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  • 1
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    Anti-CD33 monoclonal antibody and etoposide/cytosine arabinoside combinations for the ex vivo purification of bone marrow in acute nonlymphocytic leukemia (1991)
    American Society of Hematology
    Details
    Publication Date: 1991-01-15
    Description: Pharmacologic and immunologic methods of ex-vivo bone marrow (BM) purging for acute nonlymphocytic leukemia (ANLL) were combined to augment the effect of either method alone. Etoposide (VP16; 20 to 30 micrograms/mL) with or without cytosine arabinoside (Ara C; 10 mg/mL) was used in tandem with the anti-CD33 monoclonal antibody (MoAb), MY9, chosen because CD33 is found on the stem cell pool in the majority of patients with ANLL. The agents were tested singly or sequentially, with a 1-hour incubation of the drugs preceding complement-mediated lysis using MY9. VP16 combined with Ara C killed up to 3.9 +/- 0.3 and 5.11 +/- 0.4 logs of the human ANLL cell lines HL60 and K562 at drug concentrations that killed only 1.2 +/- 0.1 logs of normal committed granulocyte/macrophage stem cells (CFU-GM). Adding a single exposure of the MY9 and complement (C′) to the drug-treated cells, greater than 5.4 logs of HL60 were killed. Similar to other pharmacologic agents, no differential kill for clonagenic leukemic cells (colony-forming unit- leukemia; CFU-L) from patients with ANLL was seen for drug only treated blasts versus normal CFU-granulocyte-macrophage (CFU-GM), with less than 1 log CFU-L kill at drug concentrations that spared 1 log of CFU- GM. Similarly, only 1.1 +/- 0.3 logs of ANLL CFU-L were eliminated using MY9 and C′. However, with the sequential VP16/Ara C----MY9 + C′ treatment, synergy was demonstrated and 2.6 +/- 0.3 logs of CFU-L were eliminated. Because CD33 is also found on the normal CFU-GM pool, two- stage long-term BM cultures were performed to determine pluripotent stem cell elimination by the drug/MoAb purging combination. No difference of CFU-GM or BFU-E production at 4 to 6 weeks of culture for VP16/Ara C, MY9 + C′, or VP16/AraC----My9 + C′ treated cells was seen compared with untreated controls indicating sparing of early progenitor cells. Sequential ex vivo treatment of human ANLL CFU-L with VP16/Ara C followed by complement-mediated lysis using MY9 synergistically kills CFU-L while sparing early normal hematopoietic progenitor cells, and thus may be a more effective way to purge BM than either alone.
    Print ISSN: 0006-4971
    Electronic ISSN: 1528-0020
    Topics: Biology , Medicine
    Published by American Society of Hematology
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  • 2
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    Anti-CD33 monoclonal antibody and etoposide/cytosine arabinoside combinations for the ex vivo purification of bone marrow in acute nonlymphocytic leukemia (1991)
    American Society of Hematology
    Details
    Publication Date: 1991-01-15
    Description: Pharmacologic and immunologic methods of ex-vivo bone marrow (BM) purging for acute nonlymphocytic leukemia (ANLL) were combined to augment the effect of either method alone. Etoposide (VP16; 20 to 30 micrograms/mL) with or without cytosine arabinoside (Ara C; 10 mg/mL) was used in tandem with the anti-CD33 monoclonal antibody (MoAb), MY9, chosen because CD33 is found on the stem cell pool in the majority of patients with ANLL. The agents were tested singly or sequentially, with a 1-hour incubation of the drugs preceding complement-mediated lysis using MY9. VP16 combined with Ara C killed up to 3.9 +/- 0.3 and 5.11 +/- 0.4 logs of the human ANLL cell lines HL60 and K562 at drug concentrations that killed only 1.2 +/- 0.1 logs of normal committed granulocyte/macrophage stem cells (CFU-GM). Adding a single exposure of the MY9 and complement (C′) to the drug-treated cells, greater than 5.4 logs of HL60 were killed. Similar to other pharmacologic agents, no differential kill for clonagenic leukemic cells (colony-forming unit- leukemia; CFU-L) from patients with ANLL was seen for drug only treated blasts versus normal CFU-granulocyte-macrophage (CFU-GM), with less than 1 log CFU-L kill at drug concentrations that spared 1 log of CFU- GM. Similarly, only 1.1 +/- 0.3 logs of ANLL CFU-L were eliminated using MY9 and C′. However, with the sequential VP16/Ara C----MY9 + C′ treatment, synergy was demonstrated and 2.6 +/- 0.3 logs of CFU-L were eliminated. Because CD33 is also found on the normal CFU-GM pool, two- stage long-term BM cultures were performed to determine pluripotent stem cell elimination by the drug/MoAb purging combination. No difference of CFU-GM or BFU-E production at 4 to 6 weeks of culture for VP16/Ara C, MY9 + C′, or VP16/AraC----My9 + C′ treated cells was seen compared with untreated controls indicating sparing of early progenitor cells. Sequential ex vivo treatment of human ANLL CFU-L with VP16/Ara C followed by complement-mediated lysis using MY9 synergistically kills CFU-L while sparing early normal hematopoietic progenitor cells, and thus may be a more effective way to purge BM than either alone.
    Print ISSN: 0006-4971
    Electronic ISSN: 1528-0020
    Topics: Biology , Medicine
    Published by American Society of Hematology
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  • 3
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    Regulation of area identity in the mammalian neocortex by Emx2 and Pax6 (2000)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2000-04-15
    Description: The contribution of extrinsic and genetic mechanisms in determining areas of the mammalian neocortex has been a contested issue. This study analyzes the roles of the regulatory genes Emx2 and Pax6, which are expressed in opposing gradients in the neocortical ventricular zone, in specifying areas. Changes in the patterning of molecular markers and area-specific connections between the cortex and thalamus suggest that arealization of the neocortex is disproportionately altered in Emx2 and Pax6 mutant mice in opposing manners predicted from their countergradients of expression: rostral areas expand and caudal areas contract in Emx2 mutants, whereas the opposite effect is seen in Pax6 mutants. These findings suggest that Emx2 and Pax6 cooperate to regulate arealization of the neocortex and to confer area identity to cortical cells.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Bishop, K M -- Goudreau, G -- O'Leary, D D -- NS31558/NS/NINDS NIH HHS/ -- New York, N.Y. -- Science. 2000 Apr 14;288(5464):344-9.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Molecular Neurobiology Laboratory, The Salk Institute for Biological Studies, 10010 North Torrey Pines Road, La Jolla, CA 92037, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/10764649" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Brain Mapping ; Cadherins/biosynthesis/genetics ; DNA-Binding Proteins/*genetics/physiology ; Eye Proteins ; *Gene Expression ; Gene Expression Regulation, Developmental ; *Genes, Homeobox ; *Genes, Regulator ; Homeodomain Proteins/*genetics/physiology ; Mice ; Mice, Inbred C57BL ; Mice, Inbred DBA ; Mice, Mutant Strains ; Morphogenesis ; Neocortex/*embryology/metabolism ; Neural Pathways ; Occipital Lobe/embryology/metabolism ; Paired Box Transcription Factors ; Repressor Proteins ; Somatosensory Cortex/embryology/metabolism ; Thalamus/embryology ; Transcription Factors ; Visual Cortex/embryology/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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  • 4
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    Enhanced CpG mutability and tumorigenesis in MBD4-deficient mice (2002)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2002-07-20
    Description: The mammalian protein MBD4 contains a methyl-CpG binding domain and can enzymatically remove thymine (T) or uracil (U) from a mismatched CpG site in vitro. These properties suggest that MBD4 might function in vivo to minimize the mutability of 5-methylcytosine by removing its deamination product from DNA. We tested this hypothesis by analyzing Mbd4-/- mice and found that the frequency of of C --〉 T transitions at CpG sites was increased by a factor of three. On a cancer-susceptible Apc(Min/+) background, Mbd4-/- mice showed accelerated tumor formation with CpG --〉 TpG mutations in the Apc gene. Thus MBD4 suppresses CpG mutability and tumorigenesis in vivo.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Millar, Catherine B -- Guy, Jacky -- Sansom, Owen J -- Selfridge, Jim -- MacDougall, Eilidh -- Hendrich, Brian -- Keightley, Peter D -- Bishop, Stefan M -- Clarke, Alan R -- Bird, Adrian -- New York, N.Y. -- Science. 2002 Jul 19;297(5580):403-5.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Wellcome Trust Centre for Cell Biology, The King's Buildings, Edinburgh University, Edinburgh EH9 3JR, UK.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/12130785" target="_blank"〉PubMed〈/a〉
    Keywords: 5-Methylcytosine ; Alleles ; Amino Acid Sequence ; Animals ; Base Pair Mismatch ; Cytosine/*analogs & derivatives/metabolism ; DNA Methylation ; DNA Repair ; Deamination ; Dinucleoside Phosphates/*genetics ; Endodeoxyribonucleases/*genetics/*physiology ; Female ; Gene Targeting ; Genes, APC ; Genetic Predisposition to Disease ; Intestinal Neoplasms/etiology/*genetics ; Intestine, Large ; Loss of Heterozygosity ; Male ; Mice ; Mice, Inbred C57BL ; Molecular Sequence Data ; *Point Mutation ; Suppression, Genetic
    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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  • 5
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    Sustained loss of a neoplastic phenotype by brief inactivation of MYC (2002)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2002-07-06
    Description: Pharmacological inactivation of oncogenes is being investigated as a possible therapeutic strategy for cancer. One potential drawback is that cessation of such therapy may allow reactivation of the oncogene and tumor regrowth. We used a conditional transgenic mouse model for MYC-induced tumorigenesis to demonstrate that brief inactivation of MYC results in the sustained regression of tumors and the differentiation of osteogenic sarcoma cells into mature osteocytes. Subsequent reactivation of MYC did not restore the cells' malignant properties but instead induced apoptosis. Thus, brief MYC inactivation appears to cause epigenetic changes in tumor cells that render them insensitive to MYC-induced tumorigenesis. These results raise the possibility that transient inactivation of MYC may be an effective therapy for certain cancers.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Jain, Meenakshi -- Arvanitis, Constadina -- Chu, Kenneth -- Dewey, William -- Leonhardt, Edith -- Trinh, Maxine -- Sundberg, Christopher D -- Bishop, J Michael -- Felsher, Dean W -- K08-CA75967-01/CA/NCI NIH HHS/ -- R01-CA85610/CA/NCI NIH HHS/ -- R01-CA89305-01/CA/NCI NIH HHS/ -- New York, N.Y. -- Science. 2002 Jul 5;297(5578):102-4.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Division of Oncology, Departments of Medicine and Pathology, Stanford University, Stanford, CA 94305-5151, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/12098700" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Antineoplastic Agents/administration & dosage/therapeutic use ; Apoptosis ; Cell Differentiation ; Cell Division ; Doxycycline/pharmacology ; Gene Expression/drug effects ; *Gene Silencing ; *Genes, myc ; Mice ; Mice, Transgenic ; Neoplasm Transplantation ; Osteocytes/cytology ; Osteosarcoma/drug therapy/*genetics/*pathology ; Phenotype ; Transgenes ; Tumor Cells, Cultured
    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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    Cancer: what should be done? (1998)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1998-02-12
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Bishop, J M -- New York, N.Y. -- Science. 1997 Nov 7;278(5340):995.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/9381206" target="_blank"〉PubMed〈/a〉
    Keywords: Diet ; Environmental Pollution/adverse effects ; Helicobacter Infections/complications ; Helicobacter pylori ; Humans ; Neoplasms/*etiology/*prevention & control ; Smoking ; Virus Diseases/complications
    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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  • 7
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    The search for an amyloid solution (2002)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2002-11-06
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Robinson, Stephen R -- Bishop, Glenda M -- New York, N.Y. -- Science. 2002 Nov 1;298(5595):962-4; author reply 962-4.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/12416505" target="_blank"〉PubMed〈/a〉
    Keywords: Alzheimer Disease/*etiology/metabolism/pathology/therapy ; Amyloid beta-Peptides/chemistry/*metabolism ; Brain/*metabolism ; Down Syndrome/metabolism ; Humans ; Nerve Degeneration ; Peptide Fragments/chemistry/*metabolism ; Plaque, Amyloid/pathology ; Solubility
    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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    Re-aim blame for NIH's hard times (2006)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2006-04-29
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Bishop, J Michael -- Varmus, Harold -- New York, N.Y. -- Science. 2006 Apr 28;312(5773):499.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/16645053" target="_blank"〉PubMed〈/a〉
    Keywords: Biomedical Research/economics ; Budgets ; National Institutes of Health (U.S.)/*economics/organization & administration ; Politics ; Research Support as Topic ; United States
    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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  • 9
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    Through the glass lightly (1995)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1995-03-17
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Bishop, J M -- New York, N.Y. -- Science. 1995 Mar 17;267(5204):1617.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/17808172" target="_blank"〉PubMed〈/a〉
    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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  • 10
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    Through the glass lightly (1995)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1995-03-17
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Bishop, J M -- New York, N.Y. -- Science. 1995 Mar 17;267(5204):1613.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/17808144" target="_blank"〉PubMed〈/a〉
    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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