Journal ArticleDOI
c-MYC: more than just a matter of life and death.
TLDR
Regulatable transgenic mouse models of oncogenesis have shed light on the role of c-MYC in tumour progression and provide hope for effective cancer therapies.Abstract:
Deregulated expression of c-MYC occurs in a broad range of human cancers and is often associated with poor prognosis, indicating a key role for this oncogene in tumour progression. However, as established human tumours often bear multiple genetic lesions, it is difficult to determine whether c-MYC is instrumental in the initiation/progression of the tumour, or indeed whether inactivating c-MYC would lead to tumour regression. Regulatable transgenic mouse models of oncogenesis have shed light on these issues and provide hope for effective cancer therapies.read more
Citations
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Tumorigenesis and the angiogenic switch
TL;DR: A more detailed understanding of the complex parameters that govern the interactions between the tumour and vascular compartments will help to improve anti-angiogenic strategies — not only for cancer treatment, but also for preventing recurrence.
Journal ArticleDOI
Direct observation of individual endogenous protein complexes in situ by proximity ligation
Ola Söderberg,Mats Gullberg,Malin Jarvius,Karin Ridderstråle,Karl-Johan Leuchowius,Jonas Jarvius,Kenneth Wester,Per Hydbring,Fuad Bahram,Lars-Gunnar Larsson,Ulf Landegren +10 more
TL;DR: This method is used to show specific regulation of protein-protein interactions between endogenous Myc and Max oncogenic transcription factors in response to interferon-γ (IFN-γ) signaling and low-molecular-weight inhibitors.
Journal ArticleDOI
Elucidation of a universal size-control mechanism in Drosophila and mammals.
Jixin Dong,Georg Feldmann,Jianbin Huang,Shian Wu,Nailing Zhang,Sarah A. Comerford,Mariana F. Gayyed,Robert A. Anders,Anirban Maitra,Duojia Pan +9 more
TL;DR: It is demonstrated that a single phosphorylation site in Yki mediates the growth-suppressive output of the Hippo pathway, and that its dysregulation leads to tumorigenesis, uncovering a universal size-control mechanism in metazoan.
Journal ArticleDOI
Reflecting on 25 years with MYC
Natalie Meyer,Linda Z. Penn +1 more
TL;DR: Just over 25 years ago, MYC, the human homologue of a retroviral oncogene, was identified and each incremental insight into MYC regulation and function has had an impact on numerous biological disciplines, including the understanding of molecular oncogenesis in general.
Journal ArticleDOI
Targeting G-quadruplexes in gene promoters: a novel anticancer strategy?
TL;DR: The evidence for G-quadruplexes in gene promoters is described and their potential as therapeutic targets are discussed, as well as progress in the development of strategies to harness this potential through intervention with small-molecule ligands.
References
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Journal ArticleDOI
Patterns and Emerging Mechanisms of the Angiogenic Switch during Tumorigenesis
TL;DR: The work from the authors' laboratories reviewed herein was supported by grants from the National Cancer Institute.
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Proliferation, cell cycle and apoptosis in cancer
Gerard I. Evan,Karen H. Vousden +1 more
TL;DR: Deregulated cell proliferation provides a minimal 'platform' necessary to support further neoplastic progression and should be targeted withroit targeting to have potent and specific therapeutic consequences.
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Induction of apoptosis in fibroblasts by c-myc protein
Gerard I. Evan,Andrew H. Wyllie,Christopher S. Gilbert,Trevor Littlewood,Hartmut Land,Mary W. Brooks,Catherine M. Waters,Linda Z. Penn,David C. Hancock +8 more
TL;DR: It is demonstrated that deregulated c-myc expression induces apoptosis in cells growth arrested by a variety of means and at various points in the cell cycle.
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Serine Phosphorylation of Death Agonist BAD in Response to Survival Factor Results in Binding to 14-3-3 Not BCL-XL
TL;DR: The rapid phosphorylation of BAD following IL-3 connects a proximal survival signal with the BCL-2 family, modulating this checkpoint for apoptosis and enhanced BAD's death-promoting activity.
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Tumorigenic conversion of primary embryo fibroblasts requires at least two cooperating oncogenes.
TL;DR: The embryo fibroblasts become tumorigenic if a second oncogene such as a viral or cellular myc gene or the gene for the polyoma large-T antigen is introduced together with the ras gene.