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2. Jancík S, Drábek J, Radzioch D, Hajdúch M: Clinical relevance of KRAS in human cancers. J Biomed Biotechnol; 2010;2010:150960
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  • The KRAS gene (Ki-ras2 Kirsten rat sarcoma viral oncogene homolog) is an oncogene that encodes a small GTPase transductor protein called KRAS.
  • Activating mutations in the KRAS gene impair the ability of the KRAS protein to switch between active and inactive states, leading to cell transformation and increased resistance to chemotherapy and biological therapies targeting epidermal growth factor receptors.
  • It also underlines the importance of activating mutations in the KRAS gene in relation to carcinogenesis and their importance as diagnostic biomarkers, providing clues regarding human cancer patients' prognosis and indicating potential therapeutic approaches.

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  • (PMID = 20617134.001).
  • [ISSN] 1110-7251
  • [Journal-full-title] Journal of biomedicine & biotechnology
  • [ISO-abbreviation] J. Biomed. Biotechnol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't; Review
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / KRAS protein, human; 0 / Proto-Oncogene Proteins; EC 3.6.5.2 / ras Proteins
  • [Other-IDs] NLM/ PMC2896632
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3. Petre PM, Baciewicz FA Jr, Tigan S, Spears JR: Hyperbaric oxygen as a chemotherapy adjuvant in the treatment of metastatic lung tumors in a rat model. J Thorac Cardiovasc Surg; 2003 Jan;125(1):85-95; discussion 95
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  • [Title] Hyperbaric oxygen as a chemotherapy adjuvant in the treatment of metastatic lung tumors in a rat model.
  • OBJECTIVES: The objectives of the study were to test the hypothesis that hyperbaric levels of oxygen enhance the sensitivity of a sarcoma cell line to doxorubicin (Adriamycin) both in vitro and in vivo in a rat model of pulmonary metastases and to test the feasibility of arterialization of mixed venous blood by direct injection of aqueous oxygen into the pulmonary artery in a rat model.
  • METHODS: Rat sarcoma (MCA-2) cells were incubated in the presence of increasing concentrations of doxorubicin (0.1-2.0 micromol/L).
  • A dose-dependent toxicity relationship at 12 hours of treatment was examined with and without pretreatment with hyperbaric oxygen (3.7 atm absolute for 1.5-3.5 hours).
  • At that time the animals were divided into four groups: control (no treatment), doxorubicin at 2 mg/kg, hyperbaric oxygen (oxygen at 2 atm absolute for 30 minutes), and hyperbaric oxygen plus doxorubicin.
  • Seven days after treatment, the numbers of lung nodules were counted and the lung weights were determined.
  • CONCLUSIONS: Hyperbaric oxygen enhanced the chemotherapeutic effect of doxorubicin both in cell culture and in the rat model.
  • [MeSH-major] Antineoplastic Agents / therapeutic use. Doxorubicin / therapeutic use. Hyperbaric Oxygenation. Lung Neoplasms / therapy. Sarcoma, Experimental / therapy

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  • (PMID = 12538989.001).
  • [ISSN] 0022-5223
  • [Journal-full-title] The Journal of thoracic and cardiovascular surgery
  • [ISO-abbreviation] J. Thorac. Cardiovasc. Surg.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 80168379AG / Doxorubicin
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4. Puhlmann M, Brown CK, Gnant M, Huang J, Libutti SK, Alexander HR, Bartlett DL: Vaccinia as a vector for tumor-directed gene therapy: biodistribution of a thymidine kinase-deleted mutant. Cancer Gene Ther; 2000 Jan;7(1):66-73
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  • [Title] Vaccinia as a vector for tumor-directed gene therapy: biodistribution of a thymidine kinase-deleted mutant.
  • Tumor-directed gene therapy, such as "suicide gene" therapy, requires high levels of gene expression in a high percentage of tumor cells in vivo to be effective.
  • This report introduces the attenuated (thymidine kinase (TK)-negative) replication-competent vaccinia virus (VV) as a potential vector for tumor-directed gene therapy by studying the biodistribution of VV in animal tumor models.
  • Three other in vivo tumor models were examined for tumor-specific gene expression after intravenous delivery of VV (human melanoma in nude mice, adenocarcinoma liver metastasis in immunocompetent mice, and subcutaneous sarcoma in the rat).
  • [MeSH-major] Genetic Therapy. Genetic Vectors / genetics. Neoplasms, Experimental / therapy. Thymidine Kinase / genetics. Vaccinia virus / genetics
  • [MeSH-minor] Animals. Biomarkers, Tumor. Disease Models, Animal. Ficusin / pharmacology. Gene Expression / drug effects. Gene Expression / radiation effects. HT29 Cells. Humans. Luciferases / biosynthesis. Mice. Mice, Inbred C57BL. Mice, Nude. Mutation. Photosensitizing Agents / pharmacology. Rats. Rats, Inbred F344. Transfection / drug effects. Transfection / radiation effects. Tumor Cells, Cultured. Ultraviolet Rays. Virus Replication

