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  • 1
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    De novo crypt formation and juvenile polyposis on BMP inhibition in mouse intestine (2004)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2004-03-16
    Description: Little is known about the signaling mechanisms that determine the highly regular patterning of the intestinal epithelium into crypts and villi. With the use of mouse models, we show that bone morphogenetic protein (BMP)-4 expression occurs exclusively in the intravillus mesenchyme. Villus epithelial cells respond to the BMP signal. Inhibition of BMP signaling by transgenic expression of noggin results in the formation of numerous ectopic crypt units perpendicular to the crypt-villus axis. These changes phenocopy the intestinal histopathology of patients with the cancer predisposition syndrome juvenile polyposis (JP), including the frequent occurrence of intraepithelial neoplasia. Many JP cases are known to harbor mutations in BMP pathway genes. These data indicate that intestinal BMP signaling represses de novo crypt formation and polyp growth.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Haramis, Anna-Pavlina G -- Begthel, Harry -- van den Born, Maaike -- van Es, Johan -- Jonkheer, Suzanne -- Offerhaus, G Johan A -- Clevers, Hans -- New York, N.Y. -- Science. 2004 Mar 12;303(5664):1684-6.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Hubrecht Laboratory, Netherlands Institute for Developmental Biology, Uppsalalaan 8, 3584 CT Utrecht, Netherlands.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/15017003" target="_blank"〉PubMed〈/a〉
    Keywords: Adenoma/pathology ; Animals ; Bone Morphogenetic Protein 4 ; Bone Morphogenetic Proteins/antagonists & inhibitors/genetics/*metabolism ; Carrier Proteins ; Cell Differentiation ; Cytoskeletal Proteins/metabolism ; Intestinal Mucosa/embryology/*growth & development/metabolism ; Intestinal Neoplasms/pathology ; Intestinal Polyposis/metabolism/*pathology ; Intestine, Small/embryology/*growth & development/metabolism ; Mesoderm/metabolism ; Mice ; Mice, Transgenic ; Proteins/genetics/metabolism ; *Signal Transduction ; Trans-Activators/metabolism ; Xenopus ; Xenopus Proteins ; beta Catenin
    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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    Regulation of cell fate decision of undifferentiated spermatogonia by GDNF (2000)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2000-02-26
    Description: The molecular control of self-renewal and differentiation of stem cells has remained enigmatic. Transgenic loss-of-function and overexpression models now show that the dosage of glial cell line-derived neurotrophic factor (GDNF), produced by Sertoli cells, regulates cell fate decisions of undifferentiated spermatogonial cells that include the stem cells for spermatogenesis. Gene-targeted mice with one GDNF-null allele show depletion of stem cell reserves, whereas mice overexpressing GDNF show accumulation of undifferentiated spermatogonia. They are unable to respond properly to differentiation signals and undergo apoptosis upon retinoic acid treatment. Nonmetastatic testicular tumors are regularly formed in older GDNF-overexpressing mice. Thus, GDNF contributes to paracrine regulation of spermatogonial self-renewal and differentiation.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Meng, X -- Lindahl, M -- Hyvonen, M E -- Parvinen, M -- de Rooij, D G -- Hess, M W -- Raatikainen-Ahokas, A -- Sainio, K -- Rauvala, H -- Lakso, M -- Pichel, J G -- Westphal, H -- Saarma, M -- Sariola, H -- New York, N.Y. -- Science. 2000 Feb 25;287(5457):1489-93.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Research Programs of Developmental Biology, Molecular Neurobiology, Electron Microscopy Unit, Institute of Biotechnology, Viikki Biocenter, Finland.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/10688798" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Apoptosis/drug effects ; Cell Cycle ; Cell Differentiation/drug effects ; Cobalt/metabolism ; *Drosophila Proteins ; Female ; Gene Expression ; Gene Targeting ; Glial Cell Line-Derived Neurotrophic Factor ; Glial Cell Line-Derived Neurotrophic Factor Receptors ; Male ; Mice ; Mice, Transgenic ; Mitosis ; *Nerve Growth Factors ; Nerve Tissue Proteins/genetics/*physiology ; Proto-Oncogene Proteins/genetics/metabolism ; Proto-Oncogene Proteins c-ret ; Receptor Protein-Tyrosine Kinases/genetics/metabolism ; Sertoli Cells/cytology/physiology ; *Spermatogenesis ; Spermatogonia/*cytology/drug effects ; Stem Cells/*cytology ; Testicular Neoplasms/pathology ; Testis/anatomy & histology ; Vitamin A/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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  • 3
