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1. Reelfs O, Xu YZ, Massey A, Karran P, Storey A: Thiothymidine plus low-dose UVA kills hyperproliferative human skin cells independently of their human papilloma virus status. Mol Cancer Ther; 2007 Sep;6(9):2487-95
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  • [Title] Thiothymidine plus low-dose UVA kills hyperproliferative human skin cells independently of their human papilloma virus status.
  • The UV absorbance spectrum of S(4)TdR and its incorporation into DNA suggests that it might act synergistically with nonlethal doses of UVA to selectively kill hyperproliferative or cancerous skin cells.
  • We show here that nontoxic concentrations of S(4)TdR combine with nonlethal doses of UVA to kill proliferating cultured skin cells.
  • Although S(4)TdR plus UVA treatment induces stabilization of p53, cell death, as measured by apoptosis or clonal survival, occurs to a similar extent in both p53 wild-type and p53-null backgrounds.
  • Furthermore, different types of human papilloma virus E6 proteins, which protect against UVB-induced apoptosis, have little effect on killing by S(4)TdR/UVA.
  • S(4)TdR/UVA offers a possible therapeutic intervention strategy that seems to be applicable to human papilloma virus-associated skin lesions.
  • [MeSH-major] Apoptosis. Fibrosarcoma / therapy. Papillomaviridae / genetics. Papillomavirus Infections / virology. Skin Neoplasms / therapy. Thymidine / analogs & derivatives. Ultraviolet Rays
  • [MeSH-minor] Animals. Blotting, Western. Cell Proliferation / drug effects. Cell Proliferation / radiation effects. Cells, Cultured. Combined Modality Therapy. DNA Damage / drug effects. DNA Damage / radiation effects. Female. Fibroblasts / drug effects. Fibroblasts / radiation effects. Fibroblasts / virology. Flow Cytometry. Humans. Keratinocytes / drug effects. Keratinocytes / radiation effects. Keratinocytes / virology. Mice. Middle Aged. Octreotide / analogs & derivatives. Skin / cytology. Tumor Suppressor Protein p53 / genetics. Tumor Suppressor Protein p53 / physiology

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  • (PMID = 17876046.001).
  • [ISSN] 1535-7163
  • [Journal-full-title] Molecular cancer therapeutics
  • [ISO-abbreviation] Mol. Cancer Ther.
  • [Language] eng
  • [Grant] United Kingdom / Cancer Research UK / / A6695
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / 177Lu-octreotide, DOTA(0)-Tyr(3)-; 0 / 4-thiothymidine; 0 / Tumor Suppressor Protein p53; RWM8CCW8GP / Octreotide; VC2W18DGKR / Thymidine
  • [Other-IDs] NLM/ PMC2423463; NLM/ UKMS1840
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2. Kalka K, Ahmad N, Criswell T, Boothman D, Mukhtar H: Up-regulation of clusterin during phthalocyanine 4 photodynamic therapy-mediated apoptosis of tumor cells and ablation of mouse skin tumors. Cancer Res; 2000 Nov 1;60(21):5984-7
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  • [Title] Up-regulation of clusterin during phthalocyanine 4 photodynamic therapy-mediated apoptosis of tumor cells and ablation of mouse skin tumors.
  • Photodynamic therapy (PDT) using the silicon phthalocyanine photo-sensitizer Pc 4 is an oxidative stress associated with the induction of apoptosis in many cancer cells in vitro and in vivo.
  • Clusterin, a widely expressed glycoprotein, is induced in tissues regressing as a consequence of oxidative stress-mediated cell death.
  • Treatment of apoptosis-sensitive human epidermoid carcinoma cells (A431) with PDT resulted in significant up-regulation of clusterin with a maximum at 12 h after treatment, whereas clusterin levels in Pc 4-PDT-treated, apoptosis-resistant, radiation-induced fibrosarcoma (RIF-1) cells remained unchanged.
  • The i.v. administration of Pc 4 to mice bearing chemically or UVB radiation-induced skin papillomas, followed by light application, led to increased clusterin protein expression, peaking 24 h after the treatment, when tumor regression was apparently visible.
  • These data, for the first time, demonstrate the involvement of clusterin in PDT-mediated cell death and during tumor regression.
  • This may have relevance in improving the efficacy of PDT using pharmacological inducers of clusterin.

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  • (PMID = 11085517.001).
  • [ISSN] 0008-5472
  • [Journal-full-title] Cancer research
  • [ISO-abbreviation] Cancer Res.
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / R01 CA078530; United States / NCI NIH HHS / CA / P01 CA 48735; United States / NIAMS NIH HHS / AR / P30 AR 39750; United States / NCI NIH HHS / CA / R01 CA 51802
  • [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 / CLU protein, human; 0 / Clu protein, mouse; 0 / Clusterin; 0 / Glycoproteins; 0 / Indoles; 0 / Molecular Chaperones; 0 / Photosensitizing Agents; 0 / phthalocyanine Pc 4
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3. Laihia JK, Kallio JP, Taimen P, Kujari H, Kähäri VM, Leino L: Protodynamic intracellular acidification by cis-urocanic acid promotes apoptosis of melanoma cells in vitro and in vivo. J Invest Dermatol; 2010 Oct;130(10):2431-9
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  • The extracellular tumor microenvironment is acidified, whereas the intracellular pH of tumor and stromal cells is neutral. cis-Urocanic acid (cis-UCA), an endogenous compound of the skin, can acidify the cytosol by transporting protons into the cells.
  • This phenomenon, termed the protodynamic concept, was studied here in human cancer cells. cis-UCA dose-dependently reduced the number of viable human melanoma, cervical carcinoma, and fibrosarcoma cells at weakly acidic extracellular pH.
  • [MeSH-major] Acids / metabolism. Apoptosis / drug effects. Melanoma / drug therapy. Skin Neoplasms / drug therapy. Urocanic Acid / pharmacology
  • [MeSH-minor] Animals. Cell Division / drug effects. Cell Division / physiology. Cell Line, Transformed. Cytosol / drug effects. Cytosol / metabolism. Dose-Response Relationship, Drug. Female. Fibrosarcoma / drug therapy. Fibrosarcoma / pathology. HeLa Cells. Humans. Hydrogen-Ion Concentration / drug effects. In Vitro Techniques. Mice. Mice, SCID. Uterine Cervical Neoplasms / drug therapy. Uterine Cervical Neoplasms / pathology. Xenograft Model Antitumor Assays

