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  • 1
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    Immunotoxins with silencing of T-cell epitopes [Medical Sciences] (2014)
    National Academy of Sciences
    Details
    Publication Date: 2014-06-11
    Description: Nonhuman proteins have valuable therapeutic properties, but their efficacy is limited by neutralizing antibodies. Recombinant immunotoxins (RITs) are potent anticancer agents that have produced many complete remissions in leukemia, but immunogenicity limits the number of doses that can be given to patients with normal immune systems. Using human cells, we...
    Print ISSN: 0027-8424
    Electronic ISSN: 1091-6490
    Topics: Biology , Medicine , Natural Sciences in General
    Published by National Academy of Sciences
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  • 2
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    Identification and removal of T-cell epitopes [Medical Sciences] (2012)
    National Academy of Sciences
    Details
    Publication Date: 2012-12-19
    Description: Recombinant immunotoxins (RITs) are chimeric proteins that are being developed for cancer treatment. We have produced RITs that contain PE38, a portion of the bacterial protein Pseudomonas exotoxin A. Because the toxin is bacterial, it often induces neutralizing antibodies, which limit the number of treatment cycles and the effectiveness of...
    Print ISSN: 0027-8424
    Electronic ISSN: 1091-6490
    Topics: Biology , Medicine , Natural Sciences in General
    Published by National Academy of Sciences
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  • 3
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    Synaptic integration mediated by striatal cholinergic interneurons in basal ganglia function (2000)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2000-08-01
    Description: The physiological role of striatal cholinergic interneurons was investigated with immunotoxin-mediated cell targeting (IMCT). Unilateral cholinergic cell ablation caused an acute abnormal turning behavior. These mice showed gradual recovery but displayed abnormal turning by both excess stimulation and inhibition of dopamine actions. In the acute phase, basal ganglia function was shifted to a hyperactive state by stimulation and suppression of striatonigral and striatopallidal neurons, respectively. D1 and D2 dopamine receptors were then down-regulated, relieving dopamine-predominant synaptic perturbation but leaving a defect in controlling dopamine responses. The acetylcholine-dopamine interaction is concertedly and adaptively regulated for basal ganglia synaptic integration.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Kaneko, S -- Hikida, T -- Watanabe, D -- Ichinose, H -- Nagatsu, T -- Kreitman, R J -- Pastan, I -- Nakanishi, S -- New York, N.Y. -- Science. 2000 Jul 28;289(5479):633-7.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Biological Sciences, Kyoto University Faculty of Medicine, Kyoto 606-8501, Japan.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/10915629" target="_blank"〉PubMed〈/a〉
    Keywords: Acetylcholine/*metabolism ; Animals ; Apomorphine/pharmacology ; Basal Ganglia/cytology/*physiology ; Choline O-Acetyltransferase/metabolism ; Corpus Striatum/cytology/*physiology ; Dopamine/*metabolism ; Dopamine Agonists/pharmacology ; Down-Regulation ; Enkephalins/genetics/metabolism ; Immunotoxins ; Interneurons/*physiology ; Mice ; Mice, Transgenic ; Motor Activity ; Oxidopamine/pharmacology ; Posture ; Receptors, Dopamine D1/metabolism ; Receptors, Dopamine D2/metabolism ; Receptors, Glutamate/genetics/metabolism ; Substance P/genetics/metabolism ; Synapses/metabolism/*physiology
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
    Published by American Association for the Advancement of Science (AAAS)
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  • 4
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    Selection of drug-resistant bone marrow cells in vivo after retroviral transfer of human MDR1 (1992)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1992-07-03
    Description: Experiments were performed to determine if retroviral-mediated transfer of the human multidrug resistance 1 gene (MDR1) into murine bone marrow cells would confer drug resistance to the cells and whether the MDR1 gene could be used as a dominant selectable marker in vivo. When mice transplanted with bone marrow cells containing a transferred MDR1 gene were treated with the cytotoxic drug taxol, a substantial enrichment for transduced bone marrow cells was observed. This demonstration of positive selection establishes the ability to amplify clones of transduced hematopoietic cells in vivo and suggests possible applications in human therapy.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Sorrentino, B P -- Brandt, S J -- Bodine, D -- Gottesman, M -- Pastan, I -- Cline, A -- Nienhuis, A W -- New York, N.Y. -- Science. 1992 Jul 3;257(5066):99-103.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Clinical Hematology Branch, National Heart, Lung, and Blood Institute, National Institutes of Health, Bethesda, MD 20892.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/1352414" target="_blank"〉PubMed〈/a〉
    Keywords: Alkaloids/*pharmacology ; Antineoplastic Agents, Phytogenic/*pharmacology ; Base Sequence ; Bone Marrow/*physiology ; Bone Marrow Transplantation/*physiology ; DNA/genetics/isolation & purification ; Drug Resistance/*genetics ; Erythrocytes/physiology ; Genetic Vectors ; Hematopoietic Stem Cells/*cytology/drug effects ; Humans ; Molecular Sequence Data ; Oligodeoxyribonucleotides ; Paclitaxel ; Polymerase Chain Reaction/methods ; Proviruses/genetics ; Retroviridae/genetics ; *Transfection
