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  • 1
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    Analysis of neural crest-derived clones reveals novel aspects of facial development (2016)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2016-08-05
    Description: Cranial neural crest cells populate the future facial region and produce ectomesenchyme-derived tissues, such as cartilage, bone, dermis, smooth muscle, adipocytes, and many others. However, the contribution of individual neural crest cells to certain facial locations and the general spatial clonal organization of the ectomesenchyme have not been determined. We investigated how neural crest cells give rise to clonally organized ectomesenchyme and how this early ectomesenchyme behaves during the developmental processes that shape the face. Using a combination of mouse and zebrafish models, we analyzed individual migration, cell crowd movement, oriented cell division, clonal spatial overlapping, and multilineage differentiation. The early face appears to be built from multiple spatially defined overlapping ectomesenchymal clones. During early face development, these clones remain oligopotent and generate various tissues in a given location. By combining clonal analysis, computer simulations, mouse mutants, and live imaging, we show that facial shaping results from an array of local cellular activities in the ectomesenchyme. These activities mostly involve oriented divisions and crowd movements of cells during morphogenetic events. Cellular behavior that can be recognized as individual cell migration is very limited and short-ranged and likely results from cellular mixing due to the proliferation activity of the tissue. These cellular mechanisms resemble the strategy behind limb bud morphogenesis, suggesting the possibility of common principles and deep homology between facial and limb outgrowth.
    Electronic ISSN: 2375-2548
    Topics: Natural Sciences in General
    Published by American Association for the Advancement of Science (AAAS)
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  • 2
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    The serine-threonine kinase LKB1 is essential for survival under energetic stress in zebrafish [Genetics] (2011)
    National Academy of Sciences
    Details
    Publication Date: 2011-03-16
    Description: Mutations in the serine-threonine kinase (LKB1) lead to a gastrointestinal hamartomatous polyposis disorder with increased predisposition to cancer (Peutz–Jeghers syndrome). LKB1 has many targets, including the AMP-activated protein kinase (AMPK) that is phosphorylated under low-energy conditions. AMPK phosphorylation in turn, affects several processes, including inhibition of the target of rapamycin (TOR) pathway, and leads to proliferation inhibition. To gain insight into how LKB1 mediates its effects during development, we generated zebrafish mutants in the single LKB1 ortholog. We show that in zebrafish lkb1 is dispensable for embryonic survival but becomes essential under conditions of energetic stress. After yolk absorption, lkb1 mutants rapidly exhaust their energy resources and die prematurely from starvation. Notably, intestinal epithelial cells were polarized properly in the lkb1 mutants. We show that attenuation of metabolic rate in lkb1 mutants, either by application of the TOR inhibitor rapamycin or by crossing with von Hippel–Lindau (vhl) mutant fish (in which constitutive hypoxia signaling results in reduced metabolic rate), suppresses key aspects of the lkb1 phenotype. Thus, we demonstrate a critical role for LKB1 in regulating energy homeostasis at the whole-organism level in a vertebrate. Zebrafish models of Lkb1 inactivation could provide a platform for chemical genetic screens to identify compounds that target accelerated metabolism, a key feature of tumor cells.
    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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    Synergy between tumor suppressor APC and the beta-catenin-Tcf4 target Tcf1 (1999)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1999-09-18
    Description: Mutations in APC or beta-catenin inappropriately activate the transcription factor Tcf4, thereby transforming intestinal epithelial cells. Here it is shown that one of the target genes of Tcf4 in epithelial cells is Tcf1. The most abundant Tcf1 isoforms lack a beta-catenin interaction domain. Tcf1(-/-) mice develop adenomas in the gut and mammary glands. Introduction of a mutant APC allele into these mice substantially increases the number of these adenomas. Tcf1 may act as a feedback repressor of beta-catenin-Tcf4 target genes and thus may cooperate with APC to suppress malignant transformation of epithelial cells.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Roose, J -- Huls, G -- van Beest, M -- Moerer, P -- van der Horn, K -- Goldschmeding, R -- Logtenberg, T -- Clevers, H -- New York, N.Y. -- Science. 1999 Sep 17;285(5435):1923-6.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Immunology and Center for Biomedical Genetics, Department of Pathology, University Medical Center Utrecht, Post Office Box 85500, 3508 GA Utrecht, Netherlands.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/10489374" target="_blank"〉PubMed〈/a〉