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  • (PMID = 20520626.001).
  • [ISSN] 1523-1747
  • [Journal-full-title] The Journal of investigative dermatology
  • [ISO-abbreviation] J. Invest. Dermatol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Acids; G8D26XJJ3B / Urocanic Acid
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4. Barber LG, Sørenmo KU, Cronin KL, Shofer FS: Combined doxorubicin and cyclophosphamide chemotherapy for nonresectable feline fibrosarcoma. J Am Anim Hosp Assoc; 2000 Sep-Oct;36(5):416-21
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  • [Title] Combined doxorubicin and cyclophosphamide chemotherapy for nonresectable feline fibrosarcoma.
  • A retrospective evaluation was performed on 12 cats with nonresectable, histopathologically confirmed fibrosarcomas that were treated with doxorubicin and cyclophosphamide chemotherapy.
  • All cats developed progressive disease.
  • When animals that received other treatments after doxorubicin-based chemotherapy were eliminated from the analysis, median survival time was significantly longer for cats that responded to chemotherapy compared with the median survival time for nonresponders (242 and 83 days, respectively).
  • These findings may serve as a basis for further evaluating the role of chemotherapy in the treatment of vaccine-associated sarcomas.
  • [MeSH-major] Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Cat Diseases / drug therapy. Fibrosarcoma / veterinary. Skin Neoplasms / veterinary
  • [MeSH-minor] Animals. Cats. Cyclophosphamide / administration & dosage. Disease-Free Survival. Doxorubicin / administration & dosage. Female. Male. Records as Topic / veterinary. Retrospective Studies. Treatment Outcome. Vaccines / adverse effects

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  • (PMID = 10997517.001).
  • [ISSN] 0587-2871
  • [Journal-full-title] Journal of the American Animal Hospital Association
  • [ISO-abbreviation] J Am Anim Hosp Assoc
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] UNITED STATES
  • [Chemical-registry-number] 0 / Vaccines; 80168379AG / Doxorubicin; 8N3DW7272P / Cyclophosphamide
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5. Holán V, Zajícová A, Krulova M, Blahoutová V, Wilczek H: Augmented production of proinflammatory cytokines and accelerated allotransplantation reactions in heroin-treated mice. Clin Exp Immunol; 2003 Apr;132(1):40-5
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  • Heroin treatment or abusive drug addiction influences many physiological functions, including the reactions of the immune system.
  • In contrast, the production of anti-inflammatory cytokines IL-4 and IL-10 was at the same time rather decreased.
  • As a consequence, skin allografts in heroin-treated mice were rejected more promptly than in untreated or vehicle-treated recipients.
  • These results show that heroin treatment augments production of proinflammatory cytokines and accelerates allotransplantation reactions.
  • The observations thus illustrate the complexity of the effects of heroin on the immune system and should be taken into account during medical treatment of opiate addicts and in the use of morphine to decrease pain in various clinical situations.
  • [MeSH-major] Cytokines / blood. Heroin / pharmacology. Narcotics / pharmacology. Skin Transplantation / immunology. Transplantation Immunology / drug effects
  • [MeSH-minor] Animals. Cells, Cultured. Female. Fibrosarcoma / drug therapy. Fibrosarcoma / immunology. Interferon-gamma / biosynthesis. Interleukin-1 / biosynthesis. Interleukin-10 / biosynthesis. Interleukin-12 / biosynthesis. Interleukin-2 / biosynthesis. Interleukin-4 / biosynthesis. Macrophages, Peritoneal / metabolism. Male. Mice. Mice, Inbred BALB C. Mice, Inbred C57BL. Naltrexone / pharmacology. Narcotic Antagonists / pharmacology. Neoplasms, Experimental / drug therapy. Neoplasms, Experimental / immunology. Nitric Oxide / metabolism. Spleen / immunology. Transplantation, Homologous

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  • (PMID = 12653834.001).
  • [ISSN] 0009-9104
  • [Journal-full-title] Clinical and experimental immunology
  • [ISO-abbreviation] Clin. Exp. Immunol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Cytokines; 0 / Interleukin-1; 0 / Interleukin-2; 0 / Narcotic Antagonists; 0 / Narcotics; 130068-27-8 / Interleukin-10; 187348-17-0 / Interleukin-12; 207137-56-2 / Interleukin-4; 31C4KY9ESH / Nitric Oxide; 5S6W795CQM / Naltrexone; 70D95007SX / Heroin; 82115-62-6 / Interferon-gamma
  • [Other-IDs] NLM/ PMC1808676
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6. Brekken RA, Overholser JP, Stastny VA, Waltenberger J, Minna JD, Thorpe PE: Selective inhibition of vascular endothelial growth factor (VEGF) receptor 2 (KDR/Flk-1) activity by a monoclonal anti-VEGF antibody blocks tumor growth in mice. Cancer Res; 2000 Sep 15;60(18):5117-24
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  • At the present time there are two well-characterized receptors for VEGF that are selectively expressed on endothelium.
  • 2C3 blocks the VEGF-induced vascular permeability increase in guinea pig skin.
  • [MeSH-minor] Animals. Capillary Permeability / drug effects. Carcinoma, Non-Small-Cell Lung / pathology. Carcinoma, Non-Small-Cell Lung / therapy. Cell Division / drug effects. Enzyme-Linked Immunosorbent Assay. Fibrosarcoma / pathology. Fibrosarcoma / therapy. Guinea Pigs. Humans. Lung Neoplasms / pathology. Lung Neoplasms / therapy. Male. Mice. Neoplasm Transplantation. Phosphorylation / drug effects. Proto-Oncogene Proteins / metabolism. Receptors, Vascular Endothelial Growth Factor. Rhabdomyosarcoma / pathology. Rhabdomyosarcoma / therapy. Skin / blood supply. Substrate Specificity. Transplantation, Heterologous. Vascular Endothelial Growth Factor A. Vascular Endothelial Growth Factor Receptor-1. Vascular Endothelial Growth Factors

