Note to users. If you're seeing this message, it means that your browser cannot find this page's style/presentation instructions -- or possibly that you are using a browser that does not support current Web standards. Find out more about why this message is appearing, and what you can do to make your experience of our site the best it can be.

Science 12 February 1988:
Vol. 239. no. 4841, pp. 775 - 777
DOI: 10.1126/science.3422516
Prev | Table of Contents | Next

Articles

Science, Vol 239, Issue 4841, 775-777
Copyright © 1988 by American Association for the Advancement of Science

articles

Expression of a distinctive BCR-ABL oncogene in Ph1-positive acute lymphocytic leukemia (ALL)

SS Clark, J McLaughlin, M Timmons, AM Pendergast, Y Ben-Neriah, LW Dow, W Crist, G Rovera, SD Smith, and ON Witte

Department of Microbiology, UCLA 90024.

The Philadelphia chromosome (Ph1) is a translocation between chromosomes 9 and 22 that is found in chronic myelogenous leukemia (CML) and a subset of acute lymphocytic leukemia patients (ALL). In CML, this results in the expression of a chimeric 8.5-kilobase BCR-ABL transcript that encodes the P210BCR-ABL tyrosine kinase. The Ph1 chromosome in ALL expresses a distinct ABL-derived 7-kilobase messenger RNA that encodes the P185ALL-ABL protein. Since the expression of different oncogene products may play a role in the distinctive presentation of Ph1-positive ALL versus CML, it is necessary to understand the molecular basis for the expression of P185ALL-ABL. Both P210BCR-ABL and P185ALL-ABL are recognized by an antiserum directed to BCR determinants in the amino-terminal region of both proteins. Antisera to BCR determinants proximal to the BCR-ABL junction in CML immunoprecipitated P210BCR-ABL but not P185ALL-ABL. Nucleotide sequence analysis of complementary DNA clones made from RNA from the Ph1-positive ALL SUP-B15 cell line, and S1 nuclease protection analysis confirmed the presence of BCR-ABL chimeric transcripts in Ph1-positive ALL cells. In Ph1-positive ALL, ABL sequences were joined to BCR sequences approximately 1.5 kilobases 5' of the CML junction. P185ALL-ABL represents the product of a BCR-ABL fusion gene in Ph1-positive ALL that is distinct from the BCR-ABL fusion gene of CML.