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  • (PMID = 10678358.001).
  • [ISSN] 0929-1903
  • [Journal-full-title] Cancer gene therapy
  • [ISO-abbreviation] Cancer Gene Ther.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] ENGLAND
  • [Chemical-registry-number] 0 / Biomarkers, Tumor; 0 / Photosensitizing Agents; EC 1.13.12.- / Luciferases; EC 2.7.1.21 / Thymidine Kinase; KTZ7ZCN2EX / Ficusin
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5. Babincov M, Altanerov V, Altaner C, Bergemann C, Babinec P: In vitro analysis of cisplatin functionalized magnetic nanoparticles in combined cancer chemotherapy and electromagnetic hyperthermia. IEEE Trans Nanobioscience; 2008 Mar;7(1):15-9
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  • [Title] In vitro analysis of cisplatin functionalized magnetic nanoparticles in combined cancer chemotherapy and electromagnetic hyperthermia.
  • A novel platform has been developed for combined cancer chemotherapy and hyperthermia based on iron oxide magnetic nanoparticles functionalized with cis-diamminedichloroplatinum(II) (cisplatin).
  • The capabilities of this system for heating and controlled drug release were investigated, and the system was tested in vitro by the treatment of BP6 rat sarcoma cells, where we demonstrated a synergism between the effects of cisplatin-targetMAG nanoparticles and the application of electromagnetic field.
  • [MeSH-major] Cisplatin / administration & dosage. Drug Carriers / administration & dosage. Hyperthermia, Induced / methods. Magnetics / therapeutic use. Nanoparticles / administration & dosage. Sarcoma / pathology. Sarcoma / therapy
  • [MeSH-minor] Animals. Antineoplastic Agents / administration & dosage. Cell Line, Tumor. Combined Modality Therapy. Drug Therapy / methods. Rats. Treatment Outcome

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  • (PMID = 18334449.001).
  • [ISSN] 1536-1241
  • [Journal-full-title] IEEE transactions on nanobioscience
  • [ISO-abbreviation] IEEE Trans Nanobioscience
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / Drug Carriers; Q20Q21Q62J / Cisplatin
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6. Durrleman N, El Hamamsy I, Demaria R, Carrier M, Perrault LP, Albat B: [Is Dacron carcinogenic? Apropos of a case and review of the literature]. Arch Mal Coeur Vaiss; 2004 Mar;97(3):267-70
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  • Malignant lymphoma is a haematological form of sarcoma.
  • Survival after "pure" medical therapy (chemotherapy alone or associated with radiotherapy) is 6 to 8 months after diagnosis.
  • Dacron has been implicated in the pathogenesis of primary cardiac sarcoma.
  • Oppenheimer demonstrated experimental induction of sarcoma in the rat by subcutaneous implantation of polymers.
  • [MeSH-minor] Abdominal Neoplasms / drug therapy. Abdominal Neoplasms / secondary. Aged. Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Asthenia / etiology. Diagnostic Errors. Fatal Outcome. Female. Humans. Mitral Valve / surgery. Multiple Organ Failure / etiology. Myxoma / diagnosis. Sarcoma / chemically induced. Thrombosis / diagnosis

