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The novel ets factor tel2 cooperates with myc in b lymphomagenesis

Academic Article
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Overview

authors

  • Cardone, M.
  • Kandilci, A.
  • Carella, C.
  • Nilsson, J. A.
  • Brennan, J. A.
  • Sirma, S.
  • Ozbek, U.
  • Boyd, K.
  • Cleveland, John
  • Grosveld, G. C.

publication date

  • March 2005

journal

  • Molecular and Cellular Biology  Journal

abstract

  • The human ETS family gene TEL2/ETV7 is highly homologous to TEL1/ETV6, a frequent target of chromosome translocations in human leukemia and specific solid tumors. Here we report that TEL2 augments the proliferation and survival of normal mouse B cells and dramatically accelerates lymphoma development in Emu-Myc transgenic mice. Nonetheless, inactivation of the p53 pathway was a hallmark of all TEL2/Emu-Myc lymphomas, indicating that TEL2 expression alone is insufficient to bypass this apoptotic checkpoint. Although TEL2 is infrequently up-regulated in human sporadic Burkitt's lymphoma, analysis of pediatric B-cell acute lymphocytic leukemia (B-ALL) samples showed increased coexpression of TEL2 and MYC and/or MYCN in over one-third of B-ALL patients. Therefore, TEL2 and MYC also appear to cooperate in provoking a cadre of human B-cell malignancies.

subject areas

  • Animals
  • Apoptosis
  • B-Lymphocytes
  • Burkitt Lymphoma
  • Cell Proliferation
  • Child
  • DNA-Binding Proteins
  • Female
  • Humans
  • Male
  • Mice
  • Mice, Transgenic
  • Mutation
  • Proto-Oncogene Proteins c-ets
  • Proto-Oncogene Proteins c-myc
  • Suppression, Genetic
  • Transcription Factors
  • Tumor Suppressor Protein p53
  • Up-Regulation
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Identity

International Standard Serial Number (ISSN)

  • 0270-7306

Digital Object Identifier (DOI)

  • 10.1128/mcb.25.6.2395-2405.2005

PubMed ID

  • 15743832
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Additional Document Info

start page

  • 2395

end page

  • 2405

volume

  • 25

issue

  • 6

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