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    Immunology. B cell receptor rehabilitation--pausing to reflect (2001)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2001-03-10
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉King, L B -- Monroe, J G -- New York, N.Y. -- Science. 2001 Feb 23;291(5508):1503-5.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Pathology and Laboratory Medicine, University of Pennsylvania School of Medicine, Philadelphia, PA 19104, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/11234081" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Apoptosis ; Autoantigens/immunology ; B-Lymphocytes/cytology/*immunology ; Clonal Anergy ; Clonal Deletion ; *Gene Rearrangement, B-Lymphocyte, Light Chain ; Genes, Immunoglobulin ; Hematopoietic Stem Cells/cytology/immunology ; Mice ; Mice, Transgenic ; Models, Immunological ; Receptors, Antigen, B-Cell/*genetics/*immunology ; Recombination, Genetic ; *Self Tolerance ; Signal Transduction
    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
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    Dilated cardiomyopathy and heart failure caused by a mutation in phospholamban (2003)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2003-03-01
    Description: Molecular etiologies of heart failure, an emerging cardiovascular epidemic affecting 4.7 million Americans and costing 17.8 billion health-care dollars annually, remain poorly understood. Here we report that an inherited human dilated cardiomyopathy with refractory congestive heart failure is caused by a dominant Arg --〉 Cys missense mutation at residue 9 (R9C) in phospholamban (PLN), a transmembrane phosphoprotein that inhibits the cardiac sarcoplasmic reticular Ca2+-adenosine triphosphatase (SERCA2a) pump. Transgenic PLN(R9C) mice recapitulated human heart failure with premature death. Cellular and biochemical studies revealed that, unlike wild-type PLN, PLN(R9C) did not directly inhibit SERCA2a. Rather, PLN(R9C) trapped protein kinase A (PKA), which blocked PKA-mediated phosphorylation of wild-type PLN and in turn delayed decay of calcium transients in myocytes. These results indicate that myocellular calcium dysregulation can initiate human heart failure-a finding that may lead to therapeutic opportunities.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Schmitt, Joachim P -- Kamisago, Mitsuhiro -- Asahi, Michio -- Li, Guo Hua -- Ahmad, Ferhaan -- Mende, Ulrike -- Kranias, Evangelia G -- MacLennan, David H -- Seidman, J G -- Seidman, Christine E -- New York, N.Y. -- Science. 2003 Feb 28;299(5611):1410-3.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Genetics, Harvard Medical School and Howard Hughes Medical Institute, 200 Longwood Avenue, Boston, MA 02115, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/12610310" target="_blank"〉PubMed〈/a〉
    Keywords: Amino Acid Sequence ; Amino Acid Substitution ; Animals ; Calcium/metabolism ; Calcium Signaling ; Calcium-Binding Proteins/chemistry/*genetics/*physiology ; Calcium-Transporting ATPases/antagonists & inhibitors/metabolism ; Cardiomegaly ; Cardiomyopathy, Dilated/*genetics/pathology/physiopathology ; Cell Line ; Cyclic AMP-Dependent Protein Kinases/metabolism ; Female ; Heart Failure/*genetics/pathology/physiopathology ; Heart Ventricles/metabolism/pathology ; Humans ; Lod Score ; Male ; Mice ; Mice, Transgenic ; Molecular Sequence Data ; Muscle Cells/metabolism/physiology ; *Mutation, Missense ; Myocardial Contraction ; Myocardium/pathology ; Pedigree ; Phosphorylation ; Sarcoplasmic Reticulum Calcium-Transporting ATPases
    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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    Gastric cancer originating from bone marrow-derived cells (2004)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2004-11-30