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  • (PMID = 15106752.001).
  • [ISSN] 0003-9683
  • [Journal-full-title] Archives des maladies du coeur et des vaisseaux
  • [ISO-abbreviation] Arch Mal Coeur Vaiss
  • [Language] fre
  • [Publication-type] Case Reports; English Abstract; Journal Article; Review
  • [Publication-country] France
  • [Chemical-registry-number] 0 / Polyethylene Terephthalates
  • [Number-of-references] 10
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8. Cappellacci L, Franchetti P, Vita P, Petrelli R, Grifantini M: Synthesis and antitumor activity of a heterodinucleotide of BVDU and gemcitabine. Nucleosides Nucleotides Nucleic Acids; 2008 May;27(5):460-8
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  • A heterodinucleotide comprising BVDU and Gemcitabine bound together by a 5',5'-pyrophospate bridge (BVDUp(2)dFdC) has been synthesized and evaluated as antitumor agent against AH13 rat sarcoma cells.
  • [MeSH-minor] Animals. Antiviral Agents / chemical synthesis. Antiviral Agents / chemistry. Antiviral Agents / pharmacology. Cell Line, Tumor. Drug Screening Assays, Antitumor. Rats. Sarcoma, Experimental / drug therapy

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  • (PMID = 18569785.001).
  • [ISSN] 1525-7770
  • [Journal-full-title] Nucleosides, nucleotides & nucleic acids
  • [ISO-abbreviation] Nucleosides Nucleotides Nucleic Acids
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antimetabolites, Antineoplastic; 0 / Antiviral Agents; 0W860991D6 / Deoxycytidine; 2M3055079H / brivudine; B76N6SBZ8R / gemcitabine; G34N38R2N1 / Bromodeoxyuridine
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9. Beganovic S: Clinical significance of the KRAS mutation. Bosn J Basic Med Sci; 2009 Oct;9 Suppl 1:17-20
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  • Physicians now have the opportunity to use specific biomarkers to personalize therapeutic options in various settings.
  • Recent research has demonstrated that presence of Kirsten rat sarcoma viral oncogene homolog (KRAS) mutation may directly influence medical decisions in patients with colon and lung cancer.
  • Use of KRAS oncogene as a selection marker for specific treatment is a good example of individualized medicine approach to cancer treatment.

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  • (PMID = 19912113.001).
  • [ISSN] 1512-8601
  • [Journal-full-title] Bosnian journal of basic medical sciences
  • [ISO-abbreviation] Bosn J Basic Med Sci
  • [Language] ENG
  • [Publication-type] Journal Article
  • [Publication-country] Bosnia and Herzegovina
  • [Chemical-registry-number] 0 / Antibodies, Monoclonal; 0 / Antibodies, Monoclonal, Humanized; 0 / KRAS protein, human; 0 / Proto-Oncogene Proteins; 0 / Quinazolines; 2S9ZZM9Q9V / Bevacizumab; DA87705X9K / Erlotinib Hydrochloride; EC 2.7.10.1 / Receptor, Epidermal Growth Factor; EC 3.6.5.2 / ras Proteins
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10. García-Foncillas J, Díaz-Rubio E: Progress in metastatic colorectal cancer: growing role of cetuximab to optimize clinical outcome. Clin Transl Oncol; 2010 Aug;12(8):533-42
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  • The prognosis of metastatic colorectal cancer remains poor despite advances made in recent years, particularly with new treatments directed towards molecular targets.
  • There is evidence of the role of cetuximab not only in irinotecan-refractory or heavily pretreated patients, but also of the efficacy and safety of the addition of this agent to FOLFIRI (irinotecan/5-fluorouracil/leucovorin) in first-line metastatic colorectal cancer, with an enhanced effect in 5-fluorouracil patients with Kirsten rat sarcoma (KRAS) wild-type tumours.
  • In these patients, a recent meta-analysis of the pooled Cetuximab Combined with Irinotecan in First-Line Therapy for Metastatic Colorectal Cancer (CRYSTAL) and Oxaliplatin and Cetuximab in First-Line Treatment of mCRC (OPUS) patient populations confirms that the addition of cetuximab to first-line chemotherapy achieves a statistically significant improvement in the best overall response, overall survival time, and progression-free survival (PSF) compared with chemotherapy alone.
  • Also, preliminary data indicate that cetuximab can be administered in a more convenient 2-week schedule in combination with standard chemotherapy.
  • Up to the present time, the results obtained with targeted therapy combinations are not as encouraging as initially expected.
  • Clinical and molecular predictive markers of response are under active evaluation in order to better select patients who could benefit from cetuximab treatment, with the aim of both optimising patient outcomes and avoiding unnecessary toxicities.
  • [MeSH-major] Antibodies, Monoclonal / therapeutic use. Antineoplastic Agents / therapeutic use. Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Colorectal Neoplasms / pathology. Liver Neoplasms / drug therapy. Liver Neoplasms / secondary
  • [MeSH-minor] Antibodies, Monoclonal, Humanized. Antimetabolites, Antineoplastic / administration & dosage. Antineoplastic Agents, Phytogenic / administration & dosage. Biomarkers, Tumor. Camptothecin / administration & dosage. Camptothecin / analogs & derivatives. Camptothecin / therapeutic use. Cetuximab. Fluorouracil / administration & dosage. Fluorouracil / therapeutic use. Humans. Leucovorin / administration & dosage. Leucovorin / therapeutic use. Organoplatinum Compounds / administration & dosage. Organoplatinum Compounds / therapeutic use. Proto-Oncogene Proteins / genetics. Proto-Oncogene Proteins / metabolism. Proto-Oncogene Proteins p21(ras). Receptor, Epidermal Growth Factor / antagonists & inhibitors. Vitamin B Complex / administration & dosage. ras Proteins / genetics. ras Proteins / metabolism

