Response and resistance to MEK inhibition in leukaemias initiated by hyperactive Ras

Nature

Volumn 461, Issue 7262, 2009, Pages 411-414

  Lauchle, Jennifer O ^a   Kim, Doris ^a   Le, Doan T ^a   Akagi, Keiko ^b   Crone, Michael ^a   Krisman, Kimberly ^a   Warner, Kegan ^a   Bonifas, Jeannette M ^a   Li, Qing ^a   Coakley, Kristen M ^a   Diaz Flores, Ernesto ^a   Gorman, Matthew ^a   Przybranowski, Sally ^c   Tran, Mary ^a   Kogan, Scott C ^a   Roose, Jeroen P ^a   Copeland, Neal G ^d   Jenkins, Nancy A ^d   Parada, Luis ^e   Wolff, Linda ^b   Sebolt Leopold, Judith ^c   Shannon, Kevin ^a   more..

^a UNIVERSITY OF CALIFORNIA   (United States)

^b NATIONAL CANCER INSTITUTE   (United States)

^c PFIZER INC   (United States)

^d INSTITUTE OF MOLECULAR AND CELL BIOLOGY   (Singapore)

^e UNIVERSITY OF TEXAS SOUTHWESTERN MEDICAL CENTER   (United States)

Author keywords

[No Author keywords available]

Indexed keywords

2 (2 CHLORO 4 IODOANILINO) N CYCLOPROPYLMETHOXY 3,4 DIFLUOROBENZAMIDE; 4 (4 FLUOROPHENYL) 2 (4 HYDROXYPHENYL) 5 (4 PYRIDYL)IMIDAZOLE; GRANULOCYTE MACROPHAGE COLONY STIMULATING FACTOR; MITOGEN ACTIVATED PROTEIN KINASE; MITOGEN ACTIVATED PROTEIN KINASE P38; N (2,3 DIHYDROXYPROPOXY) 3,4 DIFLUORO 2 (2 FLUORO 4 IODOANILINO)BENZAMIDE; RETROVIRUS VECTOR;

BIOACTIVITY; CANCER; COMPARATIVE STUDY; DISEASE TREATMENT; DRUG RESISTANCE; ENZYME ACTIVITY; GENE EXPRESSION; MUTATION; REGRESSION ANALYSIS;

ACUTE GRANULOCYTIC LEUKEMIA; ANIMAL CELL; ANIMAL EXPERIMENT; ANIMAL MODEL; ANIMAL TISSUE; ARTICLE; BONE MARROW; CANCER CELL; CANCER GROWTH; CANCER RESISTANCE; CONTROLLED STUDY; GENE MUTATION; GENETIC RESISTANCE; INDEL MUTATION; MOLECULAR CLONING; MOUSE; MUTAGENESIS; MYELOPROLIFERATIVE DISORDER; NONHUMAN; ONCOGENE RAS; PRIORITY JOURNAL; RADIATION DOSE; REVERSE TRANSCRIPTION POLYMERASE CHAIN REACTION; SINGLE DRUG DOSE;

ANIMALS; BENZAMIDES; DRUG RESISTANCE, NEOPLASM; GENES, RAS; GUANINE NUCLEOTIDE EXCHANGE FACTORS; LEUKEMIA, MYELOID, ACUTE; MICE; MITOGEN-ACTIVATED PROTEIN KINASE 14; MITOGEN-ACTIVATED PROTEIN KINASE KINASES; RAS PROTEINS;

EID: 70349273655     PISSN: 00280836     EISSN: 14764687     Source Type: Journal    
DOI: 10.1038/nature08279     Document Type: Article

References (25)