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  • (PMID = 11016638.001).
  • [ISSN] 0008-5472
  • [Journal-full-title] Cancer research
  • [ISO-abbreviation] Cancer Res.
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / 1RO1 CA74951; United States / NCI NIH HHS / CA / 5RO CA54168; United States / NIGMS NIH HHS / GM / T32 GM07062; etc
  • [Publication-type] Journal Article; Research Support, U.S. Gov't, P.H.S.
  • [Publication-country] UNITED STATES
  • [Chemical-registry-number] 0 / Antibodies, Monoclonal; 0 / Endothelial Growth Factors; 0 / Growth Inhibitors; 0 / Lymphokines; 0 / Proto-Oncogene Proteins; 0 / Receptors, Growth Factor; 0 / Vascular Endothelial Growth Factor A; 0 / Vascular Endothelial Growth Factors; EC 2.7.10.1 / Receptor Protein-Tyrosine Kinases; EC 2.7.10.1 / Receptors, Vascular Endothelial Growth Factor; EC 2.7.10.1 / Vascular Endothelial Growth Factor Receptor-1
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7. Sjöblom T, Shimizu A, O'Brien KP, Pietras K, Dal Cin P, Buchdunger E, Dumanski JP, Ostman A, Heldin CH: Growth inhibition of dermatofibrosarcoma protuberans tumors by the platelet-derived growth factor receptor antagonist STI571 through induction of apoptosis. Cancer Res; 2001 Aug 1;61(15):5778-83
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  • Dermatofibrosarcoma protuberans (DFSP) and giant cell fibroblastoma (GCF) are recurrent, infiltrative skin tumors that presently are treated with surgery.
  • DFSP and GCF tumors are genetically characterized by chromosomal rearrangements fusing the collagen type Ialpha1 (COLIA1) gene to the platelet-derived growth factor B-chain (PDGFB) gene.
  • Three of the primary cultures were further characterized; their in vitro growth displayed an increased sensitivity to treatment with the PDGF receptor tyrosine kinase inhibitor STI571, as compared with normal fibroblasts.
  • Treatment of tumor-bearing severe combined immunodeficient mice with STI571 reduced tumor growth.
  • These findings suggest targeting of PDGF receptors as a novel treatment strategy for DFSP and GCF.
  • [MeSH-major] Antineoplastic Agents / pharmacology. Apoptosis / drug effects. Dermatofibrosarcoma / pathology. Piperazines / pharmacology. Pyrimidines / pharmacology. Receptor, Platelet-Derived Growth Factor beta / antagonists & inhibitors
  • [MeSH-minor] Adult. Animals. Benzamides. Cell Division / drug effects. Cell Division / physiology. Child, Preschool. Female. Fibrosarcoma / blood supply. Fibrosarcoma / drug therapy. Fibrosarcoma / pathology. Giant Cell Tumors / blood supply. Giant Cell Tumors / drug therapy. Giant Cell Tumors / pathology. Growth Inhibitors / pharmacology. Humans. Imatinib Mesylate. Infant. Male. Mice. Mice, Inbred BALB C. Mice, Nude. Mice, SCID. Neovascularization, Pathologic / drug therapy. Oncogene Proteins, Fusion / biosynthesis. Oncogene Proteins, Fusion / genetics. Skin Neoplasms / blood supply. Skin Neoplasms / drug therapy. Skin Neoplasms / pathology. Xenograft Model Antitumor Assays

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  • (PMID = 11479215.001).
  • [ISSN] 0008-5472
  • [Journal-full-title] Cancer research
  • [ISO-abbreviation] Cancer Res.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / Benzamides; 0 / COLIA1-PDGFB fusion protein, human; 0 / Growth Inhibitors; 0 / Oncogene Proteins, Fusion; 0 / Piperazines; 0 / Pyrimidines; 8A1O1M485B / Imatinib Mesylate; EC 2.7.10.1 / Receptor, Platelet-Derived Growth Factor beta
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8. Chen B, Ahmed B, Landuyt W, Ni Y, Gaspar R, Roskams T, de Witte PA: Potentiation of photodynamic therapy with hypericin by mitomycin C in the radiation-induced fibrosarcoma-1 mouse tumor model. Photochem Photobiol; 2003 Sep;78(3):278-82
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  • [Title] Potentiation of photodynamic therapy with hypericin by mitomycin C in the radiation-induced fibrosarcoma-1 mouse tumor model.
  • We investigated the combination of hypericin-photodynamic therapy (PDT) and a bioreductive drug mitomycin C (MMC) in the present study.
  • The radiation-induced fibrosarcoma-1 tumors were exposed to laser light (120 J/cm2 at 595 nm) 24 h after an intravenous injection of hypericin (1 mg/kg).
  • Hypericin-PDT alone significantly decreased tumor perfusion and oxygen tension as demonstrated by India ink staining technique and OxyLite pO2 measurement, respectively.
  • No greater skin reaction was observed after the combination of MMC and PDT than after PDT alone.
  • [MeSH-major] Disease Models, Animal. Fibrosarcoma / drug therapy. Mitomycin / pharmacology. Perylene / analogs & derivatives. Perylene / pharmacology
  • [MeSH-minor] Animals. Drug Synergism. Female. Mice

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  • (PMID = 14556315.001).
  • [ISSN] 0031-8655
  • [Journal-full-title] Photochemistry and photobiology
  • [ISO-abbreviation] Photochem. Photobiol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 50SG953SK6 / Mitomycin; 5QD5427UN7 / Perylene; 7V2F1075HD / hypericin
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9. Barthomeuf C, Lamy S, Blanchette M, Boivin D, Gingras D, Béliveau R: Inhibition of sphingosine-1-phosphate- and vascular endothelial growth factor-induced endothelial cell chemotaxis by red grape skin polyphenols correlates with a decrease in early platelet-activating factor synthesis. Free Radic Biol Med; 2006 Feb 15;40(4):581-90
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  • [Title] Inhibition of sphingosine-1-phosphate- and vascular endothelial growth factor-induced endothelial cell chemotaxis by red grape skin polyphenols correlates with a decrease in early platelet-activating factor synthesis.
  • The red grape skin polyphenolic extract (SGE) both prevents and inhibits angiogenesis in the Matrigel model, decreases the basal motility of endothelial and cancer cells, and reverses the chemotactic effect of S1P and VEGF on bovine aortic endothelial cells (BAECs) as well as the chemotactic effect of conditioned medium on human HT-1080 fibrosarcoma, human U-87 glioblastoma, and human DAOY medulloblastoma cells.
  • [MeSH-major] Chemotaxis. Endothelium, Vascular / drug effects. Flavonoids / therapeutic use. Lysophospholipids / pharmacology. Phenols / therapeutic use. Platelet Activating Factor / metabolism. Sphingosine / analogs & derivatives. Vascular Endothelial Growth Factor A / pharmacology. Vitis
  • [MeSH-minor] Animals. Aorta / cytology. Aorta / drug effects. Aorta / metabolism. Cattle. Cell Movement / drug effects. Cells, Cultured. Fibrosarcoma / drug therapy. Fibrosarcoma / metabolism. Fibrosarcoma / pathology. Glioblastoma / drug therapy. Glioblastoma / metabolism. Glioblastoma / pathology. Humans. Medulloblastoma / drug therapy. Medulloblastoma / metabolism. Medulloblastoma / pathology. Mitogen-Activated Protein Kinase 1 / antagonists & inhibitors. Mitogen-Activated Protein Kinase 1 / metabolism. Mitogen-Activated Protein Kinase 3 / antagonists & inhibitors. Mitogen-Activated Protein Kinase 3 / metabolism. Neovascularization, Pathologic. Neovascularization, Physiologic. Phosphorylation / drug effects. Platelet Membrane Glycoproteins / antagonists & inhibitors. Platelet Membrane Glycoproteins / metabolism. Polyphenols. Receptors, G-Protein-Coupled / antagonists & inhibitors. Receptors, G-Protein-Coupled / metabolism. p38 Mitogen-Activated Protein Kinases / antagonists & inhibitors. p38 Mitogen-Activated Protein Kinases / metabolism