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  • (PMID = 20709651.001).
  • [ISSN] 1699-3055
  • [Journal-full-title] Clinical & translational oncology : official publication of the Federation of Spanish Oncology Societies and of the National Cancer Institute of Mexico
  • [ISO-abbreviation] Clin Transl Oncol
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] Italy
  • [Chemical-registry-number] 0 / Antibodies, Monoclonal; 0 / Antibodies, Monoclonal, Humanized; 0 / Antimetabolites, Antineoplastic; 0 / Antineoplastic Agents; 0 / Antineoplastic Agents, Phytogenic; 0 / Biomarkers, Tumor; 0 / KRAS protein, human; 0 / Organoplatinum Compounds; 0 / Proto-Oncogene Proteins; 04ZR38536J / oxaliplatin; 0H43101T0J / irinotecan; 12001-76-2 / Vitamin B Complex; EC 2.7.10.1 / Receptor, Epidermal Growth Factor; EC 3.6.5.2 / Proto-Oncogene Proteins p21(ras); EC 3.6.5.2 / ras Proteins; PQX0D8J21J / Cetuximab; Q573I9DVLP / Leucovorin; U3P01618RT / Fluorouracil; XT3Z54Z28A / Camptothecin; Folfox protocol; IFL protocol
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11. Mordant P, Loriot Y, Leteur C, Calderaro J, Bourhis J, Wislez M, Soria JC, Deutsch E: Dependence on phosphoinositide 3-kinase and RAS-RAF pathways drive the activity of RAF265, a novel RAF/VEGFR2 inhibitor, and RAD001 (Everolimus) in combination. Mol Cancer Ther; 2010 Feb;9(2):358-68
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  • Activation of phosphatidylinositol-3-kinase (PI3K)-AKT and Kirsten rat sarcoma viral oncogene homologue (KRAS) can induce cellular immortalization, proliferation, and resistance to anticancer therapeutics such as epidermal growth factor receptor inhibitors or chemotherapy.
  • [MeSH-minor] Animals. Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Eukaryotic Initiation Factor-4E / metabolism. Everolimus. Genes, ras. Humans. Immunosuppressive Agents / pharmacology. Intracellular Signaling Peptides and Proteins / metabolism. Mice. Mutation. Protein-Serine-Threonine Kinases / metabolism. TOR Serine-Threonine Kinases


