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  • 1
    Online Resource
    Online Resource
    Obesity and Breast Cancer : The Role of Dysregulated Estrogen Metabolism. (2013)
    New York, NY :Springer,
    Details
    Keywords: Enzymes. ; Metabolism -- Disorders. ; Obesity. ; Oncology. ; Electronic books.
    Description / Table of Contents: This book discusses the connection between obesity and breast cancer in older women. It explores the application of novel therapies to inhibit aromatase in the breast.
    Type of Medium: Online Resource
    Pages: 1 online resource (60 pages)
    Edition: 1st ed.
    ISBN: 9781489980021
    Series Statement: SpringerBriefs in Cancer Research Series
    URL: https://ebookcentral.proquest.com/lib/geomar/detail.action?docID=1592715
    DDC: 572.6
    Language: English
    Note: Intro -- Acknowledgments -- Contents -- Introduction -- 1 Estrogens, Adiposity and the Menopause -- 2 The Link Between Obesity and Breast Cancer Risk: Epidemiological Evidence -- 2.1…BMI and Breast Cancer Risk -- 2.2…BMI and Breast Tumor Hormone Receptor Status -- 2.3…Obesity and Mammographic Density -- 2.4…Waist-to-Hip Ratio and Breast Cancer -- 2.5…The Metabolic Syndrome, Diabetes Mellitus and Breast Cancer -- 2.6…Breast Size and Breast Cancer -- 2.7…Effect of Obesity on Disease-Free Survival -- 3 Adipose-Derived and Obesity-Related Factors and Breast Cancer -- 3.1…Adipokines -- 3.2…Inflammatory Factors -- 3.3…Insulin and Insulin-Like Growth Factor-1 (IGF-1) -- 3.4…Estrogens -- 4 Estrogen Biosynthesis -- 4.1…Source of Estrogens in Pre-versus Postmenopausal Women -- 4.2…The Aromatase Enzyme -- 4.3…Local Aromatase Expression in Breast Cancer -- 4.4…The CYP19A1 Gene and Tissue-Specific Expression -- 4.5…Promoter-Specific Regulation of Aromatase in Obesity and Breast Cancer -- 4.5.1 Prostaglandin E2 -- 4.5.2 Leptin -- 4.5.3 Adiponectin -- 4.5.4 IL-6 -- 4.5.5 TNF alpha -- 4.5.6 Insulin and IGF-1 -- 4.5.7 Other Tumor-Derived Factors -- 5 Therapy Aimed at Breaking the Linkage Between Obesity and Breast Cancer -- 5.1…Effect of Obesity on Endocrine Therapy Efficacy -- 5.2…Targeting Obesity-Related Estrogen Biosynthesis -- 5.2.1 Weight Loss, Exercise and Bariatric Surgery: Effect on Breast Cancer Risk and Estrogen Levels -- 5.2.2 Insulin Sensitizers and Anti-diabetics -- 5.2.3 Other Targeted Therapies -- Conclusions -- References.
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  • 2
    Electronic Resource
    Electronic Resource
    τ Regulation of Microtubule-Microtubule Spacing and Bundling (1994)
    Oxford, UK : Blackwell Science Ltd
    Journal of neurochemistry 63 (1994), S. 0 
    Details
    ISSN: 1471-4159
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Notes: Abstract: τ proteins are microtubule-associated proteins that promote microtubule polymerization in vitro and in vivo. They are a family of neuronal proteins with apparent molecular weights in the range 50,000–68,000 determined by sodium dodecyl sulfate-polyacrylamide gel electrophoresis. Recently, a new member of this family has been described and its cDNA has been cloned. It has an apparent molecular weight of 116,000 and has been called high-molecular-weight τ (HMW τ). All the τ proteins are encoded by a single gene, which undergoes complex alternative splicing. In the present study, we have cloned into the baculovirus a cDNA fully encoding HMW τ as well as a truncated cDNA encoding a protein beginning 13 amino acids in front of the τ microtubule-binding domain. HMW τ-recombinant-virus-infected Sf9 cells overexpressed HMW τ, which induced the polymerization of microtubules and the formation of long cellular processes similar to those induced by low-molecular-weight τ (LMW τ) overexpression. Process cross sections revealed a larger spacing (≈35 nm) between microtubules when induced by HMW τ than when induced by LMW τ (≈20 nm). The truncated construct also induces processes, where microtubules were packed far more closely together (≈10 nm). Although branching did not occur in processes induced by intact τs, 10% of the processes induced by the truncated τ protein branched.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1046/j.1471-4159.1994.63062288.x
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    Paper (German National Licenses)
    Fulltext
  • 3
    Electronic Resource
    Electronic Resource
    Mutations in the neurofilament light gene linked to Charcot-Marie-Tooth disease cause defects in transport (2005)
    Oxford, UK : Blackwell Science Ltd
    Journal of neurochemistry 93 (2005), S. 0 
    Details
    ISSN: 1471-4159