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  • [CommentIn] Free Radic Biol Med. 2007 Jan 15;42(2):311 [17189836.001]
  • (PMID = 16458188.001).
  • [ISSN] 0891-5849
  • [Journal-full-title] Free radical biology & medicine
  • [ISO-abbreviation] Free Radic. Biol. Med.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Flavonoids; 0 / Lysophospholipids; 0 / Phenols; 0 / Platelet Activating Factor; 0 / Platelet Membrane Glycoproteins; 0 / Polyphenols; 0 / Receptors, G-Protein-Coupled; 0 / VEGFA protein, human; 0 / Vascular Endothelial Growth Factor A; 0 / platelet activating factor receptor; 26993-30-6 / sphingosine 1-phosphate; EC 2.7.11.24 / Mitogen-Activated Protein Kinase 1; EC 2.7.11.24 / Mitogen-Activated Protein Kinase 3; EC 2.7.11.24 / p38 Mitogen-Activated Protein Kinases; NGZ37HRE42 / Sphingosine
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10. Hebbar SA, Mitra AK, George KC, Verma NC: Caffeine ameliorates radiation-induced skin reactions in mice but does not influence tumour radiation response. J Radiol Prot; 2002 Mar;22(1):63-9
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  • [Title] Caffeine ameliorates radiation-induced skin reactions in mice but does not influence tumour radiation response.
  • Intramuscular administration of caffeine at a dose of 80 mg kg(-1) body weight to the gastrocnemius muscles of Swiss mice 5 min prior to local irradiation (35 Gy) of the leg delayed the progression of radiation-induced skin reactions in such animals.
  • While 90% epilation with reddening of the skin was noted in animals treated with radiation alone, animals pretreated with caffeine suffered only partial hair loss with slight reddening of the skin on the 16th and 20th days post-irradiation.
  • Beyond the 28th day, damage scores in irradiated feet for both the groups were similar (score 3) and remained unchanged until the 32nd day and then decreased and disappeared completely in both treatment groups by the 40th day after irradiation.
  • In addition, the effect of caffeine on the radiation response of a mouse fibrosarcoma was investigated.
  • Results showed that intratumoral administration of caffeine at a dose of 80 mg kg(-1) body weight 5 min prior to local exposure of tumours to 10 Gy of 60Co gamma-rays did not influence the response of tumours to radiation.
  • The present study thus showed that although caffeine ameliorated radiation-induced skin reactions in the mouse leg, it did not affect the tumour radiation response, indicating its potential application in cancer radiotherapy.
  • [MeSH-major] Caffeine / pharmacology. Radiation Injuries / drug therapy. Skin / drug effects. Skin / radiation effects. Skin Neoplasms / radiotherapy

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  • (PMID = 11929115.001).
  • [ISSN] 0952-4746
  • [Journal-full-title] Journal of radiological protection : official journal of the Society for Radiological Protection
  • [ISO-abbreviation] J Radiol Prot
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 3G6A5W338E / Caffeine
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11. Davies MM, Burke D, Carnochan P, Glover C, Kaur S, Allen-Mersh TG: Basic fibroblast growth factor infusion increases tumour vascularity, blood flow and chemotherapy uptake. Acta Oncol; 2002;41(1):84-90
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  • [Title] Basic fibroblast growth factor infusion increases tumour vascularity, blood flow and chemotherapy uptake.
  • We determined whether basic fibroblast growth factor (bFGF) infusion increased tumour vascularity, blood flow and cytotoxic drug uptake.
  • Blood flow and drug uptake were studied using a radiotracer method.
  • The effects were independent of tumour type, and could be produced by bFGF administration after initial tumour growth. bFGF infusion increased tumour fluorouracil uptake.
  • [MeSH-major] Adenocarcinoma / blood supply. Antimetabolites, Antineoplastic / pharmacokinetics. Fibroblast Growth Factor 2 / administration & dosage. Fibrosarcoma / blood supply. Fluorouracil / pharmacokinetics. Liver Neoplasms, Experimental / blood supply. Neovascularization, Pathologic / metabolism. Skin Neoplasms / blood supply
  • [MeSH-minor] Animals. Blood Flow Velocity / drug effects. Infusions, Intravenous. Male. Rats. Rats, Inbred Strains

