Price of freedom

Nature

Volumn 485, Issue 7397, 2012, Pages 260-263

  Smith, Catherine C ^a   Wang, Qi ^b   Chin, Chen Shan ^c   Salerno, Sara ^a   Damon, Lauren E ^a   Levis, Mark J ^d   Perl, Alexander E ^e   Travers, Kevin J ^c   Wang, Susana ^c   Hunt, Jeremy P ^f,g   Zarrinkar, Patrick P ^f,g   Schadt, Eric E ^c,g   Kasarskis, Andrew ^c,g   Kuriyan, John ^b   Shah, Neil P ^a  

^a UNIVERSITY OF CALIFORNIA   (United States)

^b UNIVERSITY OF CALIFORNIA   (United States)

^c PACIFIC BIOSCIENCES   (United States)

^d JOHNS HOPKINS UNIVERSITY   (United States)

^e UNIVERSITY OF PENNSYLVANIA   (United States)

^f Ambit Biosciences   (United States)

^g DiscoveRx Corporation   (United States)

Author keywords

[No Author keywords available]

Indexed keywords

CD135 ANTIGEN; CYTARABINE; ETOPOSIDE; KIT PROTEIN; MITOXANTRONE; PLATELET DERIVED GROWTH FACTOR ALPHA RECEPTOR; PLATELET DERIVED GROWTH FACTOR BETA RECEPTOR; PROTEIN; PROTEIN RET; QUIZARTINIB; UNCLASSIFIED DRUG; BENZOTHIAZOLE DERIVATIVE; CARBANILAMIDE DERIVATIVE; FLT3 PROTEIN, HUMAN;

AMINO ACID; CANCER; DISCRIMINANT ANALYSIS; ENZYME ACTIVITY; INHIBITOR; MUTATION; PATHOGENICITY;

ACUTE GRANULOCYTIC LEUKEMIA; ADULT; AGED; AMINO ACID SUBSTITUTION; CONTROLLED STUDY; DRUG TARGETING; FEMALE; HUMAN; IN VITRO STUDY; INTERNAL TANDEM DUPLICATION MUTATION; MALE; MUTATION; POINT MUTATION; PRIORITY JOURNAL; REVIEW; VALIDATION STUDY; ARTICLE; CHEMICAL STRUCTURE; DRUG ANTAGONISM; DRUG RESISTANCE; GENETICS; METABOLISM; MOLECULARLY TARGETED THERAPY; NUCLEOTIDE SEQUENCE; PROTEIN BINDING; PROTEIN TERTIARY STRUCTURE; RECURRENT DISEASE; REPRODUCIBILITY; TUMOR CELL LINE;

BENZOTHIAZOLES; CELL LINE, TUMOR; DNA MUTATIONAL ANALYSIS; DRUG RESISTANCE, NEOPLASM; FMS-LIKE TYROSINE KINASE 3; HUMANS; LEUKEMIA, MYELOID, ACUTE; MODELS, MOLECULAR; MOLECULAR STRUCTURE; MOLECULAR TARGETED THERAPY; MUTATION; PHENYLUREA COMPOUNDS; PROTEIN BINDING; PROTEIN STRUCTURE, TERTIARY; RECURRENCE; REPRODUCIBILITY OF RESULTS;

EID: 84860747223     PISSN: 00280836     EISSN: None     Source Type: Journal    
DOI: 10.1038/nature11016     Document Type: Article

References (33)