1. Downward, J. Targeting RAS signalling pathways in cancer therapy. Nature Rev. Cancer 3, 11-22 (2003).
2. Schubbert, S., Shannon, K. & Bollag, G. Hyperactive Ras in developmental disorders and cancer. Nature Rev. Cancer 7, 295-308 (2007).
3. Van Etten, R. A. & Shannon, K. M. Focus on myeloproliferative diseases and myelodysplastic syndromes. Cancer Cell 6, 547-552 (2004).
4. Lauchle, J. O., Braun, B. S., Loh, M. L. & Shannon, K. Inherited predispositions and hyperactive Ras in myeloid leukemogenesis. Pediatr. Blood Cancer 46, 579-585 (2006).
5. Shannon, K. M. et al. Loss of the normal NF1 allele from the bone marrow of children with type 1 neurofibromatosis and malignant myeloid disorders. N. Engl. J. Med. 330, 597-601 (1994).
6. Bollag, G. et al. Loss of NF1 results in activation of the Ras signaling pathway and leads to aberrant growth in murine and human hematopoietic cells. Nature Genet. 12, 144-148 (1996). (Pubitemid 26051293)
7. Side, L. et al. Homozygous inactivation of the NF1 gene in bone marrow cells from children with neurofibromatosis type 1 and malignant myeloid disorders. N. Engl. J. Med. 336, 1713-1720 (1997).
8. Le, D. T. et al. Somatic inactivation of Nf1 in hematopoietic cells results in a progressive myeloproliferative disorder. Blood 103, 4243-4250 (2004).
9. Wolff, L., Koller, R., Hu, X. & Anver, M. R. A Moloney murine leukemia virus-based retrovirus with 4070A long terminal repeat sequences induces a high incidence of myeloid as well as lymphoid neoplasms. J. Virol. 77, 4965-4971 (2003).
10. Sebolt-Leopold, J. S. et al. Blockade of the MAP kinase pathway suppresses growth of colon tumors in vivo. Nature Med. 5, 810-816 (1999).
11. Brown, A. P., Carlson, T. C., Loi, C. M. & Graziano, M. J. Pharmacodynamic and toxicokinetic evaluation of the novel MEK inhibitor, PD0325901, in the rat following oral and intravenous administration. Cancer Chemother. Pharmacol. 59, 671-679 (2007).
12. Dupuy, A. J. et al. Mammalian mutagenesis using a highly mobile somatic Sleeping Beauty transposon system. Nature 436, 221-226 (2005).
13. Stone, J. C. Regulation of Ras in lymphocytes: get a GRP. Biochem. Soc. Trans. 34, 858-861 (2006).
14. Das, J. et al. Digital signaling and hysteresis characterize ras activation in lymphoid cells. Cell 136, 337-351 (2009).
15. Bain, J. et al. The selectivity of protein kinase inhibitors: a further update. Biochem. J. 408, 297-315 (2007).
16. Fabian, M. A. et al. A small molecule-kinase interaction map for clinical kinase inhibitors. Nature Biotechnol. 23, 329-336 (2005).
17. Druker, B. J. et al. Activity of a specific inhibitor of the BCR-ABL tyrosine kinase in the blast crisis of chronic myeloid leukemia and acute lymphoblastic leukemia with the Philadelphia chromosome. N. Engl. J. Med. 344, 1038-1042 (2001).
18. Shah, N. P. et al. 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).
19. Choi, S. et al. Relapse in children with acute lymphoblastic leukemia involving selection of a preexisting drug-resistant subclone. Blood 110, 632-639 (2007).
20. Mullighan, C. G. et al. Genomic analysis of the clonal origins of relapsed acute lymphoblastic leukemia. Science 322, 1377-1380 (2008).
21. Sharma, S. V. et al. A common signaling cascade may underlie 'addiction' to the Src, BCR-ABL, and EGF receptor oncogenes. Cancer Cell 10, 425-435 (2006).
22. Parmar, S. et al. Role of the p38 mitogen-activated protein kinase pathway in the generation of the effects of imatinib mesylate (STI571) in BCR-ABL-expressing cells. J. Biol. Chem. 279, 25345-32532 (2004).
23. Kogan, S. C. et al. Bethesda proposals for classification of nonlymphoid hematopoietic neoplasms in mice. Blood 100, 238-245 (2002).
24. Akagi, K. et al. RTCGD: retroviral tagged cancer gene database. Nucleic Acids Res. 32 (Database issue), D523-D527 (2004).
25. Curtiss, N. P. et al. Isolation and analysis of candidate myeloid tumor suppressor genes from a commonly deleted segment of 7q22. Genomics 85, 600-607 (2005).