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  • (PMID = 11990524.001).
  • [ISSN] 0284-186X
  • [Journal-full-title] Acta oncologica (Stockholm, Sweden)
  • [ISO-abbreviation] Acta Oncol
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Norway
  • [Chemical-registry-number] 0 / Antimetabolites, Antineoplastic; 103107-01-3 / Fibroblast Growth Factor 2; U3P01618RT / Fluorouracil
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12. Miracco C, Materno M, De Santi MM, Pirtoli L, Ninfo V: Unusual second malignancies following radiation therapy: subcutaneous pleomorphic rhabdomyosarcoma and cutaneous melanoma. Two case reports. J Cutan Pathol; 2000 Sep;27(8):419-22
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  • [Title] Unusual second malignancies following radiation therapy: subcutaneous pleomorphic rhabdomyosarcoma and cutaneous melanoma. Two case reports.
  • We report a high-grade sarcoma with rhabdomyoblastic differentiation, which appeared 30 years after megavoltage irradiation for an endometrial adenocarcinoma, and a malignant melanoma which arose after 6 years in the irradiation field of a fibrosarcoma.
  • In the second case, a lentigoid malignant melanoma was histologically and immunohistochemically demonstrated, whereas the previously resected tumor was a fibrosarcoma negative to melanoma markers.
  • CONCLUSIONS: Rare cases of rhabdomyosarcomas and melanomas are induced by irradiation, although in some cases other factors (i.e., genetic risk, chemotherapy) may have a prominent etiopathogenetic role in their development.
  • A close follow-up and a careful examination of the irradiated area should facilitate an early diagnosis of these aggressive postradiation second neoplasms.
  • [MeSH-major] Adenocarcinoma / radiotherapy. Endometrial Neoplasms / radiotherapy. Fibrosarcoma / radiotherapy. Melanoma / etiology. Neoplasms, Radiation-Induced / etiology. Rhabdomyosarcoma / etiology. Skin Neoplasms / etiology. Skin Neoplasms / radiotherapy

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  • (PMID = 10955690.001).
  • [ISSN] 0303-6987
  • [Journal-full-title] Journal of cutaneous pathology
  • [ISO-abbreviation] J. Cutan. Pathol.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] DENMARK
  • [Chemical-registry-number] 0 / Biomarkers, Tumor; 0 / Neoplasm Proteins
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13. Fedorocko P, Hoferová Z, Hofer M, Brezáni P: Administration of liposomal muramyl tripeptide phosphatidylethanolamine (MTP-PE) and diclofenac in the combination attenuates their anti-tumor activities. Neoplasma; 2003;50(3):176-84
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  • The anti-tumor effects of i.p. administered cyclooxygenase inhibitor - diclofenac and i.v. administered liposomal muramyl tripeptide phosphatidylethanolamine (MTP-PE) were investigated using a s.c. growing murine fibrosarcoma tumor.
  • Both of the drugs were administered either alone or in combination.
  • However, the volume of tumors and the survival time in tumor bearing mice treated with the two agents were similar to untreated counterparts.
  • Thus, these data suggest the anti-tumor activity of either of the two drugs is lost when they are used in combination.
  • Hematological examinations confirmed previously observed hematopoiesis-stimulating activities of the drugs when given alone.
  • Our findings corroborate the recommendation that the interactions of drugs used for the treatment of tumors must be carefully checked, if the drugs are applied in combination.
  • [MeSH-major] Acetylmuramyl-Alanyl-Isoglutamine / administration & dosage. Acetylmuramyl-Alanyl-Isoglutamine / analogs & derivatives. Antineoplastic Combined Chemotherapy Protocols / administration & dosage. Diclofenac / administration & dosage. Fibrosarcoma / drug therapy. Phosphatidylethanolamines / administration & dosage. Skin Neoplasms / drug therapy. Tumor Cells, Cultured / drug effects
  • [MeSH-minor] Animals. Cell Division / drug effects. Drug Carriers. Drug Interactions. Liposomes. Male. Mice. Mice, Inbred C3H. Survival Rate

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  • (PMID = 12937850.001).
  • [ISSN] 0028-2685
  • [Journal-full-title] Neoplasma
  • [ISO-abbreviation] Neoplasma
  • [Language] eng
  • [Publication-type] Comparative Study; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Slovakia
  • [Chemical-registry-number] 0 / Drug Carriers; 0 / Liposomes; 0 / Phosphatidylethanolamines; 144O8QL0L1 / Diclofenac; 53678-77-6 / Acetylmuramyl-Alanyl-Isoglutamine; EQD2NNX741 / mifamurtide
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14. Kale SN, Arora S, Bhayani KR, Paknikar KM, Jani M, Wagh UV, Kulkarni SD, Ogale SB: Cerium doping and stoichiometry control for biomedical use of La0.7Sr0.3MnO3 nanoparticles: microwave absorption and cytotoxicity study. Nanomedicine; 2006 Dec;2(4):217-21
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  • Considering hyperthermia as one of the possible application domains of such materials, the cytotoxicity studies were done on human skin carcinoma and human fibrosarcoma cell lines.
  • [MeSH-minor] Cell Line, Tumor. Cell Survival. Fever. Fibrosarcoma / drug therapy. Humans. Nanostructures / chemistry. Skin Neoplasms / drug therapy

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  • (PMID = 17292146.001).
  • [ISSN] 1549-9642
  • [Journal-full-title] Nanomedicine : nanotechnology, biology, and medicine
  • [ISO-abbreviation] Nanomedicine
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Manganese Compounds; 0 / Oxides; 0 / manganite; 1317-35-7 / manganese oxide; 30K4522N6T / Cerium; 6I3K30563S / Lanthanum; YZS2RPE8LE / Strontium
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15. Wacnik PW, Kehl LJ, Trempe TM, Ramnaraine ML, Beitz AJ, Wilcox GL: Tumor implantation in mouse humerus evokes movement-related hyperalgesia exceeding that evoked by intramuscular carrageenan. Pain; 2003 Jan;101(1-2):175-86
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  • In this paper we compare two innovative models of movement-related pain: tumor-induced nociception following implantation of fibrosarcoma cells into bone and muscle inflammation-induced nociception following injection of the irritant carrageenan into muscle.
  • Movement-related hyperalgesia, known clinically as a specific type of 'breakthrough pain', is a common feature of bone cancer and is thought to be a predictor of poor response to conventional analgesic pharmacotherapy (Bruera et al., 1995, J.
  • Control groups receiving implants of vehicle or no treatment at all did not manifest this forelimb hyperalgesia.
  • B6C3/F1 mice implanted with non-lysis-inducing G3.26 melanoma cells or vehicle did not manifest significant hyperalgesia when compared to B6C3/F1 mice receiving fibrosarcoma cells, indicating a dependence on bone involvement for induction of hyperalgesia in this model.
  • Tumor-implanted mice with a level of hyperalgesia comparable to that induced by carrageenan required almost three times more morphine (ED(50) 18.5mg/kg) for equivalent attenuation of forelimb hyperalgesia.
  • Importantly, they may also aid in predicting differences in analgesic efficacy in different types of musculoskeletal pain.
  • [MeSH-major] Bone Neoplasms / complications. Fibrosarcoma / complications. Hyperalgesia / physiopathology. Movement
  • [MeSH-minor] Analgesics, Opioid / pharmacology. Animals. Carrageenan. Disease Models, Animal. Forelimb / physiology. Hand Strength. Humerus. Injections, Intramuscular. Male. Melanoma / complications. Melanoma / pathology. Mice. Mice, Inbred C3H. Morphine / pharmacology. Neoplasm Transplantation. Physical Stimulation. Skin

