Search our Database of Scientific Publications and Authors

I’m looking for a
    When LMO1 Meets MYCN, Neuroblastoma Is Metastatic.
    Cancer Cell 2017 09;32(3):273-275
    Pediatric Oncology Branch, National Cancer Institute, Center for Cancer Research, 9000 Rockville Pike, Bethesda, MD 20892, USA. Electronic address:
    LMO1 is a high-risk neuroblastoma susceptibility gene, but how LMO1 cooperates with MYCN in neuroblastoma tumorigenesis is unclear. In this issue of Cancer Cell, Zhu et al. develop a novel zebrafish model that elucidates a mechanism by which LMO1 and MYCN synergistically initiate neuroblastoma and contribute to metastatic disease progression.

    Similar Publications

    LMO1 Synergizes with MYCN to Promote Neuroblastoma Initiation and Metastasis.
    Cancer Cell 2017 Sep 31;32(3):310-323.e5. Epub 2017 Aug 31.
    Department of Pediatric Oncology, Dana-Farber Cancer Institute, Harvard Medical School, Boston, MA 02115, USA. Electronic address:
    A genome-wide association study identified LMO1, which encodes an LIM-domain-only transcriptional cofactor, as a neuroblastoma susceptibility gene that functions as an oncogene in high-risk neuroblastoma. Here we show that dβh promoter-mediated expression of LMO1 in zebrafish synergizes with MYCN to increase the proliferation of hyperplastic sympathoadrenal precursor cells, leading to a reduced latency and increased penetrance of neuroblastomagenesis. The transgenic expression of LMO1 also promoted hematogenous dissemination and distant metastasis, which was linked to neuroblastoma cell invasion and migration, and elevated expression levels of genes affecting tumor cell-extracellular matrix interaction, including loxl3, itga2b, itga3, and itga5. Read More
    Dissection of the oncogenic MYCN transcriptional network reveals a large set of clinically relevant cell cycle genes as drivers of neuroblastoma tumorigenesis.
    Mol Carcinog 2011 Jun 28;50(6):403-11. Epub 2010 Dec 28.
    Departments of Cancer Genetics, Royal College of Surgeons in Ireland, York House, Dublin, Ireland.
    Amplification of the oncogenic transcription factor MYCN plays a major role in the pathogenesis of several pediatric cancers, including neuroblastoma, medulloblastoma, and rhabodomyosarcoma. For neuroblastoma, MYCN amplification is the most powerful genetic predictor of poor patient survival, yet the mechanism by which MYCN drives tumorigenesis is only partially understood. To gain an insight into the distribution of MYCN binding and to identify clinically relevant MYCN target genes, we performed an integrated analysis of MYCN ChIP-chip and mRNA expression using the MYCN repressible SHEP-21N neuroblastoma cell line. Read More
    Mdm2 deficiency suppresses MYCN-Driven neuroblastoma tumorigenesis in vivo.
    Neoplasia 2009 Aug;11(8):753-62
    Texas Children's Cancer Center and Center for Cell and Gene Therapy, Baylor College of Medicine, Houston, TX 77030, USA.
    Neuroblastoma is derived from neural crest precursor components of the peripheral sympathetic nervous system and accounts for more than 15% of all pediatric cancer deaths. A clearer understanding of the molecular basis of neuroblastoma is required for novel therapeutic approaches to improve morbidity and mortality. Neuroblastoma is uniformly p53 wild type at diagnosis and must overcome p53-mediated tumor suppression during pathogenesis. Read More
    MycN is a transcriptional regulator of livin in neuroblastoma.
    Oncol Rep 2009 Oct;22(4):831-5
    Department of Pediatrics, Emory University School of Medicine, Atlanta, GA 30322, USA.
    Our previous studies have suggested that MycN may have a role in regulating livin expression in neuroblastoma. Here, we show that siRNA-mediated repression of MycN in neuroblastoma cells with both elevated MycN and livin expression resulted in significant downregulation of livin. Conversely, induction of MycN in neuroblastoma cells with low endogenous levels of MycN and livin protein upregulated livin expression. Read More