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Blood, 15 February 2006, Vol. 107, No. 4, pp. 1599-1607. Prepublished online as a Blood First Edition Paper on October 25, 2005; DOI 10.1182/blood-2005-04-1629. This Article Full Text (PDF) Supplemental Figure All Versions of this Article: 2005-04-1629v1 107/4/1599    most recent Alert me when this article is cited Alert me if a correction is posted Services Email this article to a friend Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Rights and Permissions Citing Articles Citing Articles via HighWire Citing Articles via CrossRef Citing Articles via Google Scholar Google Scholar Articles by Margalit, O. Articles by Rechavi, G. Search for Related Content PubMed PubMed Citation Articles by Margalit, O. Articles by Rechavi, G. Related Collections Related Article in Blood Online Social Bookmarking                   What's this?  Previous Article  |  Next Article  Submitted April 21, 2005 Accepted October 7, 2005 BCL6 is regulated by p53 through a response element frequently disrupted in B-cell non-Hodgkin's lymphoma Ofer Margalit, Hila Amram, Ninette Amariglio, Amos J Simon, Sigal Shaklai, Galit Granot, Neri Minsky, Avichai Shimoni, Alon Harmelin, David Givol, Mordechai Shohat, Moshe Oren, and Gideon Rechavi* Pediatric Hematology-Oncology, Safra Children's Hospital, Tel-Hashomer, Israel; Sackler School of Medicine, Tel-Aviv University, Tel-Aviv, Israel Molecular Cell Biology, Weizmann Institute of Science, Rehovot, Israel Division of Hematology and Bone Marrow Transplantation, Chaim Sheba Medical Center, Tel-Hashomer and Sackler School of Medicine, Tel-Hashomer, Israel; Sackler School of Medicine, Tel-Aviv University, Tel-Aviv, Israel Veterinary Resources, Weizmann Institute of Science, Rehovot, Israel Molecular Genetics, Felstein Medical Research Center, Rabin Medical Center, Petah-Tikva, Israel * Corresponding author; email: gidi.rechavi{at}sheba.health.gov.il. The BCL6 transcriptional repressor mediates survival, proliferation and differentiation blockade of B-cells during the germinal-center reaction, and is frequently misregulated in B-cell non-Hodgkin's lymphoma (BNHL). The p53 tumor suppressor gene is central to tumorigenesis. Microarray analysis identified BCL6 as a primary target of p53. The BCL6 intron 1 contains a region in which 3 types of genetic alterations are frequent in BNHL: chromosomal translocations, point mutations and internal deletions. We therefore defined it as TMDR - Translocations, Mutations and Deletions Region. The BCL6 gene contains a p53-response element (p53RE) residing within the TMDR. This p53RE contains a motif known to be preferentially targeted by somatic hypermutation. This p53RE is evolutionary conserved only in primates. p53 binds to this RE in vitro and in vivo. Reporter assays revealed that the BCL6 p53RE can confer p53-dependent transcriptional activation. BCL6 mRNA and protein levels increased after chemo/radiotherapy in human, but not in murine tissues. The increase in BCL6 mRNA levels was attenuated by the p53 inhibitor PFT-. Thus, we define the BCL6 gene as a new p53 target, regulated through a RE frequently disrupted in BNHL. CiteULike    Connotea    Del.icio.us    Digg    Reddit    Technorati    What's this? Related Article in Blood Online: Closing the loop: p53-BCL6 feedback Izidore S. Lossos Blood 2006 107: 1246-1247. [Full Text] [PDF] This article has been cited by other articles: S. R. Walker, E. A. Nelson, L. Zou, M. Chaudhury, S. Signoretti, A. Richardson, and D. A. Frank Reciprocal Effects of STAT5 and STAT3 in Breast Cancer Mol. Cancer Res., June 1, 2009; 7(6): 966 - 976. [Abstract] [Full Text] [PDF]

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