    Keywords: Adenoma/genetics/metabolism/pathology ; Adenomatous Polyposis Coli Protein ; Animals ; Cytoskeletal Proteins/*metabolism ; DNA-Binding Proteins/*genetics/metabolism ; Female ; Gene Expression Regulation, Neoplastic ; Genes, Tumor Suppressor ; Hepatocyte Nuclear Factor 1-alpha ; Humans ; Intestinal Neoplasms/genetics/metabolism/pathology ; Lymphoid Enhancer-Binding Factor 1 ; Male ; Mammary Neoplasms, Experimental/genetics/metabolism/pathology ; Mice ; Neoplasm Proteins/metabolism ; Promoter Regions, Genetic ; T Cell Transcription Factor 1 ; TCF Transcription Factors ; *Trans-Activators ; Transcription Factor 7-Like 2 Protein ; Transcription Factors/*genetics/*metabolism ; Transfection ; Tumor Cells, Cultured ; 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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  • 4
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    Constitutive transcriptional activation by a beta-catenin-Tcf complex in APC-/- colon carcinoma (1997)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1997-03-21
    Description: The adenomatous polyposis coli (APC) tumor suppressor protein binds to beta-catenin, a protein recently shown to interact with Tcf and Lef transcription factors. The gene encoding hTcf-4, a Tcf family member that is expressed in colonic epithelium, was cloned and characterized. hTcf-4 transactivates transcription only when associated with beta-catenin. Nuclei of APC-/- colon carcinoma cells were found to contain a stable beta-catenin-hTcf-4 complex that was constitutively active, as measured by transcription of a Tcf reporter gene. Reintroduction of APC removed beta-catenin from hTcf-4 and abrogated the transcriptional transactivation. Constitutive transcription of Tcf target genes, caused by loss of APC function, may be a crucial event in the early transformation of colonic epithelium.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Korinek, V -- Barker, N -- Morin, P J -- van Wichen, D -- de Weger, R -- Kinzler, K W -- Vogelstein, B -- Clevers, H -- CA57345/CA/NCI NIH HHS/ -- New York, N.Y. -- Science. 1997 Mar 21;275(5307):1784-7.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Immunology, University Hospital, Post Office Box 85500, 3508 GA Utrecht, Netherlands.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/9065401" target="_blank"〉PubMed〈/a〉
    Keywords: Adenomatous Polyposis Coli Protein ; Amino Acid Sequence ; Animals ; Cell Line ; Cell Transformation, Neoplastic ; Cloning, Molecular ; Colon/metabolism ; Colonic Neoplasms/*genetics/metabolism ; Cytoskeletal Proteins/genetics/*metabolism ; Gene Expression Regulation, Neoplastic ; *Genes, APC ; Genes, Reporter ; Humans ; Intestinal Mucosa/metabolism ; Mice ; Molecular Sequence Data ; Signal Transduction ; TCF Transcription Factors ; *Trans-Activators ; Transcription Factor 7-Like 2 Protein ; Transcription Factors/chemistry/genetics/*metabolism ; *Transcriptional Activation ; Transfection ; Tumor Cells, Cultured ; 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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  • 5
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    Single Lgr5 stem cells build crypt-villus structures in vitro without a mesenchymal niche (2009)
    Nature Publishing Group (NPG)
    Details
    Publication Date: 2009-03-31
    Description: The intestinal epithelium is the most rapidly self-renewing tissue in adult mammals. We have recently demonstrated the presence of about six cycling Lgr5(+) stem cells at the bottoms of small-intestinal crypts. Here we describe the establishment of long-term culture conditions under which single crypts undergo multiple crypt fission events, while simultanously generating villus-like epithelial domains in which all differentiated cell types are present. Single sorted Lgr5(+) stem cells can also initiate these cryptvillus organoids. Tracing experiments indicate that the Lgr5(+) stem-cell hierarchy is maintained in organoids. We conclude that intestinal cryptvillus units are self-organizing structures, which can be built from a single stem cell in the absence of a non-epithelial cellular niche.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Sato, Toshiro -- Vries, Robert G -- Snippert, Hugo J -- van de Wetering, Marc -- Barker, Nick -- Stange, Daniel E -- van Es, Johan H -- Abo, Arie -- Kujala, Pekka -- Peters, Peter J -- Clevers, Hans -- England -- Nature. 