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  • 1
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    Cancer regression in patients after transfer of genetically engineered lymphocytes (2006)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2006-09-02
    Description: Through the adoptive transfer of lymphocytes after host immunodepletion, it is possible to mediate objective cancer regression in human patients with metastatic melanoma. However, the generation of tumor-specific T cells in this mode of immunotherapy is often limiting. Here we report the ability to specifically confer tumor recognition by autologous lymphocytes from peripheral blood by using a retrovirus that encodes a T cell receptor. Adoptive transfer of these transduced cells in 15 patients resulted in durable engraftment at levels exceeding 10% of peripheral blood lymphocytes for at least 2 months after the infusion. We observed high sustained levels of circulating, engineered cells at 1 year after infusion in two patients who both demonstrated objective regression of metastatic melanoma lesions. This study suggests the therapeutic potential of genetically engineered cells for the biologic therapy of cancer.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2267026/" target="_blank"〉〈img src="https://static.pubmed.gov/portal/portal3rc.fcgi/4089621/img/3977009" border="0"〉〈/a〉   〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2267026/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Morgan, Richard A -- Dudley, Mark E -- Wunderlich, John R -- Hughes, Marybeth S -- Yang, James C -- Sherry, Richard M -- Royal, Richard E -- Topalian, Suzanne L -- Kammula, Udai S -- Restifo, Nicholas P -- Zheng, Zhili -- Nahvi, Azam -- de Vries, Christiaan R -- Rogers-Freezer, Linda J -- Mavroukakis, Sharon A -- Rosenberg, Steven A -- Z01 BC010763-01/Intramural NIH HHS/ -- Z01 SC003811-32/Intramural NIH HHS/ -- Z99 CA999999/Intramural NIH HHS/ -- New York, N.Y. -- Science. 2006 Oct 6;314(5796):126-9. Epub 2006 Aug 31.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Surgery Branch, Center for Cancer Research, National Cancer Institute, National Institutes of Health, 10 Center Drive, Bethesda, MD 20892, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/16946036" target="_blank"〉PubMed〈/a〉
    Keywords: *Adoptive Transfer ; Adult ; Antigens, Neoplasm/*immunology ; CD8-Positive T-Lymphocytes/*immunology ; Cancer Vaccines/therapeutic use ; Cells, Cultured ; Electroporation ; Female ; Genetic Engineering ; *Genetic Therapy ; HLA-A Antigens/immunology ; HLA-A2 Antigen ; Humans ; Interleukin-2/immunology/therapeutic use ; MART-1 Antigen ; Male ; Melanoma/immunology/secondary/*therapy ; Middle Aged ; Neoplasm Proteins/*immunology ; Receptors, Antigen, T-Cell, alpha-beta/*genetics/*immunology ; Transduction, Genetic ; Transgenes
    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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  • 2
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    Fc and C3b receptors on pulmonary endothelial cells: induction by injury (1981)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1981-10-30
    Description: Receptors for the activated third component of complement and for the Fc portion of immunoglobulin G are not expressed by apparently normal bovine pulmonary endothelial cells, but are expressed when the cells are exposed to white cell lysates or are infected with influenza or cytomegalovirus. The unmasking of these latent receptors may contribute to the pulmonary inflammatory response characteristic of, for example, anaphylaxis and to those lung diseases characterized by the deposition of immune complexes.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Ryan, U S -- Schultz, D R -- Ruan, J W -- HL 21568/HL/NHLBI NIH HHS/ -- HL 22087/HL/NHLBI NIH HHS/ -- New York, N.Y. -- Science. 1981 Oct 30;214(4520):557-8.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/6270789" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Cattle ; Cells, Cultured ; Complement C3b/metabolism ; Cytomegalovirus Infections/physiopathology ; Endothelium/metabolism ; Orthomyxoviridae Infections/physiopathology ; Pulmonary Artery/*cytology ; Receptors, Complement/*metabolism ; Receptors, Fc/*metabolism
