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Prepublished online as a Blood First Edition Paper on February 6, 2003; DOI 10.1182/blood-2001-11-0142. This Article Full Text (PDF) All Versions of this Article: 2001-11-0142v1 101/12/4937    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 Sexl, V. Articles by Ihle, J. N Search for Related Content PubMed PubMed Citation Articles by Sexl, V. Articles by Ihle, J. N Social Bookmarking                   What's this? Submitted November 30, 2001 Accepted February 1, 2003 Jak1 deficiency leads to enhanced Abelson-induced B-cell tumor formation Veronika Sexl*, Boris Kovacic, Roland Piekorz, Richard Moriggl, Dagmar Stoiber, Angelika Hoffmeyer, Rita Liebminger, Oliver Kudlacek, Eva Weisz, Kristen Rothammer, and James N Ihle Department of Pharmacology, Vienna University, Vienna, Austria Howard Hughes Medical Institute, Memphis, TN, USA Department of Biochemistry, St. Jude Children's Hospital, Memphis, TN, USA * Corresponding author; email: veronika.sexl{at}univie.ac.at. The Janus kinase Jak1 has been implicated in tumor formation by the Abelson oncogene. In this study we show that loss of Jak1 does not affect in vitro transformation by v-abl as defined by the ability to induce cytokine independent B-cell colony formation or establishment of B cell lines. However, Jak1 deficient, v-abl transformed cell lines were more tumorgenic than wild type cells when transplanted subcutaneously into SCID mice or injected intraveinously into nude mice. Jak1 deficiency was associated with a loss in the ability of interferon- (IFN-) to induce growth arrest and/or apoptosis of v-abl transformed pre-B cells or tumor growth in SCID mice. Moreover, IFN- mRNA could be detected in growing tumors, and tumor cells explanted from SCID mice had lost the ability to respond to IFN- in 9/20 cases, whereas the response to interferon- (IFN-) remained intact. Importantly, a similar increase in tumorgenicity was observed when IFN- deficient cells were injected into SCID mice identifying the tumor cell itself as the main source of IFN-. These findings demonstrate that Jak1, rather than promoting tumorgenesis as previously proposed, is critical in mediating an intrinsic IFN- dependent tumor surveillance. CiteULike    Connotea    Del.icio.us    Digg    Reddit    Technorati    What's this? This article has been cited by other articles: Y. Takahashi, M. Takahashi, N. Carpino, S.-T. Jou, J.-R. Chao, S. Tanaka, Y. Shigeyoshi, E. Parganas, and J. N. Ihle Leukemia Inhibitory Factor Regulates Trophoblast Giant Cell Differentiation via Janus Kinase 1-Signal Transducer and Activator of Transcription 3-Suppressor of Cytokine Signaling 3 Pathway Mol. Endocrinol., July 1, 2008; 22(7): 1673 - 1681. [Abstract] [Full Text] [PDF] A. Hoelbl, B. Kovacic, M. A. Kerenyi, O. Simma, W. Warsch, Y. Cui, H. Beug, L. Hennighausen, R. Moriggl, and V. Sexl Clarifying the role of Stat5 in lymphoid development and Abelson-induced transformation Blood, June 15, 2006; 107(12): 4898 - 4906. [Abstract] [Full Text] [PDF] A. P. Szremska, L. Kenner, E. Weisz, R. G. Ott, E. Passegue, M. Artwohl, M. Freissmuth, R. Stoxreiter, H.-C. Theussl, S. B. Parzer, et al. JunB inhibits proliferation and transformation in B-lymphoid cells Blood, December 1, 2003; 102(12): 4159 - 4165. [Abstract] [Full Text] [PDF]

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