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 5
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    Recombinant toxins for cancer treatment (1991)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1991-11-22
    Description: Recombinant toxins target cell surface receptors and antigens on tumor cells. They kill by mechanisms different from conventional chemotherapy, so that cross resistance to conventional chemotherapeutic agents should not be a problem. Furthermore, they are not mutagens and should not induce secondary malignancies or accelerate progression of benign malignancies. They can be mass-produced cheaply in bacteria as homogeneous proteins. Either growth factor-toxin fusions or antibody-toxin fusions can be chosen, depending on the cellular target.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Pastan, I -- FitzGerald, D -- New York, N.Y. -- Science. 1991 Nov 22;254(5035):1173-7.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Division of Cancer Biology, National Cancer Institute, National Institutes of Health, Bethesda, MD 20892.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/1683495" target="_blank"〉PubMed〈/a〉
    Keywords: *ADP Ribose Transferases ; Antigens, Neoplasm/metabolism ; *Bacterial Toxins ; Exotoxins/administration & dosage ; Humans ; Immunotoxins/therapeutic use ; Neoplasms/*therapy ; Proto-Oncogene Proteins/metabolism ; Receptor, Epidermal Growth Factor/metabolism ; Receptor, ErbB-2 ; Receptors, Immunologic/metabolism ; Receptors, Interleukin-2/metabolism ; Receptors, Interleukin-6 ; Recombinant Fusion Proteins ; Toxins, Biological/*administration & dosage ; *Virulence Factors
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 6
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    Modulation of activity of the promoter of the human MDR1 gene by Ras and p53 (1992)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1992-01-24
    Description: Drug resistance in human cancer is associated with overexpression of the multidrug resistance (MDR1) gene, which confers cross-resistance to hydrophobic natural product cytotoxic drugs. Expression of the MDR1 gene can occur de novo in human cancers in the absence of drug treatment. The promoter of the human MDR1 gene was shown to be a target for the c-Ha-Ras-1 oncogene and the p53 tumor suppressor gene products, both of which are associated with tumor progression. The stimulatory effect of c-Ha-Ras-1 was not specific for the MDR1 promoter alone, whereas a mutant p53 specifically stimulated the MDR1 promoter and wild-type p53 exerted specific repression. These results imply that the MDR1 gene could be activated during tumor progression associated with mutations in Ras and p53.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Chin, K V -- Ueda, K -- Pastan, I -- Gottesman, M M -- New York, N.Y. -- Science. 1992 Jan 24;255(5043):459-62.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Laboratory of Cell Biology, National Cancer Institute, Bethesda, MD 20892.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/1346476" target="_blank"〉PubMed〈/a〉
    Keywords: 3T3 Cells ; Animals ; Cell Line ; Drug Resistance ; *Gene Expression Regulation ; Genes, Tumor Suppressor ; Genes, ras ; In Vitro Techniques ; Membrane Glycoproteins/*genetics ; Mice ; P-Glycoprotein ; *Promoter Regions, Genetic ; Proto-Oncogene Proteins p21(ras)/*physiology ; Transcription, Genetic ; Tumor Suppressor Protein p53/*physiology
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 7
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    Amplification and enhanced expression of the epidermal growth factor receptor gene in A431 human carcinoma cells (1984)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1984-04-27
    Description: The sequence of the human epidermal growth factor (EGF) receptor shows great homology with the avian erythroblastosis virus v-erb B oncogene, raising the possibility that the receptor gene is identical to the c-erb B protooncogene. Human A431 epidermoid carcinoma cells, which have an unusually high number of EGF receptors, were examined to determine whether elevated EGF receptor levels correlate with gene amplification. Southern blots of genomic DNA's from A431 and other human cell lines were probed with either a v-erb B gene fragment or a human EGF receptor complementary DNA clone (pE7), previously isolated from an A431 complementary DNA library. When either probe was used to analyze Eco RI- or Hind III-generated DNA fragments, EGF receptor DNA sequences were amplified about 30-fold in A431. Differences in the banding pattern of A431 DNA fragments relative to normal fibroblast DNA indicate the occurrence of a rearrangement in the region of the receptor gene. Furthermore, A431 cells contain a characteristic, prominent 2.9-kilobase RNA. These results are consistent with the hypothesis that, in A431 cells, gene amplification, possibly associated with a translocation event, may result in the overproduction of EGF receptor protein or the appearance of the transformed phenotype (or both).〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Merlino, G T -- Xu, Y H -- Ishii, S -- Clark, A J -- Semba, K -- Toyoshima, K -- Yamamoto, T -- Pastan, I -- New York, N.Y. -- Science. 1984 Apr 27;224(4647):417-9.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/6200934" target="_blank"〉PubMed〈/a〉