THIS ARTICLE HAS BEEN CITED BY OTHER ARTICLES:
Impaired V(D)J recombination and increased apoptosis among B cell precursors in the bone marrow of c-Abl-deficient mice.
Q. L. K. Lam, C. K. C. Lo, B.-J. Zheng, K.-H. Ko, D. G. Osmond, G. E. Wu, R. Rottapel, and L. Lu (2007)
Int. Immunol. 19, 267-276
   Abstract »    Full Text »    PDF »
High Complete Remission Rate and Promising Outcome by Combination of Imatinib and Chemotherapy for Newly Diagnosed BCR-ABL-Positive Acute Lymphoblastic Leukemia: A Phase II Study by the Japan Adult Leukemia Study Group.
M. Yanada, J. Takeuchi, I. Sugiura, H. Akiyama, N. Usui, F. Yagasaki, T. Kobayashi, Y. Ueda, M. Takeuchi, S. Miyawaki, et al. (2006)
J. Clin. Oncol. 24, 460-466
   Abstract »    Full Text »    PDF »
NS-187, a potent and selective dual Bcr-Abl/Lyn tyrosine kinase inhibitor, is a novel agent for imatinib-resistant leukemia.
S. Kimura, H. Naito, H. Segawa, J. Kuroda, T. Yuasa, K. Sato, A. Yokota, Y. Kamitsuji, E. Kawata, E. Ashihara, et al. (2005)
Blood 106, 3948-3954
   Abstract »    Full Text »    PDF »
Bcr-Abl regulates osteopontin transcription via Ras, PI-3K, aPKC, Raf-1, and MEK.
F. B. Hickey, K. England, and T. G. Cotter (2005)
J. Leukoc. Biol. 78, 289-300
   Abstract »    Full Text »    PDF »
Combination of intensive chemotherapy and imatinib can rapidly induce high-quality complete remission for a majority of patients with newly diagnosed BCR-ABL-positive acute lymphoblastic leukemia.
M. Towatari, M. Yanada, N. Usui, J. Takeuchi, I. Sugiura, M. Takeuchi, F. Yagasaki, Y. Kawai, S. Miyawaki, S. Ohtake, et al. (2004)
Blood 104, 3507-3512
   Abstract »    Full Text »    PDF »
BCR/ABL oncogenic kinase promotes unfaithful repair of the reactive oxygen species-dependent DNA double-strand breaks.
M. O. Nowicki, R. Falinski, M. Koptyra, A. Slupianek, T. Stoklosa, E. Gloc, M. Nieborowska-Skorska, J. Blasiak, and T. Skorski (2004)
Blood 104, 3746-3753
   Abstract »    Full Text »    PDF »
Biological impediments to monoclonal antibody-based cancer immunotherapy.
J. Christiansen and A. K. Rajasekaran (2004)
Mol. Cancer Ther. 3, 1493-1501
   Abstract »    Full Text »    PDF »
Bcr (breakpoint cluster region) protein binds to PDZ-domains of scaffold protein PDZK1 and vesicle coat protein Mint3.
E. K. Malmberg, C. X. Andersson, M. Gentzsch, J. H. Chen, A. Mengos, L. Cui, G. C. Hansson, and J. R. Riordan (2004)
J. Cell Sci. 117, 5535-5541
   Abstract »    Full Text »    PDF »
Chlorogenic acid inhibits Bcr-Abl tyrosine kinase and triggers p38 mitogen-activated protein kinase-dependent apoptosis in chronic myelogenous leukemic cells.
G. Bandyopadhyay, T. Biswas, K. C. Roy, S. Mandal, C. Mandal, B. C. Pal, S. Bhattacharya, S. Rakshit, D. K. Bhattacharya, U. Chaudhuri, et al. (2004)
Blood 104, 2514-2522
   Abstract »    Full Text »    PDF »
Bcr-Abl Regulates Protein Kinase C{iota} (PKC{iota}) Transcription via an Elk1 Site in the PKC{iota} Promoter.
W. C. Gustafson, S. Ray, L. Jamieson, E. A. Thompson, A. R. Brasier, and A. P. Fields (2004)
J. Biol. Chem. 279, 9400-9408
   Abstract »    Full Text »    PDF »
Inducible expression of BCR/ABL using human CD34 regulatory elements results in a megakaryocytic myeloproliferative syndrome.
C. S. Huettner, S. Koschmieder, H. Iwasaki, J. Iwasaki-Arai, H. S. Radomska, K. Akashi, and D. G. Tenen (2003)
Blood 102, 3363-3370
   Abstract »    Full Text »    PDF »
p210 BCR/ABL kinase regulates nucleotide excision repair (NER) and resistance to UV radiation.
Y. Canitrot, R. Falinski, T. Louat, G. Laurent, C. Cazaux, J.-S. Hoffmann, D. Lautier, and T. Skorski (2003)
Blood 102, 2632-2637
   Abstract »    Full Text »    PDF »
Double jeopardy from a single translocation: deletions of the derivative chromosome 9 in chronic myeloid leukemia.
B. J. P. Huntly, A. Bench, and A. R. Green (2003)
Blood 102, 1160-1168
   Abstract »    Full Text »    PDF »
SKI-606, a 4-Anilino-3-quinolinecarbonitrile Dual Inhibitor of Src and Abl Kinases, Is a Potent Antiproliferative Agent against Chronic Myelogenous Leukemia Cells in Culture and Causes Regression of K562 Xenografts in Nude Mice.
J. M. Golas, K. Arndt, C. Etienne, J. Lucas, D. Nardin, J. Gibbons, P. Frost, F. Ye, D. H. Boschelli, and F. Boschelli (2003)
Cancer Res. 63, 375-381
   Abstract »    Full Text »    PDF »
Fusion Tyrosine Kinases Induce Drug Resistance by Stimulation of Homology-Dependent Recombination Repair, Prolongation of G2/M Phase, and Protection from Apoptosis.
A. Slupianek, G. Hoser, I. Majsterek, A. Bronisz, M. Malecki, J. Blasiak, R. Fishel, and T. Skorski (2002)
Mol. Cell. Biol. 22, 4189-4201
   Abstract »    Full Text »    PDF »
Complementary functions of the antiapoptotic protein A1 and serine/threonine kinase pim-1 in the BCR/ABL-mediated leukemogenesis.
M. Nieborowska-Skorska, G. Hoser, P. Kossev, M. A. Wasik, and T. Skorski (2002)
Blood 99, 4531-4539
   Abstract »    Full Text »    PDF »
Derivative chromosome 9 deletions in chronic myeloid leukemia: poor prognosis is not associated with loss of ABL-BCR expression, elevated BCR-ABL levels, or karyotypic instability.
B. J. P. Huntly, A. J. Bench, E. Delabesse, A. G. Reid, J. Li, M. A. Scott, L. Campbell, J. Byrne, E. Pinto, A. Brizard, et al. (2002)
Blood 99, 4547-4553
   Abstract »    Full Text »    PDF »
Expression of Constitutively Active Raf-1 in the Mitochondria Restores Antiapoptotic and Leukemogenic Potential of a Transformation-deficient BCR/ABL Mutant.
P. Salomoni, M. A. Wasik, R. F. Riedel, K. Reiss, J. K. Choi, T. Skorski, and B. Calabretta (1998)
J. Exp. Med. 187, 1995-2007
   Abstract »    Full Text »    PDF »
Association of the protein kinases c-Bcr and Bcr-Abl with proteins of the 14-3-3 family.
G. Reuther, H Fu, L. Cripe, R. Collier, and A. Pendergast (1994)
Science 266, 129-133
   Abstract »    PDF »
Differential complementation of Bcr-Abl point mutants with c-Myc.
D. Afar, A Goga, J McLaughlin, O. Witte, and C. Sawyers (1994)
Science 264, 424-426
   Abstract »    PDF »
Genetic Approaches to Defining Signaling by the CML-associated Tyrosine Kinase BCR-ABL.
D.E.H. Afar, A. Goga, L. Cohen, C.L. Sawyers, J. McLaughlin, R.N. Mohr, and O.N. Witte (1994)
Cold Spring Harb Symp Quant Biol 59, 589-594
   Abstract »    PDF »
Characterization of a zinc finger gene disrupted by the t(15;17) in acute promyelocytic leukemia.
A. Goddard, J Borrow, P. Freemont, and E Solomon (1991)
Science 254, 1371-1374
   Abstract »    PDF »
Molecular Genetic Advances in Chronic Myelogenous Leukemia.
D. E. Epner and H. P. Koeffler (1990)
Ann Intern Med 113, 3-6
   Abstract »    PDF »
Tyrosine kinase activity and transformation potency of bcr-abl oncogene products.
T. Lugo, A. Pendergast, A. Muller, and O. Witte (1990)
Science 247, 1079-1082
   Abstract »    PDF »


To Advertise     Find Products

Science. ISSN 0036-8075 (print), 1095-9203 (online)