells, Cultured. Weight Loss / drug effects. Xenograft Model Antitumor Assays

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  • (PMID = 14500389.001).
  • [ISSN] 0008-5472
  • [Journal-full-title] Cancer research
  • [ISO-abbreviation] Cancer Res.
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / P30 CA23100-1851
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't; Research Support, U.S. Gov't, P.H.S.
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Arabinonucleosides; 0 / Luminescent Proteins; 0 / red fluorescent protein; 0 / sapacitabine; 8J337D1HZY / Cytosine
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23. Suppasansatorn P, Wang G, Conway BR, Wang W, Wang Y: Skin delivery potency and antitumor activities of temozolomide ester prodrugs. Cancer Lett; 2006 Nov 28;244(1):42-52
Hazardous Substances Data Bank. DACARBAZINE .

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  • Clinical trials have shown temozolomide to be an effective agent for treatment of malignant melanoma.
  • Topical application of 5% (w/v) hexyl ester in DMSO solution on a mouse model demonstrated a significant inhibition of tumor growth.
  • These results suggest that temozolomide esters could be an effective alternative to temozolomide in the treatment of skin cancer.
  • [MeSH-major] Antineoplastic Agents, Alkylating / therapeutic use. Dacarbazine / analogs & derivatives. Drug Delivery Systems. Prodrugs / therapeutic use. Skin / drug effects. Skin Neoplasms / drug therapy
  • [MeSH-minor] Administration, Cutaneous. Animals. Cell Membrane Permeability. Cell Proliferation / drug effects. Esterases / metabolism. Esters / chemistry. Humans. Liver / enzymology. Melanoma / drug therapy. Mice. Mice, Inbred BALB C. Mice, Nude. Rats. Swine. Tumor Cells, Cultured / drug effects

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  • (PMID = 16412562.001).
  • [ISSN] 0304-3835
  • [Journal-full-title] Cancer letters
  • [ISO-abbreviation] Cancer Lett.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Ireland
  • [Chemical-registry-number] 0 / Antineoplastic Agents, Alkylating; 0 / Esters; 0 / Prodrugs; 7GR28W0FJI / Dacarbazine; 85622-93-1 / temozolomide; EC 3.1.- / Esterases
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24. Blanquicett C, Gillespie GY, Nabors LB, Miller CR, Bharara S, Buchsbaum DJ, Diasio RB, Johnson MR: Induction of thymidine phosphorylase in both irradiated and shielded, contralateral human U87MG glioma xenografts: implications for a dual modality treatment using capecitabine and irradiation. Mol Cancer Ther; 2002 Oct;1(12):1139-45
SciCrunch. DrugBank: Data: Chemical .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Induction of thymidine phosphorylase in both irradiated and shielded, contralateral human U87MG glioma xenografts: implications for a dual modality treatment using capecitabine and irradiation.
  • In the United States, tumors of the central nervous system remain the third leading cancer-related cause of death in young adults with a median survival time of < 1 year.
  • A recent case study suggested that Capecitabine (a novel, fluoropyrimidine prodrug) may be effective in the treatment of brain metastases.
  • Pharmacogenomic studies have correlated the antitumor response to Capecitabine with the expression of the drug metabolizing enzymes thymidine phosphorylase (TP) and dihydropyrimidine dehydrogenase (DPD).
  • In the current study, we examined TP and DPD expression in normal human brain tissues and in glioblastoma multiforme, the most common and malignant type of brain tumor.
  • Expression levels were determined using real-time quantitative PCR as described previously.
  • TP mRNA levels in normal mouse liver were unaltered, suggesting a tumor-associated effect.
  • The tumor-associated induction of TP in irradiated and lead-shielded tumors within the same animal may have significant implications for the combined modality treatment of cancer patients with Capecitabine in conjunction with radiotherapy and may apply to the treatment of distant tumors and or metastatic disease.
  • [MeSH-major] Deoxycytidine / analogs & derivatives. Deoxycytidine / pharmacology. Neoplasms / drug therapy. Neoplasms / radiotherapy. Thymidine Phosphorylase / metabolism
  • [MeSH-minor] Animals. Antineoplastic Agents / pharmacology. Brain / metabolism. Brain / pathology. Brain Neoplasms / metabolism. Capecitabine. Combined Modality Therapy. Cytokines / biosynthesis. Dihydrouracil Dehydrogenase (NADP). Fluorouracil / analogs & derivatives. Glioblastoma / metabolism. Humans. Interferon-gamma / pharmacology. Liver / pathology. Mice. Mice, Nude. Neoplasm Transplantation. Oxidoreductases / metabolism. RNA / metabolism. RNA, Messenger / metabolism. Reverse Transcriptase Polymerase Chain Reaction. Time Factors. Tumor Cells, Cultured. Tumor Necrosis Factor-alpha / metabolism

