Mutation of genes affecting the RAS pathway is common in childhood acute lymphoblastic leukemia

Cancer Research

Volumn 68, Issue 16, 2008, Pages 6803-6809

  Case, Marian ^a   Matheson, Elizabeth ^a   Minto, Lynne ^a   Hassan, Rosline ^c   Harrison, Christine J ^d   Bown, Nick ^a   Bailey, Simon ^b   Vormoor, Josef ^a   Hall, Andrew G ^a   Irving, Julie A E ^a  

^a NEWCASTLE UNIVERSITY   (United Kingdom)

^b ROYAL VICTORIA INFIRMARY   (United Kingdom)

^c SCHOOL OF PHYSICS   (Malaysia)

^d UNIVERSITY OF SOUTHAMPTON   (United Kingdom)

Author keywords

[No Author keywords available]

Indexed keywords

MITOGEN ACTIVATED PROTEIN KINASE 3; MITOGEN ACTIVATED PROTEIN KINASE INHIBITOR; MITOGEN ACTIVATED PROTEIN KINASE KINASE 1; RAS PROTEIN; B RAF KINASE; BRAF PROTEIN, HUMAN; CD135 ANTIGEN; ENZYME INHIBITOR; FLT3 PROTEIN, HUMAN; KRAS PROTEIN, HUMAN; MITOGEN ACTIVATED PROTEIN KINASE; MITOGEN ACTIVATED PROTEIN KINASE KINASE; ONCOPROTEIN; PEPTIDE FRAGMENT; PROTEIN TYROSINE PHOSPHATASE SHP 2; PTPN11 PROTEIN, HUMAN;

ACUTE LYMPHOBLASTIC LEUKEMIA; ADOLESCENT; ALLELE; ARTICLE; CANCER CYTODIAGNOSIS; CANCER RECURRENCE; CANCER RELAPSE; CHILD; CHILDHOOD CANCER; CLINICAL ARTICLE; CLONE; CYTOTOXICITY; DENATURING HIGH PERFORMANCE LIQUID CHROMATOGRAPHY; DIAGNOSTIC ACCURACY; DISEASE COURSE; EXON; FEMALE; FLUORESCENCE IN SITU HYBRIDIZATION; GENE MUTATION; HUMAN; HUMAN CELL; MALE; MUTATIONAL ANALYSIS; POLYMERASE CHAIN REACTION; PRIORITY JOURNAL; SOMATIC MUTATION; CELL CULTURE; CELL SURVIVAL; COHORT ANALYSIS; DRUG ANTAGONISM; GENETICS; INFANT; LYMPHATIC LEUKEMIA; METABOLISM; MUTATION; NUCLEOTIDE SEQUENCE; ONCOGENE RAS; PATHOLOGY; PHYSIOLOGY; PLOIDY; PRESCHOOL CHILD; REMISSION; SIGNAL TRANSDUCTION; TUMOR RECURRENCE; WESTERN BLOTTING;

ADOLESCENT; BLOTTING, WESTERN; CELL SURVIVAL; CHILD; CHILD, PRESCHOOL; COHORT STUDIES; DNA MUTATIONAL ANALYSIS; ENZYME INHIBITORS; EXONS; EXTRACELLULAR SIGNAL-REGULATED MAP KINASES; FEMALE; FMS-LIKE TYROSINE KINASE 3; GENES, RAS; HUMANS; IN SITU HYBRIDIZATION, FLUORESCENCE; INFANT; MALE; MITOGEN-ACTIVATED PROTEIN KINASE KINASES; MITOGEN-ACTIVATED PROTEIN KINASES; MUTATION; NEOPLASM RECURRENCE, LOCAL; PEPTIDE FRAGMENTS; PLOIDIES; PRECURSOR CELL LYMPHOBLASTIC LEUKEMIA-LYMPHOMA; PROTEIN TYROSINE PHOSPHATASE, NON-RECEPTOR TYPE 11; PROTO-ONCOGENE PROTEINS; PROTO-ONCOGENE PROTEINS B-RAF; RAS PROTEINS; REMISSION INDUCTION; SIGNAL TRANSDUCTION; TUMOR CELLS, CULTURED;

EID: 53049109135     PISSN: 00085472     EISSN: None     Source Type: Journal    
DOI: 10.1158/0008-5472.CAN-08-0101     Document Type: Article

References (35)

1. Kolch W. Ras/Raf signalling and emerging pharmacotherapeutic targets. Expert Opin Pharmacother 2002;3:709-18.
2. Lee JT, Jr., McCubrey JA. The Raf/MEK/ERK signal transduction cascade as a target for chemotherapeutic intervention in leukemia Leukemia 2002;16:486-507.
3. Platanias LC. Map kinase signaling pathways and hematologic malignancies. Blood 2003; 101:4667-79.
4. Wiemels JL, Zhang Y, Chang J, et al. RAS mutation is associated with hyperdiploidy and parental characteristics in pediatric acute lymphoblastic leukemia Leukemia 2005;19:415-9.
5. Perentesis JP, Bhatia S, Boyle E, et al. RAS oncogene mutations and outcome of therapy for childhood acute lymphoblastic leukemia. Leukemia 2004; 18:685-92.
6. Tartaglia M, Martinelli S, Cazzaniga G, et al. Genetic evidence for lineage-related and differentiation stagerelated contribution of somatic PTPN11 mutations to leukemogenesis in childhood acute leukemia. Blood 2004;104:307-13.
7. Armstrong SA, Mabon ME, Silverman LB, et al. FLT3 mutations in childhood acute lymphoblastic leukemia Blood 2004;103:3544-6.
8. Taketani T, Taki T, Sugita K, et al. FLT3 mutations in the activation loop of tyrosine kinase domain are frequently found in infant ALL with MLL rearrangements and pediatric ALL with hyperdiploidy. Blood 2004;103:1085-8.
9. Gustafsson B, Angelini S, Sander B, Christensson B, Hemminki K, Kumar R. Mutations in the BRAF and N-ras genes in childhood acute lymphoblastic leukaemia. Leukemia 2005;19:310-2.
10. Harrison CJ, Moorman AV. Barber KE, et al. Interphase molecular cytogenetic screening for chromosomal abnormalities of prognostic significance in childhood acute lymphoblastic leukaemia: a UK Cancer Cytogenetics Group Study. Br J Haematol 2005; 129:520-30.
11. Tartaglia M, Gelb BD. Noonan syndrome and related disorders: genetics and pathogenesis. Annu Rev Genomics Hum Genet 2005;6:45-68.
12. Tartaglia M, Mehler EL, Goldberg R, et al. Mutations in PTPN11, encoding the protein tyrosine phosphatase SHP-2, cause Noonan syndrome. Nat Genet 2001;29:465-8.
13. Braun BS, Tuveson DA, Kong N, et al. Somatic activation of oncogenic Kras in hematopoietic cells initiates a rapidly fatal myeloproliferative disorder. Proc Natl Acad Sci U S A 2004; 101:597-602.
14. Chan IT, Kutok JL, Williams IR, et al. Conditional expression of oncogenic K-ras from its endogenous promoter induces a myeloproliferative disease. J Clin Invest 2004;113:528-38.
15. Parikh C, Subrahmanyam R, Ren R. Oncogenic NRAS rapidly and efficiently induces CMML- and AML-like diseases in mice. Blood 2006;108:2349-57.
16. Paulsson K, Horvat A, Strombeck B, et al. Mutations of FLT3, NRAS, KRAS, and PTPN11 are frequent and possibly mutually exclusive in high hyperdiploid childhood acute lymphoblastic leukemia. Genes Chromosomes Cancer 2008;47:26-33.
17. Zhu YM, Foroni L, McQuaker IG, Papaioannou M, Haynes A, Russell HH. Mechanisms of relapse in acute leukaemia: involvement of p53 mutated subclones in disease progression in acute lymphoblastic leukaemia. Br J Cancer 1999;79:1151-7.
18. Konrad M, Metzler M, Panzer S, et al. Late relapses evolve from slow-responding subclones in t(12;21)-positive acute lymphoblastic leukemia: evidence for the persistence of a preleukemic clone. Blood 2003;101:3635-40.
19. Liang DC, Shih LY, Fu JF, et al. K-Ras mutations and N-Ras mutations in childhood acute leukemias with or without mixed-lineage leukemia gene rearrangements. Cancer 2006; 106:950-6.
20. Eisenmann DM, Kim SK. Mechanism of activation of the Caenorhabditis elegans ras homologue let-60 by a novel, temperature-sensitive, gain-of-function mutation. Genetics 1997;146:553-65.
21. COSMIC [database on the Internet]. Cambridge (UK): The Sanger Centre. 2000 [cited 2007 Nov]. Available from: http://www.sanger.ac.uk/genetics/CGP/ cosmic/.
22. Shi ZQ, Yu DH, Park M, Marshall M, Feng GS. Molecular mechanism for the Shp-2 tyrosine phosphatase function in promoting growth factor stimulation of Erk activity. Mol Cell Biol 2000;20:1526-36.
23. Bentires-Alj M, Paez JG, David FS, et al. Activating mutations of the Noonan syndrome-associated SHP2/PTPN11 gene in human solid tumors and adult acute myelogenous leukemia Cancer Res 2004;64:8816-20.
24. Yamamoto T, Isomura M, Xu Y, et al. PTPN11, RAS and FLT3 mutations in childhood acute lymphoblastic leukemia Leuk Res 2006;30:1085-9.
25. Clark JJ, Cools J, Curley DP, et al. Variable sensitivity of FLT3 activation loop mutations to the small molecule tyrosine kinase inhibitor MLN518. Blood 2004;104:2867-72.
26. Wellmann S, Moderegger E, Zelmer A, et al. FLT3 mutations in childhood acute lymphoblastic leukemia at first relapse. Leukemia 2005; 19:467-8.
27. Stam RW, den Boer ML, Schneider P, Meier M, Beverloo HB, Pieters R. D-HPLC analysis of the entire FLT3 gene in MLL rearranged and hyperdiploid acute lymphoblastic leukemia. Haematologica 2007;92:1565-8.
28. Kiyoi H, Ohno R, Ueda R, Saito H, Naoe T. Mechanism of constitutive activation of FLT3 with internal tandem duplication in the juxtamembrane domain. Oncogene 2002;21:2555-63.
29. Brown P, Levis M, Shurtleff S, Campana D, Downing J, Small D. FLT3 inhibition selectively kills childhood acute lymphoblastic leukemia cells with high levels of FLT3 expression. Blood 2005;105:812-20.
30. Davies H, Bignell GR, Cox C, et al. Mutations of the BRAF gene in human cancer. Nature 2002;417:949-54.
31. Wan PT, Garnett MJ, Roe SM, et al. Mechanism of activation of the RAF-ERK signaling pathway by oncogenic mutations of B-RAF. Cell 2004;116:855-67.
32. Gregorj C, Ricciardi MR, Petrucci MT, et al. ERK1/2 phosphorylation is an independent predictor of complete remission in newly diagnosed adult acute lymphoblastic leukemia. Blood 2007;109:5473-6.
33. Lorusso PM, Adjei AA, Varterasian M, et al. Phase I and pharmacodynamic study of the oral MEK inhibitor CI-1040 in patients with advanced malignancies. J Clin Oncol 2005:23:5281-93.
34. Rinehart J, Adjei AA, Lorusso PM, et al. Multicenter phase II study of the oral MEK inhibitor, CI-1040, in patients with advanced non-small-cell lung, breast, colon, and pancreatic cancer. J Clin Oncol 2004;22:4456-62.
35. Widemann BC, Salzer WL, Arceci RJ, et al. Phase I trial and pharmacokinetic study of the farnesyltransferase inhibitor tipifarnib in children with refractory solid tumors or neurofibromatosis type I and plexiform neurofibromas. J Clin Oncol 2006;24:507-16