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  • 1
    Publication Date: 1988-02-12
    Description: Mesoderm induction in the amphibian embryo can be studied by exposing animal region explants (destined to become ectoderm) to appropriate stimuli and assaying the appearance of mesodermal products like alpha-actin messenger RNA. Transforming growth factor beta 2 (TGF-beta 2), but not TGF-beta 1, was active in alpha-actin induction, while addition of fibroblast growth factor had a small synergistic effect. Medium conditioned by Xenopus XTC cells (XTC-CM), known to have powerful mesoderm-inducing activity, was shown to contain TGF-beta-like activity as measured by a radioreceptor binding assay, colony formation in NRK cells, and growth inhibition in CCL64 cells. The activity of XTC-CM in mesoderm induction and in growth inhibition of CCL64 cells was inhibited partially by antibodies to TGF-beta 2 but not by antibodies to TGF-beta 1. Thus, a TGF-beta 2-like molecule may be involved in mesoderm induction.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Rosa, F -- Roberts, A B -- Danielpour, D -- Dart, L L -- Sporn, M B -- Dawid, I B -- New York, N.Y. -- Science. 1988 Feb 12;239(4841 Pt 1):783-5.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Laboratory of Molecular Genetics, National Institute of Child Health and Human Development, Bethesda, MD 20892.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/3422517" target="_blank"〉PubMed〈/a〉
    Keywords: Actins/genetics ; Amphibians/*embryology ; Animals ; Cell Division/drug effects ; Cell Line ; Embryo, Nonmammalian/physiology ; Growth Substances/*physiology ; Mesoderm/*physiology ; Peptides/pharmacology/*physiology ; RNA, Messenger/genetics ; Transforming Growth Factors ; Xenopus
    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: 1990-06-29
    Description: In Rous sarcoma virus (RSV)-infected chickens, wounding leads to tumor formation with nearly 100% frequency in tissues that would otherwise remain tumor-free. Identifying molecular mediators of this phenomenon should yield important clues to the mechanisms involved in RSV tumorigenesis. Immunohistochemical staining showed that TGF-beta is present locally shortly after wounding, but not unwounded controls. In addition, subcutaneous administration of recombinant transforming growth factor-beta 1 (TGF-beta 1) could substitute completely for wounding in tumor induction. A treatment protocol of four doses of 800 nanograms of TGF-beta resulted in v-src-expressing tumors with 100% frequency; four doses of only 10 nanograms still led to tumor formation in 80% of the animals. This effect was specific, as other growth factors with suggested roles in wound healing did not elicit the same response. Epidermal growth factor (EGF) or TGF-alpha had no effect, and platelet-derived growth factor (PDGF) or insulin-like growth factor-1 (IGF-1) yielded only occasional tumors after longer latency. TGF-beta release during the wound-healing response may thus be a critical event that creates a conducive environment for RSV tumorigenesis and may act as a cofactor for transformation in this system.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Sieweke, M H -- Thompson, N L -- Sporn, M B -- Bissell, M J -- New York, N.Y. -- Science. 1990 Jun 29;248(4963):1656-60.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Cell and Molecular Biology Division, Lawrence Berkeley Laboratory, University of California, Berkeley 94720.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/2163544" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Antibodies ; Chickens ; Epidermal Growth Factor/pharmacology ; Humans ; Immunoenzyme Techniques ; Insulin-Like Growth Factor I/pharmacology ; Platelet-Derived Growth Factor/pharmacology ; Recombinant Proteins/pharmacology ; Sarcoma, Avian/complications/*pathology ; Swine ; Transforming Growth Factors/analysis/*pharmacology ; Wound Healing ; Wounds and Injuries/complications/*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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  • 3
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    American Association for the Advancement of Science (AAAS)
    Publication Date: 1997-11-14
    Description: Chemoprevention is the use of pharmacologic or natural agents that inhibit the development of invasive cancer either by blocking the DNA damage that initiates carcinogenesis or by arresting or reversing the progression of premalignant cells in which such damage has already occurred. Recent advances in our understanding of the mechanisms of carcinogenesis have led to the synthesis of new drugs that can inhibit tumor development in experimental animals by selective action on specific molecular targets, such as the estrogen, androgen, and retinoid receptors or inducible cyclooxygenase. Several of these agents (including tamoxifen, 13-cis-retinoic acid, retinyl palmitate, and an acyclic retinoid) are clinically effective in preventing the development of cancer, particularly in patients who are at high risk for developing second primary tumors after surgical removal of the initial tumor.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Hong, W K -- Sporn, M B -- New York, N.Y. -- Science. 1997 Nov 7;278(5340):1073-7.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Thoracic/Head and Neck Medical Oncology, University of Texas M. D. Anderson Cancer Center, 1515 Holcombe Boulevard, Box 80, Houston, TX 77030, USA. whong@notes.mdacc.tmc.edu〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/9353183" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Anticarcinogenic Agents/*therapeutic use ; Biomarkers, Tumor/analysis ; *Chemoprevention ; Clinical Trials as Topic ; Drug Therapy, Combination ; Humans ; Neoplasm Recurrence, Local/prevention & control ; Neoplasms/etiology/pathology/*prevention & control ; Neoplasms, Second Primary/prevention & control ; Precancerous Conditions/*drug therapy ; Risk Factors
    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: 2011-03-25
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Sporn, Michael B -- England -- Nature. 2011 Mar 24;471(7339):S10-1. doi: 10.1038/471S10a.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Dartmouth Medical School, Hanover, New Hampshire, USA. michael.b.sporn@dartmouth.edu〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/21430710" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Antineoplastic Combined Chemotherapy Protocols/economics/pharmacology/therapeutic ; use ; Clinical Trials as Topic/legislation & jurisprudence/standards ; Cooperative Behavior ; Disease Progression ; Female ; Humans ; Male ; Neoplasms/drug therapy/epidemiology/pathology/*prevention & control ; Precision Medicine/trends ; Risk ; Time Factors ; Tumor Microenvironment/drug effects ; United States ; United States Food and Drug Administration/legislation & jurisprudence
