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  • 1
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    American Association for the Advancement of Science (AAAS)
    Publication Date: 2001-02-07
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Lander, E S -- Weinberg, R A -- New York, N.Y. -- Science. 2000 Mar 10;287(5459):1777-82.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Biology at the 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/10755930" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Chromosome Mapping ; Chromosomes/genetics ; Cloning, Molecular ; DNA/chemistry/genetics ; DNA, Recombinant ; Evolution, Molecular ; Genes ; Genetic Code ; Genetics/*history/trends ; Genetics, Medical/history/trends ; History, 19th Century ; History, 20th Century ; Human Genome Project ; Humans ; Sequence Analysis, DNA
    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
    Publication Date: 1989-02-17
    Description: The retinoblastoma (Rb) antioncogene encodes a nuclear phosphoprotein, p105-Rb, that forms protein complexes with the adenovirus E1A and SV40 large T oncoproteins. A novel, aberrant Rb protein detected in J82 bladder carcinoma cells was not able to form a complex with E1A and was less stable than p105-Rb. By means of a rapid method for the detection of mutations in Rb mRNA, this defective Rb protein was observed to result from a single point mutation within a splice acceptor sequence in J82 genomic DNA. This mutation eliminates a single exon and 35 amino acids from its encoded protein product.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Horowitz, J M -- Yandell, D W -- Park, S H -- Canning, S -- Whyte, P -- Buchkovich, K -- Harlow, E -- Weinberg, R A -- Dryja, T P -- CA 08131/CA/NCI NIH HHS/ -- CA 13106/CA/NCI NIH HHS/ -- CA 39826/CA/NCI NIH HHS/ -- etc. -- New York, N.Y. -- Science. 1989 Feb 17;243(4893):937-40.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Whitehead Institute for Biomedical Research, Massachusetts Institute of Technology, Cambridge 02142.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/2521957" target="_blank"〉PubMed〈/a〉
    Keywords: Adenovirus Early Proteins ; Antigens, Polyomavirus Transforming ; Base Sequence ; DNA-Binding Proteins/metabolism ; Eye Neoplasms/*genetics ; Humans ; Molecular Sequence Data ; *Mutation ; Oncogene Proteins, Viral/metabolism ; *Oncogenes ; Phosphoproteins/*genetics/metabolism ; Retinoblastoma/*genetics ; Retinoblastoma Protein
    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: 1991-11-22
    Description: For the past decade, cellular oncogenes have attracted the attention of biologists intent on understanding the molecular origins of cancer. As the present decade unfolds, oncogenes are yielding their place at center stage to a second group of actors, the tumor suppressor genes, which promise to teach us equally important lessons about the molecular mechanisms of cancer pathogenesis.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Weinberg, R A -- 5R35-CA39826/CA/NCI NIH HHS/ -- New York, N.Y. -- Science. 1991 Nov 22;254(5035):1138-46.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Whitehead Institute for Biomedical Research, Cambridge, MA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/1659741" target="_blank"〉PubMed〈/a〉
    Keywords: Chromosome Mapping ; Colonic Neoplasms/genetics ; Genes, Neurofibromatosis 1 ; Genes, Retinoblastoma ; *Genes, Tumor Suppressor ; Humans ; Neurofibromatosis 1/genetics ; Retinoblastoma/genetics ; Tumor Suppressor Protein p53/genetics ; Wilms Tumor/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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  • 4
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    American Association for the Advancement of Science (AAAS)
    Publication Date: 1998-06-06
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Jacks, T -- Weinberg, R A -- New York, N.Y. -- Science. 1998 May 15;280(5366):1035-6.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Biology, Massachusetts Institute of Technology, Cambridge, MA 02142, USA. tjacks@mit.edu〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/9616080" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; *Cell Cycle ; *Cell Cycle Proteins ; *Cell Differentiation ; Cyclin D1/metabolism ; Cyclin-Dependent Kinase Inhibitor Proteins ; Cyclin-Dependent Kinase Inhibitor p21 ; Cyclin-Dependent Kinases/antagonists & inhibitors/metabolism ; Cyclins/*metabolism ; Enzyme Inhibitors/*metabolism ; Fungal Proteins/metabolism ; Proliferating Cell Nuclear Antigen/metabolism ; Protein-Serine-Threonine Kinases/metabolism ; Receptors, Estrogen/metabolism ; *Repressor Proteins ; Retinoblastoma Protein/metabolism ; *Saccharomyces cerevisiae Proteins
    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: 2008-02-23
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Hanahan, Douglas -- Weinberg, Robert A -- New York, N.Y. -- Science. 2008 Feb 22;319(5866):1055. doi: 10.1126/science.1156080.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Biochemistry and Biophysics, University of California-San Francisco, San Francisco, CA 94143, USA. dh@biochem.ucsf.edu〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/18292332" target="_blank"〉PubMed〈/a〉