12. Rozados VR, Sánchez AM, Gervasoni SI, Berra HH, Matar P, Graciela Scharovsky O: Metronomic therapy with cyclophosphamide induces rat lymphoma and sarcoma regression, and is devoid of toxicity. Ann Oncol; 2004 Oct;15(10):1543-50
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  • [Title] Metronomic therapy with cyclophosphamide induces rat lymphoma and sarcoma regression, and is devoid of toxicity.
  • BACKGROUND: Our aim was to investigate the clinical efficacy and toxicity of metronomic administration of low-dose cyclophosphamide (Cy) in lymphoma and sarcoma rat tumour models.
  • METHODS: Adult inbred rats were challenged with lymphoma TACB and sarcoma E100 s.c. on day 0.
  • Animals were divided into two groups: group I, control, injected with saline three times a week; and group II, treated with Cy 10 mg/kg three times a week, from day 10 until the tumour was non-palpable, or 5 mg/kg three times a week from day 7.
  • RESULTS: The administration of low-dose Cy eradicated established rat lymphomas and sarcomas; there was neither metastatic growth nor recurrence at primary sites for 100% of the lymphomas and 83% of the sarcomas.
  • In addition, the treatment did not cause weight loss, and was devoid of haematological, cardiac, hepatic and renal toxicity.
  • CONCLUSIONS: Metronomic administration of Cy at low doses on a thrice weekly schedule to already grown rat lymphomas and sarcomas demonstrated itself to be a successful antitumour therapy that did not cause weight loss and was devoid of haematological, cardiac, hepatic and renal toxicity.

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  • [CommentIn] Ann Oncol. 2005 Apr;16(4):673 [15716290.001]
  • (PMID = 15367416.001).
  • [ISSN] 0923-7534
  • [Journal-full-title] Annals of oncology : official journal of the European Society for Medical Oncology
  • [ISO-abbreviation] Ann. Oncol.
  • [Language] ENG
  • [Publication-type] Journal Article
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Antineoplastic Agents, Alkylating; 8N3DW7272P / Cyclophosphamide
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13. Yokota T, Shibata N, Ura T, Takahari D, Shitara K, Muro K, Yatabe Y: Cycleave polymerase chain reaction method is practically applicable for V-Ki-ras2 Kirsten rat sarcoma viral oncogene homolog (KRAS)/V-raf murine sarcoma viral oncogene homolog B1 (BRAF) genotyping in colorectal cancer. Transl Res; 2010 Aug;156(2):98-105
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  • [Title] Cycleave polymerase chain reaction method is practically applicable for V-Ki-ras2 Kirsten rat sarcoma viral oncogene homolog (KRAS)/V-raf murine sarcoma viral oncogene homolog B1 (BRAF) genotyping in colorectal cancer.
  • Activating V-Ki-ras2 Kirsten rat sarcoma viral oncogene homolog (KRAS) and V-raf murine sarcoma viral oncogene homolog B1 (BRAF) gene mutations are important predictive markers for antiepidermal growth factor receptor chemotherapy in colorectal cancer (CRC).
  • However, a rapid and accurate assay for KRAS/BRAF mutation detection from routine pathological specimens is lacking in clinical practice.
  • [MeSH-major] Colorectal Neoplasms / genetics. Genes, ras / genetics. Proto-Oncogene Proteins / genetics. Proto-Oncogene Proteins B-raf / genetics. Sarcoma, Experimental / genetics. ras Proteins / genetics