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  • (PMID = 12507712.001).
  • [ISSN] 0304-3959
  • [Journal-full-title] Pain
  • [ISO-abbreviation] Pain
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / 1R01-CA84233-01A2; United States / NIDCR NIH HHS / DE / 5T 32-DEO 7288-02
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't; Research Support, U.S. Gov't, P.H.S.
  • [Publication-country] Netherlands
  • [Chemical-registry-number] 0 / Analgesics, Opioid; 76I7G6D29C / Morphine; 9000-07-1 / Carrageenan
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16. Kummoona R: Periorbital and orbital malignancies: methods of management and reconstruction in Iraq. J Craniofac Surg; 2007 Nov;18(6):1370-5
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  • Tumor types were squamous cell carcinoma, basal cell carcinoma, conjunctival squamous cell carcinoma, retinoblastoma, fibrosarcoma, and ectopic mixed tumor in two, one, two, one, one, and one patients, respectively, in addition to eight patients with jaw lymphoma involving the orbit, out of 24 patients reported by us.
  • Eight patients were treated surgically with adjuvant postoperative radiotherapy, whereas eight patients with lymphoma treated with combination chemotherapy (vincristine, Adriamycin, cyclophosphamide, methotrexate, and prednisolone), the survival rate was very poor.
  • Reconstruction of the defect was accomplished using various local skin flaps and temporalis muscle flap was used for augmenting the orbit in the four exenterated patients.
  • There is no single best method for reconstruction of the periorbital and orbital defects left after tumor resection, and different flaps applied for reconstruction had given satisfactory results related to the type and complexity of the deformity.
  • [MeSH-minor] Adolescent. Adult. Aged. Carcinoma, Squamous Cell / radiotherapy. Carcinoma, Squamous Cell / surgery. Chemotherapy, Adjuvant. Child. Child, Preschool. Eye Enucleation. Female. Humans. Infant. Iraq. Lymphoma / chemistry. Lymphoma / surgery. Male. Middle Aged. Radiotherapy, Adjuvant. Skin Transplantation

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  • (PMID = 17993883.001).
  • [ISSN] 1049-2275
  • [Journal-full-title] The Journal of craniofacial surgery
  • [ISO-abbreviation] J Craniofac Surg
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
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17. Gryshuk AL, Chen Y, Potter W, Ohulchansky T, Oseroff A, Pandey RK: In vivo stability and photodynamic efficacy of fluorinated bacteriopurpurinimides derived from bacteriochlorophyll-a. J Med Chem; 2006 Mar 23;49(6):1874-81
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  • The preliminary in vivo photosensitizing efficacy of this stable bacteriopurpurinimide was determined in C3H mice bearing radiation induced fibrosarcoma tumors as a function of variable drug doses.
  • A drug dose of 1.0 micromol/kg and light exposure of 135 J/cm2 (75 mW/cm2; 24 h postinjection) at 796 nm for 30 min produced a 60% long-term tumor cure (3/5 mice were tumor-free on day 90).
  • The fluorescein-exclusion assay and histological staining of CD31 confirmed vascular stasis at various time points post-PDT (post photodynamic therapy).
  • The treatment parameters (time for maximum drug uptake and wavelength for light irradiation) were determined by in vivo reflectance spectroscopy.
  • [MeSH-minor] Animals. Benzylamines / chemistry. Cell Line, Tumor. Cell Survival / drug effects. Chromatography, High Pressure Liquid. Drug Stability. Female. Fibrosarcoma / drug therapy. Mice. Neoplasms, Radiation-Induced / drug therapy. Oxidation-Reduction. Skin / blood supply. Skin / drug effects. Skin / radiation effects

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  • (PMID = 16539373.001).
  • [ISSN] 0022-2623
  • [Journal-full-title] Journal of medicinal chemistry
  • [ISO-abbreviation] J. Med. Chem.
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / CA55791; United States / NCI NIH HHS / CA / IR 21 CA109914-01; United States / NCI NIH HHS / CA / P30CA16056
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't; Research Support, U.S. Gov't, Non-P.H.S.
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Bacteriochlorophyll A; 0 / Benzylamines; 0 / Imides; 0 / Photosensitizing Agents; 0 / Porphyrins; 25465-77-4 / purpurin 18; 284SYP0193 / Fluorine
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18. Sartippour MR, Liu C, Shao ZM, Go VL, Heber D, Nguyen M: Livistona extract inhibits angiogenesis and cancer growth. Oncol Rep; 2001 Nov-Dec;8(6):1355-7

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  • The aqueous extract inhibits the in vitro proliferation of endothelial cells and multiple tumor cell lines including mouse fibrosarcoma and human breast and colon cancer.
  • In mouse experiments, this extract suppresses the growth of the subcutaneous fibrosarcoma tumors.
  • When the seed is separated into different components, the shell including the seed skin appears more potent than the inner kernel in tumor suppression.
  • Our results suggest that the extract from the shell of Livistona chinensis may be a potential supplemental source for cancer treatment.
  • [MeSH-minor] Animals. Carcinoma / drug therapy. Cell Division / drug effects. Endothelium, Vascular / drug effects. Fibrosarcoma / drug therapy. HT29 Cells / drug effects. Humans. Mice. Mice, Inbred C3H. Seeds. Tumor Cells, Cultured. Xenograft Model Antitumor Assays

