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  • 1.
    den Hollander, Jürgen
    et al.
    III. Medical Department, Technische Universität München, Munich, Germany.
    Rimpi, Sara
    Umeå universitet, Teknisk-naturvetenskaplig fakultet, Molekylärbiologi (Teknisk-naturvetenskaplig fakultet).
    Doherty, Joanne R
    Department of Cancer Biology, The Scripps Research Institute, Scripps Florida, Jupiter, Florida, USA.
    Rudelius, Martina
    Department of Pathology, Technische Universität München, Munich, Germany.
    Buck, Andreas
    Department of Nuclear Medicine, Technische Universität München, Munich, Germany.
    Kremer, Marcus
    Department of Pathology, Technische Universität München, Munich, Germany.
    Graf, Nikolas
    III. Medical Department, Technische Universität München, Munich, Germany.
    Scheerer, Markus
    III. Medical Department, Technische Universität München, Munich, Germany.
    Hall, Mark
    Department of Cancer Biology, The Scripps Research Institute, Scripps Florida, Jupiter, Florida, USA.
    von Bubnoff, Nikolas
    III. Medical Department, Technische Universität München, Munich, Germany.
    Duyster, Justus
    III. Medical Department, Technische Universität München, Munich, Germany.
    Peschel, Christian
    III. Medical Department, Technische Universität München, Munich, Germany.
    Cleveland, John L
    Department of Cancer Biology, The Scripps Research Institute, Scripps Florida, Jupiter, Florida, USA.
    Nilsson, Jonas A
    Umeå universitet, Teknisk-naturvetenskaplig fakultet, Molekylärbiologi (Teknisk-naturvetenskaplig fakultet).
    Keller, Ulrich
    III. Medical Department, Technische Universität München, Munich, Germany.
    Aurora kinases A and B are Myc targets essential for maintenance of the malignant stateManuskript (preprint) (Övrigt vetenskapligt)
  • 2.
    Plym Forshell, Tacha Zi
    et al.
    Umeå universitet, Teknisk-naturvetenskapliga fakulteten, Institutionen för molekylärbiologi (Teknisk-naturvetenskaplig fakultet).
    Rimpi, Sara
    Umeå universitet, Teknisk-naturvetenskapliga fakulteten, Institutionen för molekylärbiologi (Teknisk-naturvetenskaplig fakultet).
    Nilsson, Jonas A
    Umeå universitet, Teknisk-naturvetenskapliga fakulteten, Institutionen för molekylärbiologi (Teknisk-naturvetenskaplig fakultet).
    Chemoprevention of B-cell lymphomas by inhibition of the Myc target spermidine synthase2010Ingår i: Cancer Prevention Research, ISSN 1940-6207, E-ISSN 1940-6215, Vol. 3, nr 2, s. 140-147Artikel i tidskrift (Refereegranskat)
    Abstract [en]

    The oncogenic transcription factor c-Myc (Myc) is frequently overexpressed in human cancers. Myc is known to induce or repress a large set of genes involved in cell growth and proliferation, explaining the selection for mutations in cancer that deregulate Myc expression. Inhibition of ornithine decarboxylase, an enzyme of the polyamine biosynthetic pathway and a Myc target, has been shown to be chemopreventive. In the present study, we have dissected the role of another enzyme in the polyamine biosynthetic pathway, spermidine synthase (Srm), in Myc-induced cancer. We find that Srm is encoded by a Myc target gene containing perfect E-boxes and that it is induced by Myc in a direct manner. RNA interference against Srm shows that it is important for Myc-induced proliferation of mouse fibroblasts but to a lesser extent for transformation. Using the compound trans-4-methylcyclohexylamine, we show that Srm inhibition can delay the onset of B-cell lymphoma development in λ-Myc transgenic mice. We therefore suggest that inhibition of Srm is an additional chemopreventive strategy that warrants further consideration.

  • 3.
    Rimpi, Sara
    Umeå universitet, Teknisk-naturvetenskaplig fakultet, Molekylärbiologi (Teknisk-naturvetenskaplig fakultet).
    Myc-induced Lymphomagenesis: In vivo assessment of downstream pathways2010Doktorsavhandling, sammanläggning (Övrigt vetenskapligt)
    Abstract [en]

    Myc oncogenes encode transcription factors that bind to E-box sequences in DNA, driving the expression of a large number of target genes and are deregulated in approximately 70% of human cancers. Deregulated Myc expression cause enhanced proliferation (which is counteracted by apoptosis), angiogenesis and cancer. Though Myc’s importance in induction of S phase has been established, less is known about its functions in the G2 and M phases of the cell cycle. Paper I addresses the targeting of the Myc targets Aurora kinase A and B that have roles in G2/M transition and provide evidence that pharmaceutical Aurora kinase inhibition causes cell cycle arrest and apoptosis in a Myc-selective manner and is useful in treating Myc-induced lymphomas in vivo.