2009 May 14;459(7244):262-5. doi: 10.1038/nature07935. Epub 2009 Mar 29.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Hubrecht Institute and University Medical Center Utrecht, Uppsalalaan 8, 3584CT Utrecht, The Netherlands.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/19329995" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Cell Culture Techniques/*methods ; Cell Lineage ; Cell Separation ; Gene Expression Regulation, Developmental ; Intestines/*anatomy & histology/*cytology/metabolism ; Mesoderm/cytology/metabolism ; Mice ; Multipotent Stem Cells/cytology/metabolism ; Organoids/*cytology/growth & development/metabolism ; Paneth Cells/metabolism ; Receptors, G-Protein-Coupled/*metabolism ; Receptors, Notch/metabolism ; Regeneration ; Stem Cell Niche ; Stem Cells/*cytology/*metabolism
    Print ISSN: 0028-0836
    Electronic ISSN: 1476-4687
    Topics: Biology , Chemistry and Pharmacology , Medicine , Natural Sciences in General , Physics
    Published by Nature Publishing Group (NPG)
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  • 6
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    Crypt stem cells as the cells-of-origin of intestinal cancer (2008)
    Nature Publishing Group (NPG)
    Details
    Publication Date: 2008-12-19
    Description: Intestinal cancer is initiated by Wnt-pathway-activating mutations in genes such as adenomatous polyposis coli (APC). As in most cancers, the cell of origin has remained elusive. In a previously established Lgr5 (leucine-rich-repeat containing G-protein-coupled receptor 5) knockin mouse model, a tamoxifen-inducible Cre recombinase is expressed in long-lived intestinal stem cells. Here we show that deletion of Apc in these stem cells leads to their transformation within days. Transformed stem cells remain located at crypt bottoms, while fuelling a growing microadenoma. These microadenomas show unimpeded growth and develop into macroscopic adenomas within 3-5weeks. The distribution of Lgr5(+) cells within stem-cell-derived adenomas indicates that a stem cell/progenitor cell hierarchy is maintained in early neoplastic lesions. When Apc is deleted in short-lived transit-amplifying cells using a different cre mouse, the growth of the induced microadenomas rapidly stalls. Even after 30weeks, large adenomas are very rare in these mice. We conclude that stem-cell-specific loss of Apc results in progressively growing neoplasia.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Barker, Nick -- Ridgway, Rachel A -- van Es, Johan H -- van de Wetering, Marc -- Begthel, Harry -- van den Born, Maaike -- Danenberg, Esther -- Clarke, Alan R -- Sansom, Owen J -- Clevers, Hans -- G0301154/Medical Research Council/United Kingdom -- Cancer Research UK/United Kingdom -- England -- Nature. 2009 Jan 29;457(7229):608-11. doi: 10.1038/nature07602. Epub 2008 Dec 17.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Hubrecht Institute for Developmental Biology and Stem Cell Research, Uppsalalaan 8, 3584CT Utrecht & University Medical Centre Utrecht, Netherlands.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/19092804" target="_blank"〉PubMed〈/a〉
    Keywords: Adenoma/genetics/metabolism/pathology ; Adenomatous Polyposis Coli Protein/*deficiency/*genetics ; Animals ; *Cell Lineage ; Cell Proliferation ; *Cell Transformation, Neoplastic/genetics/pathology ; Colonic Neoplasms/genetics/metabolism/pathology ; Genes, APC ; Intestinal Neoplasms/*genetics/metabolism/*pathology ; Mice ; Neoplastic Stem Cells/metabolism/*pathology ; Receptors, G-Protein-Coupled/analysis/genetics/metabolism ; beta Catenin/metabolism
    Print ISSN: 0028-0836
    Electronic ISSN: 1476-4687
    Topics: Biology , Chemistry and Pharmacology , Medicine , Natural Sciences in General , Physics
    Published by Nature Publishing Group (NPG)
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  • 7
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    Single-cell messenger RNA sequencing reveals rare intestinal cell types (2015)
    Nature Publishing Group (NPG)
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    Publication Date: 2015-08-20