    Keywords: Alpharetrovirus/genetics ; Base Sequence ; Carcinoma, Squamous Cell ; Cell Line ; Dna ; DNA Restriction Enzymes ; Epidermal Growth Factor/metabolism ; *Gene Amplification ; Genes, Viral ; Humans ; Nucleic Acid Hybridization ; Oncogenes ; Poly A/genetics ; RNA/genetics ; RNA, Messenger ; Receptor, Epidermal Growth Factor ; Receptors, Cell Surface/biosynthesis/*genetics ; Translocation, Genetic
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 8
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    Binding and mobility of the cell surface receptors for 3,3',5-triiodo-L-thyronine (1981)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1981-01-02
    Description: A fluorescent derivative of the thyroid hormone 3,3'-triiodo-L-thyronine binds to cultured mouse fibroblasts; such binding is saturable. Video intensification fluorescence microscopy indicates that binding occurs at the plasma membrane. Diffusion coefficients, obtained by fluorescence photobleaching recovery, are consistent with binding to a protein receptor on the cell surface.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Maxfield, F R -- Willingham, M C -- Pastan, I -- Dragsten, P -- Cheng, S Y -- New York, N.Y. -- Science. 1981 Jan 2;211(4477):63-5.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/6255563" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Carrier Proteins/*metabolism ; Cells, Cultured ; Cytoplasmic Granules/metabolism ; Diffusion ; Endocytosis ; Kinetics ; Membrane Fluidity ; Membrane Proteins/metabolism ; Mice ; Microscopy, Fluorescence ; Receptors, Cell Surface/*metabolism ; Receptors, Thyroid Hormone ; Triiodothyronine/*metabolism
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 9
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    Human multidrug-resistant cell lines: increased mdr1 expression can precede gene amplification (1986)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1986-05-02
    Description: The development of simultaneous resistance to multiple structurally unrelated drugs is a major impediment to cancer chemotherapy. Multidrug resistance in human KB carcinoma cells selected in colchicine, vinblastine, or Adriamycin is associated with amplification of specific DNA sequences (the multidrug resistance locus, mdr1). During colchicine selection resistance is initially accompanied by elevated expression of a 4.5-kilobase mdr1 messenger RNA (mRNA) without amplification of the corresponding genomic sequences. During selection for increased levels of resistance, expression of this mRNA is increased simultaneously with amplification of mdr1 DNA. Increased expression and amplification of mdr1 sequences were also found in multidrug-resistant sublines of human leukemia and ovarian carcinoma cells. These results suggest that increased expression of mdr1 mRNA is a common mechanism for multidrug resistance in human cells. Activation of the mdr1 gene by mutations or epigenetic changes may precede its amplification during the development of resistance.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Shen, D W -- Fojo, A -- Chin, J E -- Roninson, I B -- Richert, N -- Pastan, I -- Gottesman, M M -- New York, N.Y. -- Science. 1986 May 2;232(4750):643-5.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/3457471" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Cell Line ; Colchicine/pharmacology ; Cricetinae ; Cricetulus ; DNA, Neoplasm/genetics ; Doxorubicin/pharmacology ; *Drug Resistance ; Female ; *Gene Amplification ; Humans ; Leukemia, Lymphoid/drug therapy ; Neoplasms/*drug therapy/genetics ; Nucleic Acid Hybridization ; Ovarian Neoplasms/drug therapy ; RNA, Messenger/genetics ; Vinblastine/pharmacology
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 10
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    Binding of the Sp1 transcription factor by the human Harvey ras1 proto-oncogene promoter (1986)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1986-06-13
    Description: Members of the ras gene family encode proteins that when overproduced or mutated can transform immortalized mammalian cells. It is therefore important to understand the mechanisms by which the ras genes are regulated. The promoter region of the human Harvey ras proto-oncogene c-Ha-ras1 initiates RNA transcription at multiple sites and contains repeated copies of the hexanucleotide GGGCGG and its inverted complement CCGCCC, referred to as GC boxes. These GC boxes consist of sequences identical to those found in the SV40 early promoter, where the human cellular transcriptional factor Sp1 binds. Footprinting analysis with deoxyribonuclease I was used to show that Sp1 binds to six GC box sequences within the c-Ha-ras1 promoter. An in vivo transfection assay showed competition between the 21-base pair repeats of the SV40 promoter and the c-Ha-ras1 promoter for common regulatory factors. In this system the presence of Sp1 is apparently required for c-Ha-ras1 transcription. Analysis of deletions of the c-Ha-ras1 promoter region by means of a transient expression assay revealed that the three Sp1 binding sites closest to the RNA start sites were sufficient for full transcriptional activity.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Ishii, S -- Kadonaga, J T -- Tjian, R -- Brady, J N -- Merlino, G T -- Pastan, I -- New York, N.Y. -- Science. 1986 Jun 13;232(4756):1410-3.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/3012774" target="_blank"〉PubMed〈/a〉
    Keywords: Base Sequence ; Binding, Competitive ; DNA/metabolism ; DNA-Binding Proteins/metabolism ; Gene Expression Regulation ; HeLa Cells ; Humans ; *Promoter Regions, Genetic ; *Proto-Oncogenes ; Simian virus 40/genetics ; Transcription Factors/*genetics/metabolism
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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