    The assumption that the important target genes responsible for the biological effects of Myc overexpression were those encoding components of the cell cycle machinery lead to little interest in other potentially important groups of target genes. However, recent work challenged this view by indicating that Myc target genes encoding metabolic enzymes may be critical for Myc-induced tumorigenesis. Importantly, the targeting of Myc target genes encoding metabolic enzymes has the potential of providing a new treatment strategy of Myc-induced cancers. Paper II covers the pharmaceutical targeting of the Myc-induced spermidine synthase (Srm) that shows promise as a tool for chemoprevention by affecting proliferation, but not for the treatment of established tumors.

    Paper III focuses on the negligible effect an Ldha mutation has on Myc- induced lymphomagenesis. Ldha has long been known to be a Myc target gene and in vitro experiments have recently indicated it to be important for transformation. It seems the negligible effect of the Ldh mutation can be explained by the high frequency of loss of either Arf or p53 in this mouse model, since enforced Ras-Myc oncogenic cooperation in soft agar assays of Ldh mutant MEFs effectively inhibits colony formation, and λ-Myc;Ldh mutant bone marrow infected with oncogenic Ras does not give rise to tumors when transplanted into wild-type mice. A role for Ldh in the ability of tumors to evade the immune system was also indicated in this study. The combined experiences and very different outcome of the three studies included in this thesis draw attention to the value of in vivo assessment of Myc downstream targets in Myc-induced lymphomagenesis.

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  • 4.
    Rimpi, Sara
    et al.
    Umeå universitet, Teknisk-naturvetenskapliga fakulteten, Institutionen för molekylärbiologi (Teknisk-naturvetenskaplig fakultet).
    Nilsson, Jonas A
    Umeå universitet, Teknisk-naturvetenskapliga fakulteten, Institutionen för molekylärbiologi (Teknisk-naturvetenskaplig fakultet).
    Metabolic enzymes regulated by the Myc oncogene are possible targets for chemotherapy or chemoprevention.2007Ingår i: Biochem Soc Trans, ISSN 0300-5127, Vol. 35, nr Pt 2, s. 305-10Artikel i tidskrift (Refereegranskat)
    Abstract [en]

    The Myc oncogenes are dysregulated in 70% of human cancers. They encode transcription factors that bind to E-box sequences in DNA, driving the expression of a vast amount of target genes. The biological outcome is enhanced proliferation (which is counteracted by apoptosis), angiogenesis and cancer. Based on the biological effects of Myc overexpression it was originally assumed that the important Myc target genes are those encoding components of the cell cycle machinery. Recent work has challenged this notion and indicates that Myc target genes encoding metabolic enzymes deserve attention, as they may be critical arbiters of Myc in cancer. Thus targeting metabolic enzymes encoded by Myc-target genes may provide a new means to treat cancer that have arisen in response to deregulated Myc oncogenes.

  • 5.
    Rimpi, Sara
    et al.
    Umeå universitet, Teknisk-naturvetenskapliga fakulteten, Institutionen för molekylärbiologi (Teknisk-naturvetenskaplig fakultet).
    Nilsson, Lisa M
    Umeå universitet, Teknisk-naturvetenskapliga fakulteten, Institutionen för molekylärbiologi (Teknisk-naturvetenskaplig fakultet).
    Plym Forshell, Linus
    Umeå universitet, Teknisk-naturvetenskapliga fakulteten, Institutionen för molekylärbiologi (Teknisk-naturvetenskaplig fakultet).
    Pretsch, Walter
    Helmholtz Zentrum München, National Research Center for Environmental Health (GSF), Institute of Clinical Molecular Biology and Tumor Genetics, München, Germany.
    Bornkamm, Georg W
    Helmholtz Zentrum München, National Research Center for Environmental Health (GSF), Institute of Clinical Molecular Biology and Tumor Genetics, München, Germany.
    Nilsson, Jonas A
    Umeå universitet, Teknisk-naturvetenskapliga fakulteten, Institutionen för molekylärbiologi (Teknisk-naturvetenskaplig fakultet).
    Differential requirement of Ldha in Myc-induced tumorigenesis based on cooperating oncogenic lesion and tumor immunogenicityManuskript (preprint) (Övrigt vetenskapligt)
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