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  • [Copyright] Copyright (c) 2010 Mosby, Inc. All rights reserved.
  • (PMID = 20627194.001).
  • [ISSN] 1878-1810
  • [Journal-full-title] Translational research : the journal of laboratory and clinical medicine
  • [ISO-abbreviation] Transl Res
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / DNA Primers; 0 / KRAS protein, human; 0 / Proto-Oncogene Proteins; EC 2.7.11.1 / BRAF protein, human; EC 2.7.11.1 / Braf protein, mouse; EC 2.7.11.1 / Braf protein, rat; EC 2.7.11.1 / Proto-Oncogene Proteins B-raf; EC 3.6.5.2 / ras Proteins
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14. van Ijken MG, van Etten B, de Wilt JH, van Tiel ST, ten Hagen TL, Eggermont AM: Tumor necrosis factor-alpha augments tumor effects in isolated hepatic perfusion with melphalan in a rat sarcoma model. J Immunother; 2000 Jul-Aug;23(4):449-55
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  • [Title] Tumor necrosis factor-alpha augments tumor effects in isolated hepatic perfusion with melphalan in a rat sarcoma model.
  • Isolated hepatic perfusion (IHP) is an attractive approach to treating nonresectable liver tumors, because the effects of systemic chemotherapy are poor and its application is hampered by severe general toxicity.
  • In clinical and experimental settings, the efficacy of isolated limb perfusion (ILP) with tumor necrosis factor-alpha (TNF alpha) in combination with melphalan to treat melanoma in transit and soft-tissue sarcoma has been well established.
  • In an ILP model in rats, the authors previously observed synergistic anti-tumor effects of TNF and melphalan on BN 175 soft-tissue sarcoma extremity tumors.
  • The aim of the current study was to determine whether similar synergy in anti-tumor effects could be achieved by treating experimental BN 175 soft-tissue sarcoma liver tumors by IHP using these agents.
  • Thus, as in the rat ILP setting, the anti-tumor effect is augmented when TNF is added to IHP with melphalan to treat BN 175 soft-tissue sarcoma tumor-bearing rats.
  • [MeSH-major] Chemotherapy, Cancer, Regional Perfusion / methods. Liver Neoplasms / drug therapy. Liver Neoplasms / therapy. Melphalan / therapeutic use. Sarcoma, Experimental / drug therapy. Sarcoma, Experimental / therapy. Tumor Necrosis Factor-alpha / administration & dosage
  • [MeSH-minor] Adjuvants, Immunologic / administration & dosage. Animals. Antineoplastic Agents, Alkylating / therapeutic use. Combined Modality Therapy. Liver / blood supply. Male. Rats

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  • [CommentIn] J Immunother. 2000 Jul-Aug;23(4):505-6 [10916761.001]
  • (PMID = 10916754.001).
  • [ISSN] 1524-9557
  • [Journal-full-title] Journal of immunotherapy (Hagerstown, Md. : 1997)
  • [ISO-abbreviation] J. Immunother.
  • [Language] eng
  • [Publication-type] Evaluation Studies; Journal Article
  • [Publication-country] UNITED STATES
  • [Chemical-registry-number] 0 / Adjuvants, Immunologic; 0 / Antineoplastic Agents, Alkylating; 0 / Tumor Necrosis Factor-alpha; Q41OR9510P / Melphalan
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15. Al-Jamal KT, Al-Jamal WT, Akerman S, Podesta JE, Yilmazer A, Turton JA, Bianco A, Vargesson N, Kanthou C, Florence AT, Tozer GM, Kostarelos K: Systemic antiangiogenic activity of cationic poly-L-lysine dendrimer delays tumor growth. Proc Natl Acad Sci U S A; 2010 Mar 02;107(9):3966-71
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  • The PLL-dendrimer-inhibited tubule formation of SVEC4-10 murine endothelial cells and neovascularization in the chick embryo chick chorioallantoic membrane (CAM) assay.
  • Reduced vascularization of P22 rat sarcoma implanted in the dorsal window chamber of SCID mice was observed following tail vein administration (i.v.) of the PLL dendrimers.
  • Enhanced apoptosis/necrosis within tumors of PLL-dendrimer-treated animals only and reduction in the number of CD31 positive cells were observed in comparison to protamine treatment.
  • This study suggests that PLL-dendrimer molecules can exhibit a systemic antiangiogenic activity that may be used for therapy of solid tumors, and in combination with their capacity to carry other therapeutic or diagnostic agents may potentially offer capabilities for the design of theranostic systems.
  • [MeSH-major] Angiogenesis Inhibitors / pharmacology. Cell Division / drug effects. Dendrimers. Neoplasms, Experimental / pathology. Polylysine / pharmacology