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Notes: Neurofilament light gene mutations have been linked to a subset of patients with Charcot-Marie-Tooth disease, the most common inherited motor and sensory neuropathy. We have previously shown that Charcot-Marie-Tooth-linked mutant neurofilament light assembles abnormally in non-neuronal cells. In this study, we have characterized the effects of expression of mutant neurofilament light proteins on axonal transport in a neuronal cell culture model. We demonstrated that the Charcot-Marie-Tooth-linked neurofilament light mutations: (i) affect the axonal transport of mutant neurofilaments; (ii) have a dominant-negative effect on the transport of wild-type neurofilaments; (iii) affect the transport of mitochondria and the anterograde axonal transport marker human amyloid precursor protein; (iv) result in alterations of retrograde axonal transport and (v) cause fragmentation of the Golgi apparatus. Increased neuritic degeneration was observed in neuronal cells overexpressing neurofilament light mutants. Our results suggest that these generalized axonal transport defects could be responsible for the neuropathy in Charcot-Marie-Tooth disease.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1111/j.1471-4159.2005.03095.x
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    Paper (German National Licenses)
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  • 4
    Electronic Resource
    Electronic Resource
    Mutational loss of PTEN induces resistance to NOTCH1 inhibition in T-cell leukemia (2007)
    [s.l.] : Nature Publishing Group
    Nature medicine 13 (2007), S. 1203-1210 
    Details
    ISSN: 1546-170X
    Source: Nature Archives 1869 - 2009
    Topics: Biology , Medicine
    Notes: [Auszug] Gain-of-function mutations in NOTCH1 are common in T-cell lymphoblastic leukemias and lymphomas (T-ALL), making this receptor a promising target for drugs such as γ-secretase inhibitors, which block a proteolytic cleavage required for NOTCH1 activation. However, the enthusiasm for these ...
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1038/nm1636
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    Paper (German National Licenses)
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  • 5
    Electronic Resource
    Electronic Resource
    Induction of autophagy and inhibition of tumorigenesis by beclin 1 (1999)
    [s.l.] : Macmillian Magazines Ltd.
    Nature 402 (1999), S. 672-676 
    Details
    ISSN: 1476-4687
    Source: Nature Archives 1869 - 2009
    Topics: Biology , Chemistry and Pharmacology , Medicine , Natural Sciences in General , Physics
    Notes: [Auszug] The process of autophagy, or bulk degradation of cellular proteins through an autophagosomic-lysosomal pathway, is important in normal growth control and may be defective in tumour cells. However, little is known about the genetic mediators of autophagy in mammalian cells or their role in ...
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1038/45257
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    Paper (German National Licenses)
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  • 6
    Electronic Resource
    Electronic Resource
    Depletion of secondary lysosomes in mouse macrophages infected withLeishmania mexicana amazonensis: A cytochemical study (1985)
    Springer
    Parasitology research 71 (1985), S. 159-168 
    Details
    ISSN: 1432-1955
    Source: Springer Online Journal Archives 1860-2000
    Topics: Biology , Medicine
    Notes: Abstract Leishmania amastigotes lodge and multiply within parasitophorous vacuoles, which can fuse with secondary lysosomes of the host macrophages. This study examines the effect of infection with amastigotes ofL. mexicana amazonensis on the secondary lysosomes of mouse macrophage cultures. The cultures were stained for the activities of two lysosomal enzyme markers, acid phosphatase and arylsulfatase, and the light microscopic observations were supplemented by electron microscopy. Nearly all noninfected macrophages contained numerous stained secondary lysosomes. The number of such lysosomes was markedly reduced 24 h postinfection, and the reduction persisted for at least 10 days. Stained secondary lysosomes reppeared after the amastigotes were destroyed by exposure of the cultures to phenazine methosulfate or by placing them at 37.5° C. The depletion of lysosomes shown by cytochemical methods may reflect a high rate of fusion of the lysosomes with the parasitophorous vacuoles, exceeding the rate of formation of new secondary lysosomes. Alternatively, the parasites may inhibit the synthesis of lysosomal hydrolases, or the assembly or formation of primary or secondary lysosomes.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00926266
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    Paper (German National Licenses)
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