    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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  • 3
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    Endothelial cells of bovine pulmonary artery lack receptors for C3b and for the Fc portion of immunoglobulin G (1980)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1980-05-16
    Description: Bovine pulmonary endothelial cells do not possess receptors for the 3b component of complement (C3b) or for the Fc portion of immunoglobulin G. The lack of these receptors may help explain the nonthrombogenic function of endothelial cells. Our findings rule out the possibility that endothelial cells participate in pulmonary immune complex disease through the binding of C3b or Fc fragments.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Ryan, U S -- Schultz, D R -- Del Vecchio, P J -- Ryan, J W -- New York, N.Y. -- Science. 1980 May 16;208(4445):748-9.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/7367890" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Cattle ; Cells, Cultured ; Complement C3b/metabolism ; Endothelium/immunology ; Pulmonary Artery/*immunology/metabolism ; Receptors, Complement/*metabolism ; Receptors, Fc/*metabolism ; Rosette Formation
    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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    TFEB links autophagy to lysosomal biogenesis (2011)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2011-05-28
    Description: Autophagy is a cellular catabolic process that relies on the cooperation of autophagosomes and lysosomes. During starvation, the cell expands both compartments to enhance degradation processes. We found that starvation activates a transcriptional program that controls major steps of the autophagic pathway, including autophagosome formation, autophagosome-lysosome fusion, and substrate degradation. The transcription factor EB (TFEB), a master gene for lysosomal biogenesis, coordinated this program by driving expression of autophagy and lysosomal genes. Nuclear localization and activity of TFEB were regulated by serine phosphorylation mediated by the extracellular signal-regulated kinase 2, whose activity was tuned by the levels of extracellular nutrients. Thus, a mitogen-activated protein kinase-dependent mechanism regulates autophagy by controlling the biogenesis and partnership of two distinct cellular organelles.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3638014/" target="_blank"〉〈img src="https://static.pubmed.gov/portal/portal3rc.fcgi/4089621/img/3977009" border="0"〉〈/a〉   〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3638014/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Settembre, Carmine -- Di Malta, Chiara -- Polito, Vinicia Assunta -- Garcia Arencibia, Moises -- Vetrini, Francesco -- Erdin, Serkan -- Erdin, Serpil Uckac -- Huynh, Tuong -- Medina, Diego -- Colella, Pasqualina -- Sardiello, Marco -- Rubinsztein, David C -- Ballabio, Andrea -- 250154/European Research Council/International -- 5 P30 HD024064/HD/NICHD NIH HHS/ -- G0600194/Medical Research Council/United Kingdom -- P30 HD024064/HD/NICHD NIH HHS/ -- R01 NS078072/NS/NINDS NIH HHS/ -- TGM11CB6/Telethon/Italy -- Medical Research Council/United Kingdom -- Wellcome Trust/United Kingdom -- New York, N.Y. -- Science. 2011 Jun 17;332(6036):1429-33. doi: 10.1126/science.1204592. Epub 2011 May 26.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Telethon Institute of Genetics and Medicine (TIGEM), Via Pietro Castellino 111, 80131 Naples, Italy.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/21617040" target="_blank"〉PubMed〈/a〉
    Keywords: Active Transport, Cell Nucleus ; Animals ; *Autophagy ; Basic Helix-Loop-Helix Leucine Zipper Transcription Factors/genetics/*metabolism ; COS Cells ; Cell Nucleus/*metabolism ; Cells, Cultured ; Cercopithecus aethiops ; Cytoplasm/metabolism ; Gene Expression Regulation ; HeLa Cells ; Humans ; Liver/metabolism ; Lysosomes/*metabolism ; MAP Kinase Signaling System ; Mice ; Mice, Transgenic ; Microtubule-Associated Proteins/metabolism ; Mitogen-Activated Protein Kinase 1/metabolism ; Phagosomes/metabolism ; Phosphorylation ; RNA Interference ; Transcription, Genetic ; Up-Regulation
    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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