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  • (PMID = 12481438.001).
  • [ISSN] 1535-7163
  • [Journal-full-title] Molecular cancer therapeutics
  • [ISO-abbreviation] Mol. Cancer Ther.
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / CA85381
  • [Publication-type] Journal Article; Research Support, U.S. Gov't, P.H.S.
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / Cytokines; 0 / RNA, Messenger; 0 / Tumor Necrosis Factor-alpha; 0W860991D6 / Deoxycytidine; 63231-63-0 / RNA; 6804DJ8Z9U / Capecitabine; 82115-62-6 / Interferon-gamma; EC 1.- / Oxidoreductases; EC 1.3.1.2 / Dihydrouracil Dehydrogenase (NADP); EC 2.4.2.4 / Thymidine Phosphorylase; U3P01618RT / Fluorouracil
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25. Haas BR, Sontheimer H: Inhibition of the Sodium-Potassium-Chloride Cotransporter Isoform-1 reduces glioma invasion. Cancer Res; 2010 Jul 1;70(13):5597-606
MedlinePlus Health Information. consumer health - Brain Tumors.

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  • Malignant gliomas metastasize throughout the brain by infiltrative cell migration into peritumoral areas.
  • NKCC1 localizes to the leading edge of invading processes, and pharmacologic inhibition using the loop diuretic bumetanide inhibits in vitro Transwell migration by 25% to 50%.
  • Intracranial implantation of human gliomas into severe combined immunodeficient mice showed a marked reduction in cell invasion when NKCC1 function was disrupted genetically or by twice daily injection of the Food and Drug Administration-approved NKCC1 inhibitor Bumex.
  • These data support the consideration of Bumex as adjuvant therapy for patients with high-grade gliomas.

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  • [Copyright] Copyright 2010 AACR.
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  • (PMID = 20570904.001).
  • [ISSN] 1538-7445
  • [Journal-full-title] Cancer research
  • [ISO-abbreviation] Cancer Res.
  • [Language] ENG
  • [Grant] United States / PHS HHS / / R01-031234; United States / NICHD NIH HHS / HD / P30 HD038985-08; United States / NINDS NIH HHS / NS / P30 NS057098; United States / NINDS NIH HHS / NS / R01 NS031234; United States / NINDS NIH HHS / NS / R01 NS031234-18; United States / NICHD NIH HHS / HD / P30 HD038985; United States / NINDS NIH HHS / NS / NS57098; United States / NICHD NIH HHS / HD / HD038985-08; United States / NINDS NIH HHS / NS / P30 NS057098-05; United States / NINDS NIH HHS / NS / NS036692-12; United States / PHS HHS / / R01-036692; United States / NINDS NIH HHS / NS / R01 NS036692; United States / NINDS NIH HHS / NS / R01 NS036692-12
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / RNA, Small Interfering; 0 / SLC12A2 protein, human; 0 / Slc12a2 protein, mouse; 0 / Sodium Potassium Chloride Symporter Inhibitors; 0 / Sodium-Potassium-Chloride Symporters; 0 / Solute Carrier Family 12, Member 2; 0Y2S3XUQ5H / Bumetanide
  • [Other-IDs] NLM/ NIHMS207208; NLM/ PMC2896443
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26. Zamir G, Zeira E, Gelman AE, Shaked A, Olthoff KM, Eid A, Galun E: Replication-deficient adenovirus induces host topoisomerase I activity: implications for adenovirus-mediated gene expression. Mol Ther; 2007 Apr;15(4):772-81
NCI CPTC Antibody Characterization Program. NCI CPTC Antibody Characterization Program .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • Replication-deficient adenoviruses are useful vectors for the transfer of therapeutic transgenes to malignant and non-malignant tissues.
  • Although transgene expression from adenovirus vectors is initially higher than expression of transgenes transduced by other viral or non-viral vectors, it is often insufficient to generate a significant therapeutic effect.
  • Consequently, the inhibition of topoisomerase I by the anti-cancer drug topotecan greatly enhanced transgene expression in adenovirus-infected hepatic cells, colon cancer and prostate cancer cell cultures, mouse liver, human ex vivo tumor specimens, and mouse tumor in vivo.
  • These findings are significant for gene therapy as they reveal novel aspects of the host anti-adenovirus response and set the stage for the development of a rational molecular-pharmacological approach to increase the effectiveness, and safety, of adenovirus-mediated cancer therapeutics.
  • [MeSH-major] Adenoviridae / genetics. DNA Topoisomerases, Type I / biosynthesis. Defective Viruses / genetics. Genetic Vectors
  • [MeSH-minor] Animals. Base Sequence. Cell Line. DNA Primers / genetics. Enzyme Inhibitors / pharmacology. Female. Gene Expression / drug effects. Genetic Therapy / methods. Humans. In Vitro Techniques. Liver / drug effects. Liver / enzymology. Liver / virology. Mice. Mice, Inbred BALB C. Neoplasms / enzymology. Neoplasms / genetics. Neoplasms / therapy. Rats. Rats, Inbred Lew. Topoisomerase I Inhibitors. Topotecan / pharmacology. Transduction, Genetic