    Description: Understanding the development and function of an organ requires the characterization of all of its cell types. Traditional methods for visualizing and isolating subpopulations of cells are based on messenger RNA or protein expression of only a few known marker genes. The unequivocal identification of a specific marker gene, however, poses a major challenge, particularly if this cell type is rare. Identifying rare cell types, such as stem cells, short-lived progenitors, cancer stem cells, or circulating tumour cells, is crucial to acquire a better understanding of normal or diseased tissue biology. To address this challenge we first sequenced the transcriptome of hundreds of randomly selected cells from mouse intestinal organoids, cultured self-organizing epithelial structures that contain all cell lineages of the mammalian intestine. Organoid buds, like intestinal crypts, harbour stem cells that continuously differentiate into a variety of cell types, occurring at widely different abundances. Since available computational methods can only resolve more abundant cell types, we developed RaceID, an algorithm for rare cell type identification in complex populations of single cells. We demonstrate that this algorithm can resolve cell types represented by only a single cell in a population of randomly sampled organoid cells. We use this algorithm to identify Reg4 as a novel marker for enteroendocrine cells, a rare population of hormone-producing intestinal cells. Next, we use Reg4 expression to enrich for these rare cells and investigate the heterogeneity within this population. RaceID confirmed the existence of known enteroendocrine lineages, and moreover discovered novel subtypes, which we subsequently validated in vivo. Having validated RaceID we then applied the algorithm to ex vivo-isolated Lgr5-positive stem cells and their direct progeny. We find that Lgr5-positive cells represent a homogenous abundant population of stem cells mixed with a rare population of Lgr5-positive secretory cells. We envision broad applicability of our method for discovering rare cell types and the corresponding marker genes in healthy and diseased organs.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Grun, Dominic -- Lyubimova, Anna -- Kester, Lennart -- Wiebrands, Kay -- Basak, Onur -- Sasaki, Nobuo -- Clevers, Hans -- van Oudenaarden, Alexander -- England -- Nature. 2015 Sep 10;525(7568):251-5. doi: 10.1038/nature14966. Epub 2015 Aug 19.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Hubrecht Institute-KNAW (Royal Netherlands Academy of Arts and Sciences), 3584 CT Utrecht, The Netherlands. ; University Medical Center Utrecht, Cancer Genomics Netherlands, 3584 CG Utrecht, The Netherlands.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/26287467" target="_blank"〉PubMed〈/a〉
    Keywords: Algorithms ; Animals ; Biomarkers/analysis ; Cell Differentiation/genetics ; Cell Lineage ; Cell Separation/*methods ; In Situ Hybridization, Fluorescence ; Intestine, Small/*cytology ; Mice ; Neoplasm Proteins/genetics ; Organoids/cytology ; Paneth Cells/cytology/metabolism ; RNA, Messenger/*genetics ; Receptors, G-Protein-Coupled/genetics ; Reproducibility of Results ; *Sequence Analysis, RNA ; *Single-Cell Analysis ; Stem Cells/cytology/metabolism ; Transcriptome/genetics
    Print ISSN: 0028-0836
    Electronic ISSN: 1476-4687
    Topics: Biology , Chemistry and Pharmacology , Medicine , Natural Sciences in General , Physics
    Published by Nature Publishing Group (NPG)
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  • 8
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    Sequential cancer mutations in cultured human intestinal stem cells (2015)
    Nature Publishing Group (NPG)
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    Publication Date: 2015-04-30
    Description: Crypt stem cells represent the cells of origin for intestinal neoplasia. Both mouse and human intestinal stem cells can be cultured in medium containing the stem-cell-niche factors WNT, R-spondin, epidermal growth factor (EGF) and noggin over long time periods as epithelial organoids that remain genetically and phenotypically stable. Here we utilize CRISPR/Cas9 technology for targeted gene modification of four of the most commonly mutated colorectal cancer genes (APC, P53 (also known as TP53), KRAS and SMAD4) in cultured human intestinal stem cells. Mutant organoids can be selected by removing individual growth factors from the culture medium. Quadruple mutants grow independently of all stem-cell-niche factors and tolerate the presence of the P53 stabilizer nutlin-3. Upon xenotransplantation into mice, quadruple mutants grow as tumours with features of invasive carcinoma. Finally, combined loss of APC and P53 is sufficient for the appearance of extensive aneuploidy, a hallmark of tumour progression.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Drost, Jarno -- van Jaarsveld, Richard H -- Ponsioen, Bas -- Zimberlin, Cheryl -- van Boxtel, Ruben -- Buijs, Arjan -- Sachs, Norman -- Overmeer, Rene M -- Offerhaus, G Johan -- Begthel, Harry -- Korving, Jeroen -- van de Wetering, Marc -- Schwank, Gerald -- Logtenberg, Meike -- Cuppen, Edwin -- Snippert, Hugo J -- Medema, Jan Paul -- Kops, Geert J P L -- Clevers, Hans -- England -- Nature. 2015 May 7;521(7550):43-7. doi: 10.1038/nature14415. Epub 2015 Apr 29.