Selected abstracts on oncogene protein products
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Selected abstracts on oncogene protein products

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Published by U.S. Dept. of Health and Human Services, Public Health Service, National Institutes of Health, International Cancer Research Data Bank, National Cancer Institute, For sale by the Supt. of Docs., U.S. G.P.O. in Bethesda, MD, Washington, DC .
Written in English

Subjects:

  • Oncogenes -- Abstracts.,
  • Cancer -- Genetic aspects -- Abstracts.,
  • Proteins -- Abstracts.

Book details:

Edition Notes

Other titlesOncogene protein products.
StatementR.A. Weinberg, consulting reviewer.
GenreAbstracts.
SeriesOncology overview
ContributionsWeinberg, Robert A. 1942-, International Cancer Research Data Bank.
The Physical Object
Paginationviii, 75, 28, 5 p. ;
Number of Pages75
ID Numbers
Open LibraryOL17570149M

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An oncogene is a modified gene, or a set of nucleotides that codes for a protein and is believed to cause cancer. Asked in Conditions and Diseases, Cancer, Genetics.   The first Oncogene Meeting, held at Hood College 10–13 July , organized by Mariano Barbacid and Mike Wigler, was a huge success, Cited by: 2. Abstract Book of the 44th ESMO Congress (ESMO ) 27 September – 1 October , Barcelona, Spain. Vol Supplement 5, Pages v1-v (October ) Previous vol/issue. Next vol/issue. Actions for selected articles. LAPTM5 protein can regulate TGF-β mediated MAPK and smad signaling pathways in ovarian cancer cell. The interactive Book of Abstracts is available in two versions: PDF and HTML. lipid, and sugar or peptide/protein of selected species. Mass spectrometry as a tool for species determination was introduced about ten years ago. Matrix-assisted laser desorption ionization–time of flight mass spectrometry (MALDI-TOF MS) identifies microbes.

First designed and published in as a laboratory tool to study Myc perturbation, Omomyc has come a long way in the past 22 years. This dominant negative has contributed to our understanding of Myc biology when expressed, first, in normal and cancer cells, and later in genetically-engineered mice, and has shown remarkable anti-cancer properties in a wide range of tumor types. Keywords: BRAF, colorectal cancer, gene expression profile, oncogenes, signalling pathways, signatures, chromosomal instability, myotonic dystrophy protein kinase, Epithelial-Mesenchymal Transition, extracellular signal-related kinase, Host Cell Factor 1, microsatellite instability, proliferator-activated receptor, vascular endothelial growth by:   erbB Family. In , the cellular homologue of viral oncogene v-erbB, from an avian erythroblastosis virus, was shown to be a receptor that binds EGF (11–13).EGFR is a RTK found on cells of epithelial origin. Because v-erbB was found in the erythroblastosis virus, EGFR and its family of RTKs are known as erbB has six ligands: transforming growth factor-α, EGF, β cellulin Cited by: Ribosomal protein S7 as a novel modulator of pMDM2 interaction: binding to MDM2, stabilization of p53 protein, and activation of p53 function. Oncogene. ; Li .

  Human cyclin D1 is expressed as two isoforms derived by alternate RNA splicing, termed D1a and D1b, which differ for the inclusion of intron 4 in the D1b mRNA. Both isoforms are frequently upregulated in human cancers, but cyclin D1b displays relatively higher oncogenic potential. The splicing factors that regulate alternative splicing of cyclin D1b remain unknown despite the likelihood that Cited by: This book contains 18 selections. Some of the titles are: Exploring Carcinogenesis with Retroviral and Cellular Oncogenes; Retroviruses, Oncogenes and Evolution; HTLV and Human Neoplasi; Modes of Activation of cMyc Oncogene in B and T Lymphoid Tumors; The Structure and Function of the Epidermal Growth Factor Receptor: Its Relationship to the Protein Product of the V-ERB-B Oncogene; and. Ruiwen Zhang, M.D., Ph.D., D.A.B.T. Robert L. Boblitt Endowed Professor in Drug Discovery Professor of Pharmacology and Toxicology Director of UH Center for Drug Discovery Health 2 University of Houston College of Pharmacy Calhoun Road, Room Houston, TX Office: Fax: [email protected]   Some tumors are dependent on the continued activity of a single oncogene for maintenance of their malignant phenotype. The best-studied example is the Bcr-Abl fusion protein in chronic myelogenous leukemia (CML). Although the clinical success of the Abl kinase inhibitor imatinib against chronic-phase CML emphasizes the importance of developing therapeutic strategies aimed at Cited by: