BCR/ABL regulates mammalian RecA homologs, resulting in drug resistance.
Artur Slupianek,Christoph Schmutte,Gregory Tombline,Malgorzata Nieborowska-Skorska,Grazyna Hoser,Michał Nowicki,Andrew J. Pierce,Richard Fishel,Tomasz Skorski +8 more
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It is demonstrated that RAD51 is important for resistance to cisplatin and mitomycin C in cells expressing the BCR/ABL oncogenic tyrosine kinase.About:
This article is published in Molecular Cell.The article was published on 2001-10-26 and is currently open access. It has received 328 citations till now. The article focuses on the topics: ABL & RAD51.read more
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Endogenous DNA double-strand breaks: Production, fidelity of repair, and induction of cancer
TL;DR: It is concluded that rates of production of EDSBs and of ensuing spontaneous mitotic recombination events can account for a substantial fraction of the earliest oncogenic events in human carcinomas.
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The biology of cml blast crisis
Bruno Calabretta,Danilo Perrotti +1 more
TL;DR: Validation of the critical role of certain secondary changes (ie, loss of p53 or C/EBPalpha function) in murine models of CML blast crisis and in in vitro assays of BCR/ABL transformation of human hematopoietic progenitors might lead to the development of novel therapies based on targeting BCR /ABL and inhibiting or restoring the gene activity gained or lost during disease progression.
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Chronic myeloid leukaemia as a model of disease evolution in human cancer.
Junia V. Melo,David J. Barnes +1 more
TL;DR: Chronic myeloid leukaemia can be considered as a paradigm for neoplasias that evolve through a multi-step process and one of the best examples of a disease that can be targeted by molecular therapy; however, the success of new 'designer drugs' is largely restricted to the chronic phase of the disease.
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Recombinational DNA repair and human disease.
Larry H. Thompson,David Schild +1 more
TL;DR: The genes and proteins related to the homologous recombinational repair (HRR) pathway that are implicated in cancer through either genetic disorders that predispose to cancer through chromosome instability or the occurrence of somatic mutations that contribute to carcinogenesis are reviewed.
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The BCR-ABL Story: Bench to Bedside and Back
Stephane Wong,Owen N. Witte +1 more
TL;DR: Analysis of CML patients resistant to BCR-ABL suppression by Imatinib mesylate coupled with the crystallographic structure of ABL complexed to this inhibitor have shown how structural mutations in ABL can circumvent an otherwise potent anticancer drug.
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DNA Repair and Mutagenesis
TL;DR: Nucleotide excision repair in mammalian cells: genes and proteins Mismatch repair The SOS response and recombinational repair in prokaryotes Mutagenesis in proKaryote Mutagenisation in eukaryotes Other DNA damage tolerance responses in eUKaryotes.
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Effects of a selective inhibitor of the Abl tyrosine kinase on the growth of Bcr-Abl positive cells.
Brian J. Druker,Shu Tamura,Elisabeth Buchdunger,Sayuri Ohno,Gerald M. Segal,Shane Fanning,Jürg Zimmermann,Nicholas B. Lydon +7 more
TL;DR: A compound, designed to inhibit the Abl protein tyrosine kinase, was evaluated for its effects on cells containing the Bcr–Abl fusion protein and it was found that this compound may be useful in the treatment of bcr–abl–positive leukemias.
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Chronic myeloid leukemia.
TL;DR: This work has demonstrated that CML can be curable through immune-mediated elimination of leukemia cells by allogeneic T lymphocytes, and specific inhibition of signal transduction by the tyrosine kinase Bcr-Abl has been found to be active in managing the disease.
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Association of BRCA1 with Rad51 in Mitotic and Meiotic Cells
Ralph Scully,Junjie Chen,Annemieke W. Plug,Yonghong Xiao,David R. Weaver,Jean Feunteun,Terry Ashley,David M. Livingston +7 more
TL;DR: Findings suggest a functional interaction between BRCA1 and Rad51 in the meiotic and mitotic cell cycles, which, in turn, suggests a role for BRC a1 in the control of recombination and of genome integrity.
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XRCC3 promotes homology-directed repair of DNA damage in mammalian cells
TL;DR: It is demonstrated here that error-free homology-directed repair of DNA double-strand breaks is decreased 25-fold in an XR CC3-deficient hamster cell line and can be restored to wild-type levels through XRCC3 expression.