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  • (PMID = 20150514.001).
  • [ISSN] 1091-6490
  • [Journal-full-title] Proceedings of the National Academy of Sciences of the United States of America
  • [ISO-abbreviation] Proc. Natl. Acad. Sci. U.S.A.
  • [Language] eng
  • [Grant] United Kingdom / Cancer Research UK / / 9993
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Angiogenesis Inhibitors; 0 / Cations; 0 / Dendrimers; 25104-18-1 / Polylysine
  • [Other-IDs] NLM/ PMC2840079
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16. Simó S, Pujadas L, Segura MF, La Torre A, Del Río JA, Ureña JM, Comella JX, Soriano E: Reelin induces the detachment of postnatal subventricular zone cells and the expression of the Egr-1 through Erk1/2 activation. Cereb Cortex; 2007 Feb;17(2):294-303
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • Although rat sarcoma viral oncogene was weakly activated upon Reelin treatment, pharmacological inhibition of the PI3K pathway blocked Reelin-dependent ERK activation, which indicates cross talk between the ERK and PI3K pathways.
  • [MeSH-major] Cell Adhesion / physiology. Cell Adhesion Molecules, Neuronal / pharmacology. Cell Movement / physiology. Cerebral Ventricles / physiology. Early Growth Response Protein 1 / metabolism. Extracellular Matrix Proteins / pharmacology. Extracellular Signal-Regulated MAP Kinases / metabolism. Nerve Tissue Proteins / pharmacology. Neurons / physiology. Serine Endopeptidases / pharmacology
  • [MeSH-minor] Animals. Animals, Newborn. Cells, Cultured. Enzyme Activation. Gene Expression / drug effects. Gene Expression / physiology. MAP Kinase Signaling System / drug effects. MAP Kinase Signaling System / physiology. Mice