    Keywords: Angiogenesis Inhibitors/*history/therapeutic use ; Animals ; History, 20th Century ; History, 21st Century ; Humans ; Neoplasms/blood supply/drug therapy/pathology ; Neovascularization, Pathologic/*history ; United States
    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: 2011-03-26
    Description: Metastasis causes most cancer deaths, yet this process remains one of the most enigmatic aspects of the disease. Building on new mechanistic insights emerging from recent research, we offer our perspective on the metastatic process and reflect on possible paths of future exploration. We suggest that metastasis can be portrayed as a two-phase process: The first phase involves the physical translocation of a cancer cell to a distant organ, whereas the second encompasses the ability of the cancer cell to develop into a metastatic lesion at that distant site. Although much remains to be learned about the second phase, we feel that an understanding of the first phase is now within sight, due in part to a better understanding of how cancer cell behavior can be modified by a cell-biological program called the epithelial-to-mesenchymal transition.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Chaffer, Christine L -- Weinberg, Robert A -- New York, N.Y. -- Science. 2011 Mar 25;331(6024):1559-64. doi: 10.1126/science.1203543.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Whitehead Institute for Biomedical Research, 9 Cambridge Center, Cambridge, MA 02142, USA. chaffer@wi.mit.edu〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/21436443" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Epithelial-Mesenchymal Transition ; Humans ; Neoplasm Invasiveness ; *Neoplasm Metastasis ; Neoplasms/*pathology/physiopathology ; Neoplastic Cells, Circulating ; Neoplastic Stem Cells/physiology ; Tumor Microenvironment
    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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  • 7
    Publication Date: 2015-04-04
    Description: By dividing asymmetrically, stem cells can generate two daughter cells with distinct fates. However, evidence is limited in mammalian systems for the selective apportioning of subcellular contents between daughters. We followed the fates of old and young organelles during the division of human mammary stemlike cells and found that such cells apportion aged mitochondria asymmetrically between daughter cells. Daughter cells that received fewer old mitochondria maintained stem cell traits. Inhibition of mitochondrial fission disrupted both the age-dependent subcellular localization and segregation of mitochondria and caused loss of stem cell properties in the progeny cells. Hence, mechanisms exist for mammalian stemlike cells to asymmetrically sort aged and young mitochondria, and these are important for maintaining stemness properties.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4405120/" 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/PMC4405120/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Katajisto, Pekka -- Dohla, Julia -- Chaffer, Christine L -- Pentinmikko, Nalle -- Marjanovic, Nemanja -- Iqbal, Sharif -- Zoncu, Roberto -- Chen, Walter -- Weinberg, Robert A -- Sabatini, David M -- P30 CA014051/CA/NCI NIH HHS/ -- R01 CA103866/CA/NCI NIH HHS/ -- R01 CA129105/CA/NCI NIH HHS/ -- R37 AI047389/AI/NIAID NIH HHS/ -- T32 GM007287/GM/NIGMS NIH HHS/ -- Howard Hughes Medical Institute/ -- New York, N.Y. -- Science. 2015 Apr 17;348(6232):340-3. doi: 10.1126/science.1260384. Epub 2015 Apr 2.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Whitehead Institute for Biomedical Research, Boston, MA 02142, USA. Department of Biology, Massachusetts Institute of Technology (MIT), Cambridge, MA 02139, USA. Howard Hughes Medical Institute, MIT, Cambridge, MA 02139, USA. Institute of Biotechnology, University of Helsinki, P.O. Box 00014, Helsinki, Finland. pekka.katajisto@helsinki.fi sabatini@wi.mit.edu. ; Institute of Biotechnology, University of Helsinki, P.O. Box 00014, Helsinki, Finland. ; Whitehead Institute for Biomedical Research, Boston, MA 02142, USA. ; Whitehead Institute for Biomedical Research, Boston, MA 02142, USA. Department of Biology, Massachusetts Institute of Technology (MIT), Cambridge, MA 02139, USA. ; Whitehead Institute for Biomedical Research, Boston, MA 02142, USA. Department of Biology, Massachusetts Institute of Technology (MIT), Cambridge, MA 02139, USA. Howard Hughes Medical Institute, MIT, Cambridge, MA 02139, USA. ; Whitehead Institute for Biomedical Research, Boston, MA 02142, USA. Department of Biology, Massachusetts Institute of Technology (MIT), Cambridge, MA 02139, USA. Howard Hughes Medical Institute, MIT, Cambridge, MA 02139, USA. Broad Institute, Cambridge, MA 02142, USA. The David H. Koch Institute for Integrative Cancer Research at MIT, Cambridge, MA 02139, USA. pekka.katajisto@helsinki.fi sabatini@wi.mit.edu.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/25837514" target="_blank"〉PubMed〈/a〉
    Keywords: Cell Aging/genetics/*physiology ; Cell Division/genetics/*physiology ; Cell Line ; Humans ; Mitochondria/*physiology/ultrastructure ; Stem Cells/*physiology/*ultrastructure
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    Electronic ISSN: 1095-9203
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  • 8
    Publication Date: 2016-03-05
    Description: The epithelial-to-mesenchymal transition enables carcinoma cells to acquire malignancy-associated traits and the properties of tumor-initiating cells (TICs). TICs have emerged in recent years as important targets for cancer therapy, owing to their ability to drive clinical relapse and enable metastasis. Here, we propose a strategy to eliminate mesenchymal TICs by inducing their conversion to more epithelial counterparts that have lost tumor-initiating ability. We report that increases in intracellular levels of the second messenger, adenosine 3',5'-monophosphate, and the subsequent activation of protein kinase A (PKA) induce a mesenchymal-to-epithelial transition (MET) in mesenchymal human mammary epithelial cells. PKA activation triggers epigenetic reprogramming of TICs by the histone demethylase PHF2, which promotes their differentiation and loss of tumor-initiating ability. This study provides proof-of-principle for inducing an MET as differentiation therapy for TICs and uncovers a role for PKA in enforcing and maintaining the epithelial state.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Pattabiraman, Diwakar R -- Bierie, Brian -- Kober, Katharina Isabelle -- Thiru, Prathapan -- Krall, Jordan A -- Zill, Christina -- Reinhardt, Ferenc -- Tam, Wai Leong -- Weinberg, Robert A -- R01-CA078461/CA/NCI NIH HHS/ -- New York, N.Y. -- Science. 2016 Mar 4;351(6277):aad3680. doi: 10.1126/science.aad3680.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Whitehead Institute for Biomedical Research, Cambridge, MA 02142, USA. ; Whitehead Institute for Biomedical Research, Cambridge, MA 02142, USA. Genome Institute of Singapore, 60 Biopolis Street, Singapore. Cancer Science Institute of Singapore, 14 Medical Drive, Singapore. ; Whitehead Institute for Biomedical Research, Cambridge, MA 02142, USA. Department of Biology, Massachusetts Institute of Technology, Cambridge, MA 02139, USA. Ludwig Center for Molecular Oncology at MIT, Cambridge, MA 02142, USA. weinberg@wi.mit.edu.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/26941323" target="_blank"〉PubMed〈/a〉
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
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  • 9
    Publication Date: 1983-03-04
    Description: A human colonic adenocarcinoma transforming gene, recently identified as a cellular homolog of the Kirsten sarcoma gene (v-ras), was used to assign the human cellular Kirsten ras2 gene to chromosome 12 by the Southern hybridization method. A single 640 base-pair Eco RI--Hind III fragment of the transforming gene, isolated by DNA transfection and molecular cloning, can detect a single Eco RI fragment (2.9 kilobase pairs) of DNA from phenotypically normal cells. The data suggest a constant chromosomal location of c-Ki-ras2.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Sakaguchi, A Y -- Naylor, S L -- Shows, T B -- Toole, J J -- McCoy, M -- Weinberg, R A -- CA16056/CA/NCI NIH HHS/ -- CA26717/CA/NCI NIH HHS/ -- GM 20454/GM/NIGMS NIH HHS/ -- New York, N.Y. -- Science. 1983 Mar 4;219(4588):1081-3.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/6823569" target="_blank"〉PubMed〈/a〉
    Keywords: Adenocarcinoma/genetics ; Chromosome Mapping ; *Chromosomes, Human, 6-12 and X ; Colonic Neoplasms/genetics ; Humans ; Hybrid Cells ; Kirsten murine sarcoma virus/genetics ; Nucleic Acid Hybridization ; *Oncogenes
    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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    American Association for the Advancement of Science (AAAS)
    Publication Date: 1983-11-18
    Description: Two dozen cellular proto-oncogenes have been discovered to date through the study of retroviruses and the use of gene transfer. They form a structurally and functionally heterogeneous group. At least five distinct mechanisms are responsible for their conversion to active oncogenes. Recent work provides experimental strategies by which many of these oncogenes, as well as oncogenes of DNA tumor viruses, may be placed into functional categories. These procedures may lead to definition of a small number of common pathways through which the various oncogenes act to transform cells.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Land, H -- Parada, L F -- Weinberg, R A -- CA14051/CA/NCI NIH HHS/ -- CA26717/CA/NCI NIH HHS/ -- New York, N.Y. -- Science. 1983 Nov 18;222(4625):771-8.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/6356358" target="_blank"〉PubMed〈/a〉
    Keywords: Gene Expression Regulation ; Genes, Viral ; Humans ; Neoplasms/*etiology/genetics ; *Oncogenes ; Retroviridae/*genetics ; Tissue Distribution ; Transfection
    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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