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11q deletion or ALK activity curbs DLG2 expression to maintain an undifferentiated state in neuroblastoma

Joachim Tetteh Siaw, Niloufar Javanmardi, Jimmy Van den Eynden (UGent) , Dan Emil Lind, Susanne Fransson, Angela Martinez-Monleon, Anna Djos, Rose-Marie Sjöberg, Malin Östensson, Helena Carén, et al.
(2020) CELL REPORTS. 32(12).
Author
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Abstract
High-risk neuroblastomas typically display an undifferentiated or poorly differentiated morphology. It is therefore vital to understand molecular mechanisms that block the differentiation process. We identify an important role for oncogenic ALK-ERK1/2-SP1 signaling in the maintenance of undifferentiated neural crest-derived progenitors through the repression of DLG2, a candidate tumor suppressor gene in neuroblastoma. DLG2 is expressed in the murine "bridge signature'' that represents the transcriptional transition state when neural crest cells or Schwann cell precursors differentiate to chromaffin cells of the adrenal gland. We show that the restoration of DLG2 expression spontaneously drives neuroblastoma cell differentiation, high-lighting the importance of DLG2 in this process. These findings are supported by genetic analyses of high-risk 11q deletion neuroblastomas, which identified genetic lesions in the DLG2 gene. Our data also suggest that further exploration of other bridge genes may help elucidate the mechanisms underlying the differentiation of NC-derived progenitors and their contribution to neuroblastomas.
Keywords
General Biochemistry, Genetics and Molecular Biology

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MLA
Siaw, Joachim Tetteh, et al. “11q Deletion or ALK Activity Curbs DLG2 Expression to Maintain an Undifferentiated State in Neuroblastoma.” CELL REPORTS, vol. 32, no. 12, 2020, doi:10.1016/j.celrep.2020.108171.
APA
Siaw, J. T., Javanmardi, N., Van den Eynden, J., Lind, D. E., Fransson, S., Martinez-Monleon, A., … Martinsson, T. (2020). 11q deletion or ALK activity curbs DLG2 expression to maintain an undifferentiated state in neuroblastoma. CELL REPORTS, 32(12). https://doi.org/10.1016/j.celrep.2020.108171
Chicago author-date
Siaw, Joachim Tetteh, Niloufar Javanmardi, Jimmy Van den Eynden, Dan Emil Lind, Susanne Fransson, Angela Martinez-Monleon, Anna Djos, et al. 2020. “11q Deletion or ALK Activity Curbs DLG2 Expression to Maintain an Undifferentiated State in Neuroblastoma.” CELL REPORTS 32 (12). https://doi.org/10.1016/j.celrep.2020.108171.
Chicago author-date (all authors)
Siaw, Joachim Tetteh, Niloufar Javanmardi, Jimmy Van den Eynden, Dan Emil Lind, Susanne Fransson, Angela Martinez-Monleon, Anna Djos, Rose-Marie Sjöberg, Malin Östensson, Helena Carén, Gunhild Trøen, Klaus Beiske, Ana P. Berbegall, Rosa Noguera, Wei-Yun Lai, Per Kogner, Ruth H. Palmer, Bengt Hallberg, and Tommy Martinsson. 2020. “11q Deletion or ALK Activity Curbs DLG2 Expression to Maintain an Undifferentiated State in Neuroblastoma.” CELL REPORTS 32 (12). doi:10.1016/j.celrep.2020.108171.
Vancouver
1.
Siaw JT, Javanmardi N, Van den Eynden J, Lind DE, Fransson S, Martinez-Monleon A, et al. 11q deletion or ALK activity curbs DLG2 expression to maintain an undifferentiated state in neuroblastoma. CELL REPORTS. 2020;32(12).
IEEE
[1]
J. T. Siaw et al., “11q deletion or ALK activity curbs DLG2 expression to maintain an undifferentiated state in neuroblastoma,” CELL REPORTS, vol. 32, no. 12, 2020.
@article{8675878,
  abstract     = {{High-risk neuroblastomas typically display an undifferentiated or poorly differentiated morphology. It is therefore vital to understand molecular mechanisms that block the differentiation process. We identify an important role for oncogenic ALK-ERK1/2-SP1 signaling in the maintenance of undifferentiated neural crest-derived progenitors through the repression of DLG2, a candidate tumor suppressor gene in neuroblastoma. DLG2 is expressed in the murine "bridge signature'' that represents the transcriptional transition state when neural crest cells or Schwann cell precursors differentiate to chromaffin cells of the adrenal gland. We show that the restoration of DLG2 expression spontaneously drives neuroblastoma cell differentiation, high-lighting the importance of DLG2 in this process. These findings are supported by genetic analyses of high-risk 11q deletion neuroblastomas, which identified genetic lesions in the DLG2 gene. Our data also suggest that further exploration of other bridge genes may help elucidate the mechanisms underlying the differentiation of NC-derived progenitors and their contribution to neuroblastomas.}},
  articleno    = {{108171}},
  author       = {{Siaw, Joachim Tetteh and Javanmardi, Niloufar and Van den Eynden, Jimmy and Lind, Dan Emil and Fransson, Susanne and Martinez-Monleon, Angela and Djos, Anna and Sjöberg, Rose-Marie and Östensson, Malin and Carén, Helena and Trøen, Gunhild and Beiske, Klaus and Berbegall, Ana P. and Noguera, Rosa and Lai, Wei-Yun and Kogner, Per and Palmer, Ruth H. and Hallberg, Bengt and Martinsson, Tommy}},
  issn         = {{2211-1247}},
  journal      = {{CELL REPORTS}},
  keywords     = {{General Biochemistry,Genetics and Molecular Biology}},
  language     = {{eng}},
  number       = {{12}},
  pages        = {{38}},
  title        = {{11q deletion or ALK activity curbs DLG2 expression to maintain an undifferentiated state in neuroblastoma}},
  url          = {{http://doi.org/10.1016/j.celrep.2020.108171}},
  volume       = {{32}},
  year         = {{2020}},
}
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