Mechanisms of autoinhibition and STI-571/imatinib resistance revealed by mutagenesis of BCR-ABL.

By M. Azam, R. Latek, G. Daley. Cell, 2003

649 citations recorded by the source corpus.

Subfields: Genetics, Hematology, Organic Chemistry

View Paper: https://www.semanticscholar.org/paper/70732801448c353a86c9d0c473372048b0d09510

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In Genetics

1. J. Engelman
2. C. Ashby
3. Nathanael S. Gray
4. Zhesheng Chen

In Hematology

1. Jianming Zhang
2. C. Ashby
3. Levi A. Garraway
4. Nathanael S. Gray
5. Zhesheng Chen

In Organic Chemistry

1. D. Barford

Citations in the corpus

• Structural basis for the autoinhibition of c-Abl tyrosine kinase. (2003, background): “Crystal structures of the isolatedc-Abl show that the N-terminal myristoyl modification kinase domain of Abl show that STI-571 displaces ATPof c-Abl 1b binds to the kinase domain and induces and traps an inactive conformation of the kinase domainconformational changes that allow the SH2 and SH3 (Nag”
• MEK1 mutations confer resistance to MEK and B-RAF inhibition (2009, methodology): “accomplished using a modification of published methods (10), and is described”
• Paul Ehrlich's magic bullet concept: 100 years of progress (2008, background): “A point mutation like T315I, frequently found in CML patients, prevents ABL from switching to the inactive conformation to which imatinib bind”
• The structure of Dasatinib (BMS-354825) bound to activated ABL kinase domain elucidates its inhibitory activity against imatinib-resistant ABL mutants. (2006, background): “adopt a specific inactive conformation favorable to imatinib (11, 13).”
• A small molecule–kinase interaction map for clinical kinase inhibitors (2005, background): “One of the most commonly observed mutant forms in patients, T315I, is almost completely resistant to imatini”
• Mechanisms of Acquired Crizotinib Resistance in ALK-Rearranged Lung Cancers (2012, background): “Among the three new mutations, the G1202R mutation is analogous to an imatinib-resistant BCR-ABL mutation (G340W), which was identified by random mutagenesis screening (22) but has not been reported in patient samples.”
• Validation of ITD mutations in FLT3 as a therapeutic target in human acute myeloid leukaemia (2012, neutral): “1011-007 F 56 713, HAM Normal 46,XX,del(11) (p?13p?15) [12]/46,XX[9] 80 F691L D835V 4/24 5/24 11”
• Mechanism of activation of the RAF-ERK signaling pathway by oncogenic mutations of B-RAF. (2004, background): “Mechanisms of au-media containing 1% (COS cells) or 10% FCS (WM266-4 and H1666) toinhibition and STI-571/imatinib resistance revealed by mutagene-and protein extracts prepared after 48 hr. COS cells were transfected sis of BCR-ABL.”
• Characterization of AMN107, a selective inhibitor of native and mutant Bcr-Abl. (2005, methodology): “*, values as reported previously for imatinib (Azam et al., 2003) CANCER CELL : FEBRUARY 2005 normal human myeloid and erythroid progenitor cells (assayed as CFU-GM [colony-forming unit, granulocyte/macrophage] and BFU-E [burst-forming unit, erythroid]) at concentrations %100 nM, but resulted in…”
• Structure and regulation of Src family kinases (2004, background): “Thus, the myristoylated N-terminus functionally replaces the SH2–tail interaction in Abl, and, as in Src, disruption of this latch leads to oncogenic activation (Azam et al., 2003; Hantschel et al., 2003; Harrison, 2003; Nagar et al., 2003).”
• BCR-ABL tyrosine kinase inhibitors in the treatment of Philadelphia chromosome positive chronic myeloid leukemia: a review. (2010, background): “n patients with advanced-stage disease, there are frequent reports f both primary and secondary resistance [22,52,90,91].”