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  • 1
    Keywords: Oncology ; Stem Cells ; Cancer Research ; Stem Cells ; Springer eBooks
    Description / Table of Contents: Alcohol Consumption and Risk of Thyroid Cancer: A Population Based Case-Control Study in Connecticut -- Roles of Cytochrome P450 in Metabolism of Ethanol and Carcinogens -- Glutathione and Transsulfuration in Alcohol-associated Tissue Injury and Carcinogenesis -- Fatty liver disease and hepatocellular carcinoma: The pathologist’s view -- Alcoholic liver disease accelerates early hepatocellular cancer in a mouse model -- Chronic ethanol consumption and generation of etheno-DNA adducts in cancer-prone tissues -- Role of TGF-β in Alcohol-Induced Liver Disease -- NANOG-dependent metabolic reprogramming and symmetric division in tumor-initiating stem-like cells -- Diet supplementation with soy protein isolate, but not the isoflavone genistein, protects against alcohol-induced tumor progression in DEN-treated male mice -- ALDH1L1 and ALDH1L2 folate regulatory enzymes in cancer -- Developmental Morphogens & Recovery from Alcoholic Liver Disease -- Suppressed fat mobilization due to PNPLA3 rs738409 -associated liver damage in heavy drinkers: The liver damage feedback hypothesis -- Aldo-Keto Reductases: Multifunctional Proteins as Therapeutic Targets in Diabetes and Inflammatory Disease -- Engineered animal models designed for investigating ethanol metabolism, toxicity and cancer -- Index
    Abstract: Following the Third Alcohol and Cancer Conference, this volume compiles the most up-to-date research on the role of alcohol consumption in carcinogenesis, from epidemiology to pathology metabolism and stem cells. More specifically, it delves into the effects of alcohol consumption and thyroid cancer, CD133+ progenitor cells, carcinogenic iron accumulation, developmental morphogens, and cancer-inducing epigenetic changes. Alcohol and Cancer: Proceedings of the Third International Conference is a timely update to Biological Basis of Alcohol-Induced Cancer, which followed the Second Alcohol and Cancer Conference, compiling cutting-edge research from graduate students, young scientists, and researchers. It is ideal for graduate students and researchers in oncology, hepatology, epigenetics, and alcohol consumption
    Pages: XII, 271 p. 36 illus., 23 illus. in color. : online resource.
    ISBN: 9783319987880
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  • 2
    ISSN: 1432-1777
    Source: Springer Online Journal Archives 1860-2000
    Topics: Biology , Medicine
    Notes: Abstract. The aim of our study was to isolate novel gene(s) involved in cell differentiation and embryonic liver development. Mouse cded/lior was identified from subtraction hybridization of embryonic liver cDNA libraries as well as an adult mouse liver genomic DNA library. The full open reading frame of cded/lior encodes a 131-amino acid protein with 71.88% overall similarity to the PH domain of rat PLC-γ1. A gapped search with the C-terminal region of CDED/LIOR revealed a 36–41% similarity to several proteins related to signal transduction and cell replication, such as ORC1 and KSR. Northern blot analysis of adult mouse tissues shows a strong 2.6-kb transcript restricted to heart and skeletal muscle. RT-PCR utilizing cded/lior-specific primers demonstrates cded/lior mRNAs in heart, brain, and liver tissue throughout mid-embryonic mouse gestation. cded/lior maps to the distal end of mouse Chromosome (Chr) 2. Analysis of the genomic structure for cded/lior demonstrated a single exon gene that is not an alternatively spliced isoform of PLC-γ1. Analysis of the cded/lior promoter region revealed a high GC-content, high ratio of CpG/GpC, multiple GC-boxes, the lack of a TATA box, CTF/NFI element, and two MyoD-MCK binding sites. These characteristics are also found in several genes important in the regulation of cell growth or DNA synthesis, such as transforming growth factor-β1, c-Ha-ras, nerve growth factor, epidermal growth factor receptor, and DNA polymerase β. These results suggest that cded/lior is a mesoderm/muscle-specific transcript that may be involved in the mesodermal inductive and regulatory interactions required for liver formation and embryonic development.
    Type of Medium: Electronic Resource
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  • 3
    ISSN: 1600-0714
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Notes: Background:  Smad4 is vital to the roles of Smads 2 and 3 in transforming growth factor-beta (TGF)-β signal transduction, and inactivated Smad4 is common to human gastrointestinal cancers. The embryonic liver fodrin (ELF) is a β-spectrin that facilitates the nuclear translocation of activated Smad4.Methods:  Smad4 +/− mice, known to develop gastrointestinal cancer, were crossbred with elf+/− mice. The smad4+/− and smad4+/−/elf+/− offspring were autopsied as abnormalities developed.Results:  In addition to polyps and adenocarcinomas of the stomach and duodenum, the smad4+/− mice developed squamous cell carcinomas of the skin, oral mucosa and forestomach, benign neoplasms of connective tissue and lacrimal gland, and a lymphoma. The smad4+/−/elf+/− mice developed extensive hyperplasia and neoplasia of the gastric mucosa.Conclusion:  These findings indicate that investigating interactions among smad4, elf, and other genes involved in TGF-β signaling should be useful in further delineating the processes of neoplasia in a wide variety of tissues.
    Type of Medium: Electronic Resource
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