    Print ISSN: 0028-0836
    Electronic ISSN: 1476-4687
    Topics: Biology , Chemistry and Pharmacology , Medicine , Natural Sciences in General , Physics
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  • 5
    Publication Date: 1994-06-24
    Description: Maternal sources of transforming growth factor-beta 1 (TGF-beta 1) are shown here to contribute to the normal appearance and perinatal survival of TGF-beta 1 null newborn mice. Labeled TGF-beta 1 crossed the placenta and was recovered intact from various tissues after oral administration to mouse pups. TGF beta-1 protein was also detected in cells recovered from breast milk. In immunohistochemical analyses, TGF-beta 1 null embryos and null newborn pups born to TGF-beta 1 heterozygotes stained positive for TGF-beta 1, whereas those born to a null female were negative and had severe cardiac abnormalities. These results suggest an important role for maternal sources of TGF-beta 1 during development and, more generally, provide evidence for maternal rescue of targeted gene disruption in the fetus.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Letterio, J J -- Geiser, A G -- Kulkarni, A B -- Roche, N S -- Sporn, M B -- Roberts, A B -- New York, N.Y. -- Science. 1994 Jun 24;264(5167):1936-8.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Laboratory of Chemoprevention, National Cancer Institute, National Institutes of Health, Bethesda, MD 20892.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/8009224" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Animals, Newborn ; Embryonic and Fetal Development ; Female ; Fetus/*metabolism ; Heart Defects, Congenital/etiology ; Heterozygote ; Homozygote ; *Maternal-Fetal Exchange ; Mice ; Milk/chemistry ; Pregnancy ; Transforming Growth Factor beta/analysis/biosynthesis/*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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  • 6
    Publication Date: 1983-03-18
    Description: Transforming growth factors, which are polypeptides that induce the transformed phenotype in nonneoplastic cells, have been isolated in bulk amounts from bovine salivary gland and kidney. In experiments in which wound healing chambers were implanted subcutaneously in the backs of rats, these bovine transforming growth factors accelerated the accumulation of total protein, collagen, and DNA in treated chambers. These studies thus show an effect of an isolated transforming growth factor in vivo.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Sporn, M B -- Roberts, A B -- Shull, J H -- Smith, J M -- Ward, J M -- Sodek, J -- New York, N.Y. -- Science. 1983 Mar 18;219(4590):1329-31.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/6572416" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Cattle ; Growth Substances/*isolation & purification/pharmacology ; Kidney/analysis ; Peptides/*pharmacology ; Salivary Glands/analysis ; Transforming Growth Factors ; Wound Healing/*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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  • 7
    Publication Date: 1987-09-11
    Description: The role of polypeptide growth factors in the processes of inflammation and repair was investigated by analyzing the influence of transforming growth factor-beta (TGF-beta), applied directly to linear incisions made through rat dorsal skin. A dose-dependent, direct stimulatory effect of a single application of TGF-beta on the breaking strength of healing incisional wounds was demonstrated. An increase in maximum wound strength of 220 percent of control was observed at 5 days; the healing rate was accelerated by approximately 3 days for at least 14 days after production of the wound and application of TGF-beta. These increases in wound strength were accompanied by an increased influx of mononuclear cells and fibroblasts and by marked increases in collagen deposition at the site of application of TGF-beta. TGF-beta is thus a potent pharmacologic agent that can accelerate wound healing in rats.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Mustoe, T A -- Pierce, G F -- Thomason, A -- Gramates, P -- Sporn, M B -- Deuel, T F -- New York, N.Y. -- Science. 1987 Sep 11;237(4820):1333-6.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/2442813" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Growth Substances/*pharmacology ; Male ; Peptides/*pharmacology ; Rats ; Rats, Inbred Strains ; Staining and Labeling ; Transforming Growth Factors ; Wound Healing/*drug effects ; Wounds, Penetrating/*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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  • 8
    Publication Date: 1986-08-01
    Description: Transforming growth factor-beta (TGF-beta) is a multifunctional peptide that controls proliferation, differentiation, and other functions in many cell types. Many cells synthesize TGF-beta and essentially all of them have specific receptors for this peptide. TGF-beta regulates the actions of many other peptide growth factors and determines a positive or negative direction of their effects. Its marked ability to enhance formation of connective tissue in vivo suggests several therapeutic applications.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Sporn, M B -- Roberts, A B -- Wakefield, L M -- Assoian, R K -- New York, N.Y. -- Science. 1986 Aug 1;233(4763):532-4.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/3487831" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Cell Division/drug effects ; Epidermal Growth Factor/metabolism ; Genes ; Humans ; Peptides/genetics/metabolism/pharmacology/*physiology ; Platelet-Derived Growth Factor/pharmacology ; Rats ; Transforming Growth Factors
    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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  • 9
    Electronic Resource
    Electronic Resource
    Oxford, UK : Blackwell Publishing Ltd
    Annals of the New York Academy of Sciences 593 (1990), S. 0 
    ISSN: 1749-6632
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Natural Sciences in General
    Type of Medium: Electronic Resource
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  • 10
    Electronic Resource
    Electronic Resource
    Oxford, UK : Blackwell Publishing Ltd
    Annals of the New York Academy of Sciences 593 (1990), S. 0 
    ISSN: 1749-6632
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Natural Sciences in General
    Type of Medium: Electronic Resource
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