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Oncogenic signaling: new insights and controversies from chronic myeloid leukemia
Chronic myeloid leukemia (CML), which is caused by the BCR–ABL fusion tyrosine kinase, is one of the most intensively studied human cancers. ABL kinase inhibitors have been spectacularly successful in treating CML, but disease persistence and acquired drug resistance can prevent eradication and cure...
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Formato: | Texto |
Lenguaje: | English |
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The Rockefeller University Press
2007
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Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2137897/ https://www.ncbi.nlm.nih.gov/pubmed/17353369 http://dx.doi.org/10.1084/jem.20062335 |
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author | Van Etten, Richard A. |
author_facet | Van Etten, Richard A. |
author_sort | Van Etten, Richard A. |
collection | PubMed |
description | Chronic myeloid leukemia (CML), which is caused by the BCR–ABL fusion tyrosine kinase, is one of the most intensively studied human cancers. ABL kinase inhibitors have been spectacularly successful in treating CML, but disease persistence and acquired drug resistance can prevent eradication and cure of the leukemia. The development of better therapies will depend on a full understanding of signaling pathways in CML, facilitated by model studies using mutant mice. |
format | Text |
id | pubmed-2137897 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2007 |
publisher | The Rockefeller University Press |
record_format | MEDLINE/PubMed |
spelling | pubmed-21378972007-12-13 Oncogenic signaling: new insights and controversies from chronic myeloid leukemia Van Etten, Richard A. J Exp Med Commentaries Chronic myeloid leukemia (CML), which is caused by the BCR–ABL fusion tyrosine kinase, is one of the most intensively studied human cancers. ABL kinase inhibitors have been spectacularly successful in treating CML, but disease persistence and acquired drug resistance can prevent eradication and cure of the leukemia. The development of better therapies will depend on a full understanding of signaling pathways in CML, facilitated by model studies using mutant mice. The Rockefeller University Press 2007-03-19 /pmc/articles/PMC2137897/ /pubmed/17353369 http://dx.doi.org/10.1084/jem.20062335 Text en Copyright © 2007, The Rockefeller University Press This article is distributed under the terms of an Attribution–Noncommercial–Share Alike–No Mirror Sites license for the first six months after the publication date (see http://www.rupress.org/terms). After six months it is available under a Creative Commons License (Attribution–Noncommercial–Share Alike 4.0 Unported license, as described at http://creativecommons.org/licenses/by-nc-sa/4.0/). |
spellingShingle | Commentaries Van Etten, Richard A. Oncogenic signaling: new insights and controversies from chronic myeloid leukemia |
title | Oncogenic signaling: new insights and controversies from chronic myeloid leukemia |
title_full | Oncogenic signaling: new insights and controversies from chronic myeloid leukemia |
title_fullStr | Oncogenic signaling: new insights and controversies from chronic myeloid leukemia |
title_full_unstemmed | Oncogenic signaling: new insights and controversies from chronic myeloid leukemia |
title_short | Oncogenic signaling: new insights and controversies from chronic myeloid leukemia |
title_sort | oncogenic signaling: new insights and controversies from chronic myeloid leukemia |
topic | Commentaries |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2137897/ https://www.ncbi.nlm.nih.gov/pubmed/17353369 http://dx.doi.org/10.1084/jem.20062335 |
work_keys_str_mv | AT vanettenricharda oncogenicsignalingnewinsightsandcontroversiesfromchronicmyeloidleukemia |