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Science 8 June 1984:
Vol. 224. no. 4653, pp. 1117 - 1121
DOI: 10.1126/science.6585957
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Articles

Science, Vol 224, Issue 4653, 1117-1121
Copyright © 1984 by American Association for the Advancement of Science

articles

Amplification of the c-myb oncogene in a case of human acute myelogenous leukemia

PG Pelicci, L Lanfrancone, MD Brathwaite, Wolman SR, and R Dalla-Favera

Amplification is one of the mechanisms by which cellular oncogenes may be altered in their function, possibly leading to neoplastic transformation. The oncogenes c-myc, c- abl , and c-Ki-ras are amplified in several different human neoplasias. The oncogene c-myb, which is specifically expressed and regulated in hematopoietic cells, was found to be amplified in cell lines ML-1, ML-2, and ML-3, which were separately cultured from cells of a patient with acute myelogenous leukemia (AML). A five- to tenfold amplification was correlated with high levels of expression of normal size c-myb messenger RNA and with chromosomal abnormalities in the region 6q22 -24, where the c-myb locus is normally located. Amplification and cytogenetic abnormalities were detected in DNA's from primary and secondary cultures of ML cells, suggesting that they may have contributed to leukemogenesis. The similar AML cell lines HL-60 and ML's contain different amplified oncogenes: c-myc and c-myb, respectively. Alternative activation of structurally and possibly functionally similar oncogenes may distinguish--at the pathogenetic level--phenotypically similar tumors.


THIS ARTICLE HAS BEEN CITED BY OTHER ARTICLES:
c-Myb Is an Evolutionary Conserved miR-150 Target and miR-150/c-Myb Interaction Is Important for Embryonic Development.
Y.-C. Lin, M.-W. Kuo, J. Yu, H.-H. Kuo, R.-J. Lin, W.-L. Lo, and A. L. Yu (2008)
Mol. Biol. Evol. 25, 2189-2198
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Requirement of c-Myb for p210BCR/ABL-dependent transformation of hematopoietic progenitors and leukemogenesis.
M. R. Lidonnici, F. Corradini, T. Waldron, T. P. Bender, and B. Calabretta (2008)
Blood 111, 4771-4779
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Enhanced Proliferative Potential of Hematopoietic Cells Expressing Degradation-resistant c-Myb Mutants.
F. Corradini, V. Cesi, V. Bartella, E. Pani, R. Bussolari, O. Candini, and B. Calabretta (2005)
J. Biol. Chem. 280, 30254-30262
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MYB Oncogene Amplification in Hereditary BRCA1 Breast Cancer.
P. Kauraniemi, I. Hedenfalk, K. Persson, D. J. Duggan, M. Tanner, O. Johannsson, H. Olsson, J. M. Trent, J. Isola, and A. Borg (2000)
Cancer Res. 60, 5323-5328
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Distinct Cellular Factors Regulate the c-myb Promoter through Its E2F Element.
M. R. Campanero, M. Armstrong, and E. Flemington (1999)
Mol. Cell. Biol. 19, 8442-8450
   Abstract »    Full Text »    PDF »
A dominant interfering Myb mutant causes apoptosis in T cells..
D Taylor, P Badiani, and K Weston (1996)
Genes & Dev. 10, 2732-2744
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Relationship between the c-myb locus and the 6q-chromosomal aberration in leukemias and lymphomas.
C Barletta, P. Pelicci, L. Kenyon, S. Smith, and R Dalla-Favera (1987)
Science 235, 1064-1067
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Alterations of myc, myb, and rasHa proto-oncogenes in cancers are frequent and show clinical correlation.
J Yokota, Y Tsunetsugu-Yokota, H Battifora, C Le Fevre, and M. Cline (1986)
Science 231, 261-265
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The action of oncogenes in the cytoplasm and nucleus.
R. Weinberg (1985)
Science 230, 770-776
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Activated expression of the N-myc gene in human neuroblastomas and related tumors.
N. Kohl, C. Gee, and F. Alt (1984)
Science 226, 1335-1337
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