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉1] Hubrecht Institute, Royal Netherlands Academy of Arts and Sciences (KNAW) and UMC Utrecht, 3584CT Utrecht, The Netherlands [2] Cancer Genomics Netherlands, UMC Utrecht, 3584CG Utrecht, The Netherlands. ; 1] Cancer Genomics Netherlands, UMC Utrecht, 3584CG Utrecht, The Netherlands [2] Molecular Cancer Research, Centre for Molecular Medicine, UMC Utrecht, 3584CG, Utrecht, The Netherlands. ; 1] Cancer Genomics Netherlands, UMC Utrecht, 3584CG Utrecht, The Netherlands [2] Laboratory of Experimental Oncology and Radiobiology, Centre for Experimental Molecular Medicine, AMC, 1105AZ Amsterdam, The Netherlands. ; Department of Medical Genetics, UMC Utrecht, 3508AB Utrecht, The Netherlands. ; Department of Pathology, UMC Utrecht, 3584CX Utrecht, The Netherlands. ; 1] Hubrecht Institute, Royal Netherlands Academy of Arts and Sciences (KNAW) and UMC Utrecht, 3584CT Utrecht, The Netherlands [2] Cancer Genomics Netherlands, UMC Utrecht, 3584CG Utrecht, The Netherlands [3] Foundation Hubrecht Organoid Technology (HUB), 3584CT Utrecht, The Netherlands.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/25924068" target="_blank"〉PubMed〈/a〉
    Print ISSN: 0028-0836
    Electronic ISSN: 1476-4687
    Topics: Biology , Chemistry and Pharmacology , Medicine , Natural Sciences in General , Physics
    Published by Nature Publishing Group (NPG)
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  • 9
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    Cell biology. The unusual case of Porcupine (2012)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 2012-08-28
    Description: 〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4314091/" 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/PMC4314091/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Lum, Lawrence -- Clevers, Hans -- R21 HD061303/HD/NICHD NIH HHS/ -- New York, N.Y. -- Science. 2012 Aug 24;337(6097):922-3. doi: 10.1126/science.1228179.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Cell Biology, University of Texas Southwestern Medical Center, 5323 Harry Hines Boulevard, Dallas, TX 75390, USA. lawrence.lum@utsouthwestern.edu〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/22923569" target="_blank"〉PubMed〈/a〉
    Keywords: Antineoplastic Agents/pharmacology/*therapeutic use ; Clinical Trials, Phase I as Topic ; DNA-Binding Proteins/genetics ; Drug Discovery ; Enzyme Inhibitors/pharmacology/*therapeutic use ; Humans ; Membrane Proteins/*antagonists & inhibitors/genetics/*metabolism ; Molecular Targeted Therapy ; Mutation ; Neoplasms/*drug therapy/genetics/metabolism ; Oncogene Proteins/genetics ; Palmitic Acid/metabolism ; Protein-Serine-Threonine Kinases/genetics ; Wnt Proteins/*metabolism ; Wnt Signaling Pathway/*drug effects
    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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    Activation of beta-catenin-Tcf signaling in colon cancer by mutations in beta-catenin or APC (1997)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1997-03-21
    Description: Inactivation of the adenomatous polyposis coli (APC) tumor suppressor gene initiates colorectal neoplasia. One of the biochemical activities associated with the APC protein is down-regulation of transcriptional activation mediated by beta-catenin and T cell transcription factor 4 (Tcf-4). The protein products of mutant APC genes present in colorectal tumors were found to be defective in this activity. Furthermore, colorectal tumors with intact APC genes were found to contain activating mutations of beta-catenin that altered functionally significant phosphorylation sites. These results indicate that regulation of beta-catenin is critical to APC's tumor suppressive effect and that this regulation can be circumvented by mutations in either APC or beta-catenin.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Morin, P J -- Sparks, A B -- Korinek, V -- Barker, N -- Clevers, H -- Vogelstein, B -- Kinzler, K W -- CA57345/CA/NCI NIH HHS/ -- New York, N.Y. -- Science. 1997 Mar 21;275(5307):1787-90.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Howard Hughes Medical Institute and Johns Hopkins Oncology Center, 424 North Bond Street, Baltimore, MD 21231, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/9065402" target="_blank"〉PubMed〈/a〉
    Keywords: Adenomatous Polyposis Coli Protein ; Colonic Neoplasms/*genetics/metabolism ; Cytoskeletal Proteins/*genetics/*metabolism ; Gene Expression Regulation, Neoplastic ; *Genes, APC ; Genes, Reporter ; Germ-Line Mutation ; Humans ; Mutation ; Phosphorylation ; Signal Transduction ; TCF Transcription Factors ; *Trans-Activators ; Transcription Factor 7-Like 2 Protein ; Transcription Factors/*metabolism ; *Transcription, Genetic ; Transfection ; Tumor Cells, Cultured ; 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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