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  • (PMID = 17299399.001).
  • [ISSN] 1525-0016
  • [Journal-full-title] Molecular therapy : the journal of the American Society of Gene Therapy
  • [ISO-abbreviation] Mol. Ther.
  • [Language] eng
  • [Grant] United States / NIAID NIH HHS / AI / R01 AI144554
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / DNA Primers; 0 / Enzyme Inhibitors; 0 / Topoisomerase I Inhibitors; 7M7YKX2N15 / Topotecan; EC 5.99.1.2 / DNA Topoisomerases, Type I
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27. Egberts JH, Schniewind B, Pätzold M, Kettler B, Tepel J, Kalthoff H, Trauzold A: Dexamethasone reduces tumor recurrence and metastasis after pancreatic tumor resection in SCID mice. Cancer Biol Ther; 2008 Jul;7(7):1044-50
The Lens. Cited by Patents in .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • Inflammation accompanies most solid cancers including pancreatic ductal adenocarcinoma (PDAC), one of the most fatal cancers with surgery being the only potential curative therapeutic.
  • In the present work we investigated the influence of glucocorticoids on PDAC cells in vitro as well as in vivo in a pancreatic carcinoma resection mouse model.
  • In the mouse resection model subtotal pancreatectomy was performed after orthotopic inoculation of human PDAC cells.
  • DEX was administered after resection as an adjuvant treatment regime and 4 weeks later, local recurrent tumor sizes as well as number of liver and spleen metastases were analyzed.
  • In vivo, we observed a significant reduction of the local recurrent tumor volume and the number of liver and spleen metastases.
  • CONCLUSIONS: DEX has a profound influence on the malignant phenotype of PDAC tumor cells in vitro in terms of inhibition of invasiveness and pro-inflammatory signaling.
  • Therefore, DEX-treatment appears to be an interesting therapeutical option in an adjuvant setting after pancreatic cancer resection.
  • [MeSH-major] Dexamethasone / pharmacology. Pancreatic Neoplasms / drug therapy. Pancreatic Neoplasms / surgery
  • [MeSH-minor] Animals. Antineoplastic Agents, Hormonal / pharmacology. Cell Line, Tumor. Cell Proliferation. Female. Humans. Mice. Mice, SCID. Neoplasm Metastasis. Neoplasm Transplantation. Recurrence. Signal Transduction. Treatment Outcome

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  • [CommentIn] Cancer Biol Ther. 2008 Jul;7(7):1051-2 [18698168.001]
  • (PMID = 18431088.001).
  • [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 / Antineoplastic Agents, Hormonal; 7S5I7G3JQL / Dexamethasone
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