1. Thiede, C. et al. Analysis of FLT3-activating mutations in 979 patients with acute myelogenous leukemia: association with FAB subtypes and identification of subgroups with poor prognosis. Blood 99, 4326-4335 (2002).
2. Lee, B. H. etal. FLT3 internal tandem duplication mutations induce myeloproliferative or lymphoid disease in a transgenic mouse model. Oncogene 24, 7882-7892 (2005).
3. Shih, L.Y. etal. Acquisition of FLT3 orN-ras mutations is frequently associated with progression of myelodysplastic syndrome to acute myeloid leukemia. Leukemia 18, 466-475 (2004).
4. Knapper, S. etal. A phase 2 trial of the FLT3 inhibitor lestaurtinib(CEP701) as first-line treatment for older patients with acute myeloid leukemia not considered fit for intensive chemotherapy. Blood 108, 3262-3270 (2006).
5. Fischer, T. etal. Phase IIB trial of oral Midostaurin (PKC412), the FMS-like tyrosine kinase 3 receptor(FLT3) and multi-targeted kinase inhibitor, in patients with acute myeloid leukemia and high-risk myelodysplastic syndrome with either wild-type or mutated FLT3. J. Clin. Oncol. 28, 4339-4345 (2010).
6. Zarrinkar, P. P. etal. AC220 is a uniquely potent and selective inhibitor of FLT3 for the treatment of acute myeloid leukemia (AML). Blood 114, 2984-2992 (2009).
7. Cortes, J. etal. in 16th Congress of the European Hematology Association (Haematologica, 2011).
8. Heidel, F. etal. Clinical resistance to the kinase inhibitor PKC412 in acute myeloid leukemia by mutation of Asn-676 in the FLT3 tyrosine kinase domain. Blood 107, 293-300 (2006).
9. Metzelder, S. etal. Compassionate use of sorafenib in FLT3-ITD-positive acute myeloid leukemia: sustained regression before and after allogeneic stem cell transplantation. Blood 113, 6567-6571 (2009).
10. Scholl, S. etal. Secondary resistance to sorafenib in two patients with acute myeloid leukemia (AML) harboring FLT3-ITD mutations. Ann. Hematol. 90, 473-475(2011).
11. Azam, M., Latek, R. R. & Daley, G. Q. Mechanisms of autoinhibition and STI-571/imatinib resistance revealed by mutagenesis of BCR-ABL. Cell 112, 831-843 (2003).
12. Shah, N. P. etal. Multiple BCR-ABL kinase domain mutations confer polyclonal resistance to the tyrosine kinase inhibitor imatinib (STI571) in chronic phase and blast crisis chronic myeloid leukemia. Cancer Cell 2, 117-125 (2002).
13. Travers, K. J., Chin, C. S., Rank, D. R., Eid, J.S. & Turner, S. W. A flexible and efficient template format for circular consensus sequencing and SNP detection. Nucleic Acids Res. 38, e159 (2010).
14. Griffith, J. etal. The structural basis forautoinhibition of FLT3 by the juxtamembrane domain. Mol. Cell 13, 169-178 (2004).
15. Levinson, N. M. etal. ASrc-like inactive conformation in the Abl tyrosine kinase domain. PLoSBiol. 4, e144 (2006).
16. Mol, C. D. etal. Structural basis fortheautoinhibition and STI-571 inhibition of c-Kit tyrosine kinase. J. Biol. Chem. 279, 31655-31663 (2004).
17. Hubbard, S. R., Wei, L., Ellis, L. & Hendrickson, W. A. Crystal structure of the tyrosine kinase domain of the human insulin receptor. Nature 372, 746-754 (1994).
18. Mol, C. D. etal. Structure of a c-Kit product complex reveals the basis for kinase transactivation. J. Biol. Chem. 278, 31461-31464 (2003).
19. Hubbard, S. R. Crystal structureof the activated insulin receptortyrosine kinase in complex with peptide substrate and ATP analog. EMBOJ. 16, 5572-5581 (1997).
20. Wodicka, L. M. etal. Activation state-dependent binding of small molecule kinase inhibitors: structural insights from biochemistry. Chem. Biol. 17, 1241-1249 (2010).
21. Burley, S. K. & Petsko, G. A. Aromatic-aromatic interaction: a mechanism of protein structure stabilization. Science 229, 23-28 (1985).
22. Wan, P. T. etal. Mechanism of activation of the RAF-ERK signaling pathway by oncogenic mutations of B-RAF. Cell 116, 855-867 (2004).
23. Choudhary, C. etal. Activation mechanisms of STAT5 by oncogenic Flt3-ITD. Blood 110, 370-374 (2007).
24. Pao, W. etal. Acquired resistance of lung adenocarcinomas to gefitinib or erlotinib is associated with a second mutation in the EGFR kinase domain. PLoS Med. 2, e73 (2005).
25. Barbie, D. A. & Deangelo, D. J. Systemic mastocytosis: current classification and novel therapeutic options. Clin. Adv. Hematol. Oncol. 4, 768-775 (2006).
26. Anderson, K. etal. Genetic variegation of clonal architecture and propagating cells in leukaemia. Nature 469, 356-361 (2011).
27. Kralovics, R. etal. Acquisition of theV617F mutation of JAK2 is a late genetic event in a subset of patients with myeloproliferative disorders. Blood 108, 1377-1380 (2006).
28. Nazarian, R. etal. Melanomas acquire resistance to B-RAF(V600E) inhibition by RTK or N-RAS upregulation. Nature 468, 973-977 (2010).
29. Benson, G. Tandem repeats finder: a program to analyze DNA sequences. Nucleic Acids Res. 27, 573-580 (1999).
30. Yates, F. Tests of significance for 2 x 2 contingency tables. J. R. Stat. Soc.A 147, 426-463 (1984).
31. Barnard, G. A. Must clinical trials be large? The interpretation of p-valuesand the combination of test results. Stat Med. 9, 601-614 (1990).
32. Morris, G. M. etal. AutoDock4 and AutoDockTools4: automated docking with selective receptor flexibility. J. Comput. Chem. 30, 2785-2791 (2009).
33. Schuttelkopf, A. W. & van Aalten, D. M. PRODRG: a tool for high-throughput crystallography of protein-ligand complexes. Acta Crystallogr. D 60, 1355-1363 (2004).