    Description: Epithelial cancers are believed to originate from transformation of tissue stem cells. However, bone marrow-derived cells (BMDCs), which are frequently recruited to sites of tissue injury and inflammation, might also represent a potential source of malignancy. We show that although acute injury, acute inflammation, or transient parietal cell loss within the stomach do not lead to BMDC recruitment, chronic infection of C57BL/6 mice with Helicobacter, a known carcinogen, induces repopulation of the stomach with BMDCs. Subsequently, these cells progress through metaplasia and dysplasia to intraepithelial cancer. These findings suggest that epithelial cancers can originate from marrow-derived sources and thus have broad implications for the multistep model of cancer progression.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Houghton, Jeanmarie -- Stoicov, Calin -- Nomura, Sachiyo -- Rogers, Arlin B -- Carlson, Jane -- Li, Hanchen -- Cai, Xun -- Fox, James G -- Goldenring, James R -- Wang, Timothy C -- CA95103/CA/NCI NIH HHS/ -- K22 CA90518/CA/NCI NIH HHS/ -- R01 CA87958/CA/NCI NIH HHS/ -- R01 DK58/DK/NIDDK NIH HHS/ -- New York, N.Y. -- Science. 2004 Nov 26;306(5701):1568-71.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Medicine and Cancer Biology, University of Massachusetts Medical School, Worcester, MA 01605, USA. jeanmarie.houghton@umassmed.edu〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/15567866" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Apoptosis ; Bone Marrow Cells/*cytology ; Bone Marrow Transplantation ; Carcinoma in Situ/pathology ; Cell Differentiation ; Cell Fusion ; Disease Progression ; Female ; Gastric Mucosa/chemistry/pathology ; Gastritis/*pathology ; Helicobacter Infections/*pathology ; *Helicobacter felis ; Keratins/analysis ; Male ; Mesenchymal Stromal Cells/physiology ; Metaplasia ; Mice ; Mice, Inbred C57BL ; Mice, Transgenic ; Mucins/analysis ; Muscle Proteins/analysis ; Parietal Cells, Gastric/physiology ; Peptides/analysis ; Phenotype ; Stem Cells/*physiology ; Stomach Neoplasms/*pathology
    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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    Induction of tumors in mice by genomic hypomethylation (2003)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2003-04-19
    Description: Genome-wide DNA hypomethylation occurs in many human cancers, but whether this epigenetic change is a cause or consequence of tumorigenesis has been unclear. To explore this phenomenon, we generated mice carrying a hypomorphic DNA methyltransferase 1 (Dnmt1) allele, which reduces Dnmt1 expression to 10% of wild-type levels and results in substantial genome-wide hypomethylation in all tissues. The mutant mice were runted at birth, and at 4 to 8 months of age they developed aggressive T cell lymphomas that displayed a high frequency of chromosome 15 trisomy. These results indicate that DNA hypomethylation plays a causal role in tumor formation, possibly by promoting chromosomal instability.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Gaudet, Francois -- Hodgson, J Graeme -- Eden, Amir -- Jackson-Grusby, Laurie -- Dausman, Jessica -- Gray, Joe W -- Leonhardt, Heinrich -- Jaenisch, Rudolf -- CA87869/CA/NCI NIH HHS/ -- New York, N.Y. -- Science. 2003 Apr 18;300(5618):489-92.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Whitehead Institute for Biomedical Research and Department of Biology, Massachusetts Institute of Technology, Cambridge, MA 02142, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/12702876" target="_blank"〉PubMed〈/a〉
    Keywords: Alleles ; Animals ; Birth Weight ; Cell Transformation, Neoplastic ; *Chromosome Aberrations ; Chromosomes, Mammalian/*genetics/physiology ; DNA (Cytosine-5-)-Methyltransferase/genetics/metabolism ; *DNA Methylation ; Endogenous Retroviruses/genetics/physiology ; Gene Expression ; Gene Expression Regulation, Neoplastic ; Gene Rearrangement ; Gene Rearrangement, beta-Chain T-Cell Antigen Receptor ; Genes, myc ; Heterozygote ; Loss of Heterozygosity ; Lymphoma, T-Cell/*genetics/pathology ; Mice ; Mice, Transgenic ; Moloney murine leukemia virus/genetics/physiology ; Trisomy ; Virus Activation
    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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