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Blood, 15 September 2006, Vol. 108, No. 6, pp. 2029-2036.
Prepublished online as a Blood First Edition Paper on May 18, 2006; DOI 10.1182/blood-2005-10-014258.
 Previous Article | Next Article 
Submitted October 7, 2005
Accepted May 11, 2006
NPM-ALK dependent expression of the Transcription Factor
CCAAT/enhancer binding protein (C/EBP) in
Alk-positive Anaplastic Large cell Lymphomas
Leticia Quintanilla-Martinez, Stefania Pittaluga, Cornelius Miething, Margit Klier, Martina Rudelius, Theresa Davies-Hill, Natasa Anastasov, Antonio Martinez, Angelica Vivero, Justus Duyster, Elaine S Jaffe, Falko Fend, and Mark Raffeld*
Institute of Pathology, GSF-Research Center for Health and Environment
National Cancer Institute, National Intitutes of Health
Institute of Pathology, Technical University Munich
National Cancer Institute, National Institutes of Health
Department of Internal Medicine III, Technical University Munich
* Corresponding author; email: mraff{at}box-m.nih.gov.
C/EBP is one of a six-member family of
CCAAT/enhancer binding proteins (C/EBP). These
transcription factors are involved in the regulation of
various aspects of cellular growth and differentiation.
Although C/EBP has important functions in both B
and T-cell differentiation, its expression has not been
well studied in lymphoid tissues. We, therefore,
analyzed its expression by immunohistochemistry and/or
Western blot in normal lymphoid tissues and in 248 well
characterized lymphomas and lymphoma cell lines. Non-
neoplastic lymphoid tissues and the vast majority of B-
cell, T-cell, and Hodgkin lymphomas lacked detectable
C/EBP. In contrast, most cases of ALK-positive
ALCL (40/45; 88%) strongly expressed C/EBP.
Western blot analysis confirmed the C/EBP
expression in the ALK-positive ALCL cases, and
demonstrated elevated levels of the LIP isoform, which
has been associated with increased proliferation and
aggressiveness in carcinomas. Transfection of Ba/F3 and
32D cells with both NPM-ALK and a kinase-inhibitable
modified NPM-ALK resulted in the induction of C/EBP, and demonstrated dependence upon the NPM-ALK
kinase activity. In conclusion, we report the
constitutive expression of C/EBP in ALK-positive
ALCL cases, and show its relationship to NPM-ALK. We
suggest that C/EBP is likely to play an important
role in the pathogenesis and unique phenotype of this
lymphoma.
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