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  • [CommentIn] NIH Guide Grants Contracts. 2009 Feb 20;:NOT-OD-09-052 [19241492.001]
  • (PMID = 11605065.001).
  • [ISSN] 1021-335X
  • [Journal-full-title] Oncology reports
  • [ISO-abbreviation] Oncol. Rep.
  • [Language] eng
  • [Grant] United States / NCCIH NIH HHS / AT / P50 AT 00151; United States / NIDDK NIH HHS / DK / T32 DK07688
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't; Research Support, U.S. Gov't, P.H.S.
  • [Publication-country] Greece
  • [Chemical-registry-number] 0 / Angiogenesis Inhibitors; 0 / Antineoplastic Agents, Phytogenic; 0 / Plant Extracts
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19. Edelweiss M, Malpica A: Dermatofibrosarcoma protuberans of the vulva: a clinicopathologic and immunohistochemical study of 13 cases. Am J Surg Pathol; 2010 Mar;34(3):393-400
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  • One patient presented with a pigmented skin lesion.
  • Of interest, in 7 of our 13 cases, a variety of diagnoses, such as cellular dermatofibroma, cellular leiomyoma, neurofibroma, low-grade leiomyosarcoma, fibrosarcoma, low-grade malignant schwannoma, desmoplastic melanoma, cellular neurofibroma, and low-grade malignant peripheral nerve sheet tumor were initially considered.
  • One patient also developed distant metastases.
  • All recurrences were treated surgically; 1 patient also received chemotherapy and radiotherapy and another received imatinib (Gleevec).
  • [MeSH-major] Biomarkers, Tumor / analysis. Dermatofibrosarcoma / diagnosis. Immunohistochemistry. Skin Neoplasms / diagnosis. Vulvar Neoplasms / diagnosis
  • [MeSH-minor] Adult. Aged. Chemotherapy, Adjuvant. Diagnosis, Differential. Female. Gynecologic Surgical Procedures. Humans. Middle Aged. Neoplasm Recurrence, Local. Predictive Value of Tests. Radiotherapy, Adjuvant. Reoperation. Time Factors. Treatment Outcome. Young Adult

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  • (PMID = 20139758.001).
  • [ISSN] 1532-0979
  • [Journal-full-title] The American journal of surgical pathology
  • [ISO-abbreviation] Am. J. Surg. Pathol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Biomarkers, Tumor
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20. Sirvent N, Maire G, Pedeutour F: Genetics of dermatofibrosarcoma protuberans family of tumors: from ring chromosomes to tyrosine kinase inhibitor treatment. Genes Chromosomes Cancer; 2003 May;37(1):1-19
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  • [Title] Genetics of dermatofibrosarcoma protuberans family of tumors: from ring chromosomes to tyrosine kinase inhibitor treatment.
  • The preferred treatment is wide surgical excision with pathologically negative margins.
  • Recent studies have determined the molecular identity of "classical" DP, giant cell fibroblastoma, Bednar tumor, adult superficial fibrosarcoma, and the granular cell variant of DP.
  • It is encouraging that inhibitory effects of the PDGF receptor tyrosine kinase antagonist imatinib mesylate have been demonstrated in vivo; such targeted therapies might be warranted in the near future for treatment of the few DP cases not manageable by surgery.
  • [MeSH-major] Dermatofibrosarcoma / drug therapy. Dermatofibrosarcoma / genetics. Enzyme Inhibitors / therapeutic use. Ring Chromosomes. Skin Neoplasms / drug therapy. Skin Neoplasms / genetics. src-Family Kinases / antagonists & inhibitors
  • [MeSH-minor] Animals. Diagnosis, Differential. Humans

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  • [Copyright] Copyright 2003 Wiley-Liss, Inc.
  • (PMID = 12661001.001).
  • [ISSN] 1045-2257
  • [Journal-full-title] Genes, chromosomes & cancer
  • [ISO-abbreviation] Genes Chromosomes Cancer
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't; Review
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Enzyme Inhibitors; EC 2.7.10.2 / src-Family Kinases
  • [Number-of-references] 109
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21. Dreischalück J, Schwöppe C, Spieker T, Kessler T, Tiemann K, Liersch R, Schliemann C, Kreuter M, Kolkmeyer A, Hintelmann H, Mesters RM, Berdel WE: Vascular infarction by subcutaneous application of tissue factor targeted to tumor vessels with NGR-peptides: activity and toxicity profile. Int J Oncol; 2010 Dec;37(6):1389-97
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  • [Title] Vascular infarction by subcutaneous application of tissue factor targeted to tumor vessels with NGR-peptides: activity and toxicity profile.
  • tTF-NGR consists of the extracellular domain of the (truncated) tissue factor (tTF), a central molecule for coagulation in vivo, and the peptide GNGRAHA (NGR), a ligand of the surface protein aminopeptidase N (CD13).
  • Subcutaneous injection of tTF-NGR into athymic mice bearing human HT1080 fibrosarcoma tumors induced tumor growth retardation and delay.
  • Furthermore, a lack of resistance was shown by re-exposure of tumor-bearing mice to tTF-NGR after regrowth following a first cycle of treatment.
  • However, after subcutaneous (s.c.) push injection with therapeutic doses (1-5 mg/kg bw) side effects have been observed, such as skin bleeding and reduced performance.
  • Since lethality started within the therapeutic dose range (LD10 approximately 2 mg/kg bw) no safe therapeutic window could be found.
  • Thus, subcutaneous injection of tTF-NGR represents an active, but toxic application procedure and compares unfavourably to intravenous infusion.
  • [MeSH-major] Drug Delivery Systems / methods. Infarction / chemically induced. Neoplasms / blood supply. Neoplasms / drug therapy. Oligopeptides / administration & dosage. Thromboplastin / administration & dosage
  • [MeSH-minor] Angiogenesis Inhibitors / administration & dosage. Angiogenesis Inhibitors / adverse effects. Animals. Blood Vessels / drug effects. Blood Vessels / pathology. Cell Line, Tumor. Cells, Cultured. Humans. Injections, Subcutaneous. Mice. Mice, Nude. Neovascularization, Pathologic / drug therapy. Neovascularization, Pathologic / pathology. Recombinant Fusion Proteins / administration & dosage. Recombinant Fusion Proteins / adverse effects. Recombinant Fusion Proteins / chemistry. Xenograft Model Antitumor Assays