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  • (PMID = 16514107.001).
  • [ISSN] 1047-3211
  • [Journal-full-title] Cerebral cortex (New York, N.Y. : 1991)
  • [ISO-abbreviation] Cereb. Cortex
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Cell Adhesion Molecules, Neuronal; 0 / Early Growth Response Protein 1; 0 / Egr1 protein, mouse; 0 / Extracellular Matrix Proteins; 0 / Nerve Tissue Proteins; EC 2.7.11.24 / Extracellular Signal-Regulated MAP Kinases; EC 3.4.21.- / Serine Endopeptidases; EC 3.4.21.- / reelin protein
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17. Health Quality Ontario: KRAS Testing for Anti-EGFR Therapy in Advanced Colorectal Cancer: An Evidence-Based and Economic Analysis. Ont Health Technol Assess Ser; 2010;10(25):1-49
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  • [Title] KRAS Testing for Anti-EGFR Therapy in Advanced Colorectal Cancer: An Evidence-Based and Economic Analysis.
  • Within the PEPP, subgroup committees were developed for each disease area.
  • For each technology, an economic analysis was also completed by the Toronto Health Economics and Technology Assessment Collaborative (THETA) and is summarized within the reports.THE FOLLOWING REPORTS CAN BE PUBLICLY ACCESSED AT THE MAS WEBSITE AT: www.health.gov.on.ca/mas or at www.health.gov.on.ca/english/providers/program/mas/mas_about.htmlGENE EXPRESSION PROFILING FOR GUIDING ADJUVANT CHEMOTHERAPY DECISIONS IN WOMEN WITH EARLY BREAST CANCER: An Evidence-Based and Economic AnalysisEpidermal Growth Factor Receptor Mutation (EGFR) Testing for Prediction of Response to EGFR-Targeting Tyrosine Kinase Inhibitor (TKI) Drugs in Patients with Advanced Non-Small-Cell Lung Cancer: an Evidence-Based and Economic AnalysisK-RAS testing in Treatment Decisions for Advanced Colorectal Cancer: an Evidence-Based and Economic Analysis.
  • OBJECTIVE: The objective of this systematic review is to determine the predictive value of KRAS testing in the treatment of metastatic colorectal cancer (mCRC) with two anti-EGFR agents, cetuximab and panitumumab.
  • KRAS (Kristen-RAS, a member of the rat sarcoma virus (ras) gene family of oncogenes) is frequently mutated in epithelial cancers such as colorectal cancer, with mutations occurring in mutational hotspots (codons 12 and 13) of the KRAS protein.
  • Such a mutation is also hypothesized to be involved in resistance to targeted anti-EGFR (epidermal growth factor receptor with tyrosine kinase activity) treatments such as cetuximab and panitumumab, hence, the important in evaluating the evidence on the predictive value of KRAS testing in this context.
  • KRAS MUTATION TESTING IN ADVANCED COLORECTAL CANCER: Both cetuximab and panitumumab are indicated by Health Canada in the treatment of patients with metastatic colorectal cancer whose tumours are WT for the KRAS gene.
  • Cetuximab may be offered as monotherapy in patients intolerant to irinotecan-based chemotherapy or in patients who have failed both irinotecan and oxaliplatin-based regimens and who received a fluoropyrimidine.
  • It can also be administered in combination with irinotecan in patients refractory to other irinotecan-based chemotherapy regimens.
  • Panitumumab is only indicated as a single agent after failure of fluoropyrimidine-, oxaliplatin-, and irinotecan-containing chemotherapy regimens.
  • In Ontario, patients with advanced colorectal cancer who are refractory to chemotherapy may be offered the targeted anti-EGFR treatments cetuximab or panitumumab.
  • Eligibility for these treatments is based on the KRAS status of their tumour, derived from tissue collected from surgical or biopsy specimens.
  • It is believed that KRAS status is not affected by treatments, therefore, for patients for whom surgical tissue is available for KRAS testing, additional biopsies prior to treatment with these targeted agents is not necessary.
  • For patients that have not undergone surgery or for whom surgical tissue is not available, a biopsy of either the primary or metastatic site is required to determine their KRAS status.
  • RESEARCH QUESTION: To determine if there is predictive value of KRAS testing in guiding treatment decisions with anti-EGFR targeted therapies in advanced colorectal cancer patients refractory to chemotherapy.
  • In total, 14 observational studies were identified for inclusion in this EBA: 4 for cetuximab monotherapy, 7 for the cetuximab-irinotecan combination therapy, and 3 to be included in the review for panitumumab monotherapy INCLUSION CRITERIA: English-language articles, and English or French-language HTAs published from January 2005 to May 2010, inclusive.Randomized controlled trials (RCTs) or observational studies, including single arm treatment studies that include KRAS testing.Studies with data on main outcomes of interest, overall and progression-free survival.Studies of third line treatment with cetuximab or panitumumab in patients with advanced colorectal cancer refractory to chemotherapy.For the cetuximab-irinotecan evaluation, studies in which at least 70% of patients in the study received this combination therapy.
  • CETUXIMAB-IRINOTECAN COMBINATION THERAPY: There is low GRADE evidence that testing for KRAS may optimize survival benefits in patients without the KRAS mutation (KRAS wildtype, or KRAS WT) compared to those with the mutation.
  • However, cetuximab-irinotecan combination treatments based on KRAS status discount any effect of cetuximab in possibly reversing resistance to irinotecan in patients with the mutation, as observed effects were lower than for patients without the mutation.
  • Evaluation of relative cost-effectiveness, based on a decision-analytic cost-utility analysis, assessed testing for KRAS genetic mutations versus no testing in the context of treatment with cetuximab monotherapy, panitumumab monotherapy, cetuximab in combination with irinotecan, and best supportive care.
  • Of importance to note is that the cost-effectiveness analysis focused on the impact of testing for KRAS mutations compared to no testing in the context of different treatment options, and does not assess the cost-effectiveness of the drug treatments alone.
  • CONCLUSIONS: KRAS status is predictive of outcomes in cetuximab and panitumumab monotherapy, and in cetuximab-irinotecan combination therapy.
  • While KRAS testing is cost-effective for all strategies considered, it is not equally cost-effective for all treatment options.

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  • (PMID = 23074403.001).
  • [ISSN] 1915-7398
  • [Journal-full-title] Ontario health technology assessment series
  • [ISO-abbreviation] Ont Health Technol Assess Ser
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Canada
  • [Other-IDs] NLM/ PMC3377508
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