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  • 1
    Publication Date: 2016-03-17
    Description: Mutations disabling the TP53 tumour suppressor gene represent the most frequent events in human cancer and typically occur through a two-hit mechanism involving a missense mutation in one allele and a 'loss of heterozygosity' deletion encompassing the other. While TP53 missense mutations can also contribute gain-of-function activities that impact tumour progression, it remains unclear whether the deletion event, which frequently includes many genes, impacts tumorigenesis beyond TP53 loss alone. Here we show that somatic heterozygous deletion of mouse chromosome 11B3, a 4-megabase region syntenic to human 17p13.1, produces a greater effect on lymphoma and leukaemia development than Trp53 deletion. Mechanistically, the effect of 11B3 loss on tumorigenesis involves co-deleted genes such as Eif5a and Alox15b (also known as Alox8), the suppression of which cooperates with Trp53 loss to produce more aggressive disease. Our results imply that the selective advantage produced by human chromosome 17p deletion reflects the combined impact of TP53 loss and the reduced dosage of linked tumour suppressor genes.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4836395/" 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/PMC4836395/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Liu, Yu -- Chen, Chong -- Xu, Zhengmin -- Scuoppo, Claudio -- Rillahan, Cory D -- Gao, Jianjiong -- Spitzer, Barbara -- Bosbach, Benedikt -- Kastenhuber, Edward R -- Baslan, Timour -- Ackermann, Sarah -- Cheng, Lihua -- Wang, Qingguo -- Niu, Ting -- Schultz, Nikolaus -- Levine, Ross L -- Mills, Alea A -- Lowe, Scott W -- P30 CA008748/CA/NCI NIH HHS/ -- P30 CA016042/CA/NCI NIH HHS/ -- R01 CA190261/CA/NCI NIH HHS/ -- Howard Hughes Medical Institute/ -- England -- Nature. 2016 Mar 24;531(7595):471-5. doi: 10.1038/nature17157. Epub 2016 Mar 16.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Hematology and Department of Liver Surgery, State Key Laboratory of Biotherapy and Cancer Center, West China Hospital, Sichuan University and National Collaborative Innovation Center, Chengdu 610041, China. ; Department of Cancer Biology and Genetics, Memorial Sloan Kettering Cancer Center, New York, New York 10065, USA. ; Institute for Cancer Genetics, Columbia University Medical Center, New York, New York 10032, USA. ; Kravis Center for Molecular Oncology, Memorial Sloan Kettering Cancer Center, New York, New York 10065, USA. ; Department of Pediatrics, Memorial Sloan Kettering Cancer Center, New York, New York 10065, USA. ; Human Oncology &Pathogenesis Program and Leukemia Service, Memorial Sloan Kettering Cancer Center, New York, New York 10065, USA. ; Department of Hematology &Research Laboratory of Hematology, West China Hospital, Sichuan University, Chengdu 610041, China. ; Cold Spring Harbor Laboratory, Cold Spring Harbor, New York 11724, USA. ; Howard Hughes Medical Institute, New York, New York 10065, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/26982726" target="_blank"〉PubMed〈/a〉
    Keywords: Alleles ; Animals ; Cell Transformation, Neoplastic/genetics ; Chromosomes, Human, Pair 17/genetics ; Chromosomes, Mammalian/genetics ; Disease Models, Animal ; Disease Progression ; Female ; Genes, p53/*genetics ; Heterozygote ; Humans ; Leukemia, Myeloid, Acute/genetics/pathology ; Lymphoma/genetics/pathology ; Male ; Mice ; Neoplasms/*genetics/*pathology ; Peptide Initiation Factors/genetics/metabolism ; RNA-Binding Proteins/genetics/metabolism ; Sequence Deletion/*genetics ; Synteny/genetics ; Tumor Suppressor Protein p53/*deficiency
    Print ISSN: 0028-0836
    Electronic ISSN: 1476-4687
    Topics: Biology , Chemistry and Pharmacology , Medicine , Natural Sciences in General , Physics
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  • 2
    ISSN: 1572-8900
    Keywords: Biodegradation of polymers: carbon balance ; biomass ; protein assay
    Source: Springer Online Journal Archives 1860-2000
    Topics: Chemistry and Pharmacology , Energy, Environment Protection, Nuclear Power Engineering , Mechanical Engineering, Materials Science, Production Engineering, Mining and Metallurgy, Traffic Engineering, Precision Mechanics
    Notes: Abstract This article presents a method to determine the carbon content of biomass, which is formed when degrading biodegradable polymers in an aerobic aqueous test system. Existing methods for determining the carbon content of biomass (e.g., fumigazation, protein assays, dry solids) have several disadvantages when applied for polymer degradation tests. In this work a protein assay based on the Lowry method was used. It was shown that the ratio between protein and carbon content is not constant but depends on the composition of the microbial population, the growth phase, and the substrate supply. This effect was used for the method presented in this article. For determining the carbon content of biomass the absorbance obtained by the Lowry test is correlated directly with the carbon content of biomass in dependence on the duration of the degradation test. The calibration curves are obtained by a mixed population of microorganisms during the course of a degradation test.
    Type of Medium: Electronic Resource
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  • 3
    Electronic Resource
    Electronic Resource
    s.l. : American Chemical Society
    Industrial & engineering chemistry 7 (1915), S. 269-269 
    ISSN: 1520-5045
    Source: ACS Legacy Archives
    Topics: Chemistry and Pharmacology , Process Engineering, Biotechnology, Nutrition Technology
    Type of Medium: Electronic Resource
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