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  • Humans  (5)
  • *Gene Expression  (1)
  • American Association for the Advancement of Science (AAAS)  (6)
  • American Physical Society
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  • American Association for the Advancement of Science (AAAS)  (6)
  • American Physical Society
  • 1
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    American Association for the Advancement of Science (AAAS)
    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
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  • 2
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    American Association for the Advancement of Science (AAAS)
    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
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  • 3
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    American Association for the Advancement of Science (AAAS)
    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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  • 4
    Publication Date: 1984-06-08
    Description: A domain of DNA designated N-myc is amplified 20- to 140-fold in human neuroblastoma cell lines but not in cell lines from other tumor types. N-myc has now been found to be amplified in neuroblastoma tissue from 24 of 63 untreated patients (38 percent). The extent of amplification appears to be bimodal, with amplification of 100- to 300-fold in 12 cases and 3- to 10-fold in 10 others. Amplification was found in 0 of 15 patients with stage 1 or 2 disease, whereas 24 of 48 cases (50 percent) with stage 3 or 4 had evidence of N-myc amplification. These data indicate that N-myc amplification is a common event in untreated human neuroblastomas. Furthermore, N-myc amplification is highly correlated with advanced stages of disease (P less than 0.001) and with the ability to grow in vitro as an established cell line, both of which are associated with a poor prognosis.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Brodeur, G M -- Seeger, R C -- Schwab, M -- Varmus, H E -- Bishop, J M -- CA02971/CA/NCI NIH HHS/ -- CA13539/CA/NCI NIH HHS/ -- CA17829/CA/NCI NIH HHS/ -- etc. -- New York, N.Y. -- Science. 1984 Jun 8;224(4653):1121-4.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/6719137" target="_blank"〉PubMed〈/a〉
    Keywords: Adolescent ; Adult ; Aged ; Cell Line ; Child ; Child, Preschool ; DNA, Neoplasm/genetics ; Eye Neoplasms/genetics ; *Gene Amplification ; Humans ; Infant ; Lymphatic Metastasis ; Middle Aged ; Neuroblastoma/*genetics/physiopathology ; Nucleic Acid Hybridization ; *Oncogenes ; Prognosis ; Retinoblastoma/genetics
    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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    American Association for the Advancement of Science (AAAS)
    Publication Date: 1979-01-12
    Description: Both normal human serum and supernatant from explanted malignant tumors contained a heat-stable low-molecular-weight factor that inhibited monocyte activation in vitro. In contrast, serum from individuals with solid tumors enhanced monocyte activation. It is suggested that the systemic activation of monocytes that occurs in malignant disease may be an appropriate host response but that successful tumors may continue to grow because they subvert the normal physiological signal for inhibition of macrophage activation.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Rhodes, J -- Bishop, M -- Benfield, J -- New York, N.Y. -- Science. 1979 Jan 12;203(4376):179-82.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/758686" target="_blank"〉PubMed〈/a〉
    Keywords: Binding Sites ; Carcinoma/*immunology ; Carcinoma, Squamous Cell/immunology ; Chemotaxis ; Colonic Neoplasms/*immunology ; Humans ; Immunity, Cellular ; Immunoglobulin Fc Fragments ; Lung Neoplasms/*immunology ; Macrophages/*immunology ; Monocytes/*immunology ; Rosette Formation
    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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    American Association for the Advancement of Science (AAAS)
    Publication Date: 1987-01-16
    Description: The search for genetic damage in neoplastic cells now occupies a central place in cancer research. Diverse examples of such damage are in hand, and they in turn hint at biochemical explanations for neoplastic growth. The way may be open to solve the riddles of how normal cells govern their replication and why cancer cells do not.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Bishop, J M -- CA12705/CA/NCI NIH HHS/ -- SO7 RR05355/RR/NCRR NIH HHS/ -- New York, N.Y. -- Science. 1987 Jan 16;235(4786):305-11.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/3541204" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Cell Division ; Chromosome Deletion ; DNA Damage ; DNA, Neoplasm/genetics ; Gene Amplification ; Humans ; Mutation ; Neoplasms/*genetics/pathology ; *Oncogenes ; *Proto-Oncogenes ; Retroviridae/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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