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  • (PMID = 21042706.001).
  • [ISSN] 1791-2423
  • [Journal-full-title] International journal of oncology
  • [ISO-abbreviation] Int. J. Oncol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Greece
  • [Chemical-registry-number] 0 / Angiogenesis Inhibitors; 0 / NGR peptide; 0 / Oligopeptides; 0 / Recombinant Fusion Proteins; 9035-58-9 / Thromboplastin
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22. Albert A, Cruz O, Montaner A, Vela A, Badosa J, Castañón M, Morales L: [Congenital solid tumors. A thirteen-year review]. Cir Pediatr; 2004 Jul;17(3):133-6
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  • This is an interesting group of tumors because their type, relative incidence, natural history and response to treatment differ from those seen in older children.
  • There were 8 teratomas (3 sacrocoxigeal, 1 retroperitoneal, 1 in the CNS, 1 orbitary and two oronasal), two hepatic tumors (1 hepatoblastoma, 1 hemangioendothelioma, two CNS tumors, two giant nevus (one on a hamartoma), and one each Wilms tumor, infantile fibrosarcoma and myofibroblastic tumor.
  • Treatment was surgical resection alone in 17 cases (68%) and surgery + chemotherapy in 8 (32%) (5 neuroblastomas, one CNS tumor, one Wilms tumor and one presacral teratoma who developed a yolk sac tumor); 3 patients died (11%): one at surgery, one of tumoural airway obstruction at birth and one with craniopharyngioma.
  • Among the 14 tumors that were initially not malignant, two can be locally agressive, one was an immature teratoma, the giant nevus with hamartoma developed in situ melanoma, the other nevus had meningeal melanosis with hydrocephalus, and one mature presacral teratoma developed a yolk sac tumor.
  • CONCLUSIONS: Diagnosis of congenital tumors is performed earlier in recent years due to the wide use of prenatal ultrasound.
  • Complete surgical excision is the treatment of choice, most cases not need adjuvant chemotherapy.
  • We ought to pass this message on to our colleagues in prenatal diagnosis, so parents get reliable information.
  • [MeSH-major] Central Nervous System Neoplasms / congenital. Kidney Neoplasms / congenital. Liver Neoplasms / congenital. Neuroblastoma / congenital. Skin Neoplasms / congenital. Soft Tissue Neoplasms / congenital. Teratoma / congenital. Wilms Tumor / congenital
  • [MeSH-minor] Female. Follow-Up Studies. Humans. Infant, Newborn. Male. Neoplasm Recurrence, Local. Postoperative Complications. Pregnancy. Prenatal Diagnosis. Time Factors

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  • (PMID = 15503950.001).
  • [ISSN] 0214-1221
  • [Journal-full-title] Cirugía pediátrica : organo oficial de la Sociedad Española de Cirugía Pediátrica
  • [ISO-abbreviation] Cir Pediatr
  • [Language] spa
  • [Publication-type] Comparative Study; English Abstract; Journal Article
  • [Publication-country] Spain
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23. Hirao M, Onai N, Hiroishi K, Watkins SC, Matsushima K, Robbins PD, Lotze MT, Tahara H: CC chemokine receptor-7 on dendritic cells is induced after interaction with apoptotic tumor cells: critical role in migration from the tumor site to draining lymph nodes. Cancer Res; 2000 Apr 15;60(8):2209-17

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • The number of the DCs migrating into lymph nodes were greater when they were inoculated into the tumor rather than the skin.
  • Chemotaxis assay showed that CCR7 ligands, macrophage inflammatory protein 3beta and secondary lymphoid-tissue chemokine significantly (P < 0.05) induced the migration of DCs when cocultured with apoptotic tumor cells.
  • The means to promote DC delivery to tumor and to nodal sites represent novel targets for the biological therapy of cancer.
  • [MeSH-major] Apoptosis. Cell Movement. Dendritic Cells / immunology. Fibrosarcoma / pathology. Gene Expression Regulation, Neoplastic. Receptors, Chemokine / genetics
  • [MeSH-minor] Animals. Chemokine CCL4. Chemokines, CC / pharmacology. Coculture Techniques. Female. Flow Cytometry. Lymph Nodes / drug effects. Lymph Nodes / immunology. Macrophage Inflammatory Proteins / pharmacology. Mice. Mice, Inbred C57BL. RNA, Messenger / genetics. RNA, Messenger / metabolism. Receptors, CCR1. Receptors, CCR7. Th1 Cells / immunology. Transduction, Genetic. Tumor Cells, Cultured. Ultraviolet Rays

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  • (PMID = 10786686.001).
  • [ISSN] 0008-5472
  • [Journal-full-title] Cancer research
  • [ISO-abbreviation] Cancer Res.
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / 1PO1 CA73743-01; United States / NCI NIH HHS / CA / P01 CA59371
  • [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 / Ccr1 protein, mouse; 0 / Ccr7 protein, mouse; 0 / Chemokine CCL4; 0 / Chemokines, CC; 0 / Macrophage Inflammatory Proteins; 0 / RNA, Messenger; 0 / Receptors, CCR1; 0 / Receptors, CCR7; 0 / Receptors, Chemokine
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24. Busch TM, Xing X, Yu G, Yodh A, Wileyto EP, Wang HW, Durduran T, Zhu TC, Wang KK: Fluence rate-dependent intratumor heterogeneity in physiologic and cytotoxic responses to Photofrin photodynamic therapy. Photochem Photobiol Sci; 2009 Dec;8(12):1683-93
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Fluence rate-dependent intratumor heterogeneity in physiologic and cytotoxic responses to Photofrin photodynamic therapy.
  • Photodynamic therapy (PDT) can lead to the creation of heterogeneous, response-limiting hypoxia during illumination, which may be controlled in part through illumination fluence rate.
  • Regional heterogeneity in tumor response was examined through comparison of effects in the surface vs. base of tumors, i.e. along a plane parallel to the skin surface and perpendicular to the incident illumination.

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  • (PMID = 20024165.001).
  • [ISSN] 1474-9092
  • [Journal-full-title] Photochemical & photobiological sciences : Official journal of the European Photochemistry Association and the European Society for Photobiology
  • [ISO-abbreviation] Photochem. Photobiol. Sci.
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / CA085831; United States / NCI NIH HHS / CA / P01 CA087971-070006; United States / NCI NIH HHS / CA / CA87971; United States / NCI NIH HHS / CA / R01 CA085831; United States / NCI NIH HHS / CA / CA087971-070006; United States / NCI NIH HHS / CA / R01 CA085831-07; United States / NCI NIH HHS / CA / P01 CA087971
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural
  • [Publication-country] England
  • [Chemical-registry-number] 0 / 2-(2-nitroimidazol-1-yl)-N-(3,3,3-trifluoropropyl)-acetamide; 0 / Nitroimidazoles; 0 / Photosensitizing Agents; 97067-70-4 / Dihematoporphyrin Ether
  • [Other-IDs] NLM/ NIHMS171939; NLM/ PMC2834171
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