KRAS (G12D) cooperates with AML1/ETO to initiate a mouse model mimicking human acute myeloid Leukemia

Cellular Physiology and Biochemistry

Volumn 33, Issue 1, 2014, Pages 78-87

  Zhao, Shanmin ^a   Zhang, Yuxia ^a   Sha, Kun ^a   Tang, Qiu ^a   Yang, Xiaohua ^b   Yu, Chenlin ^a   Liu, Zhixue ^a   Sun, Wei ^a   Cai, Liping ^a   Xu, Chen ^a   Cui, Shufang ^a  

^a SECOND MILITARY MEDICAL UNIVERSITY   (China)

^b SHANGHAI JIAO TONG UNIVERSITY   (China)

Author keywords

Acute myeloid leukemia; AML1 ETO; K ras; Leukemogenesis; Ras mutations

Indexed keywords

AML 1 ETO PROTEIN; ENHANCED GREEN FLUORESCENT PROTEIN; HYBRID PROTEIN; K RAS PROTEIN; UNCLASSIFIED DRUG; AML1 ETO PROTEIN; CD11B ANTIGEN; GR 1 PROTEIN; MESSENGER RNA; MITOGEN ACTIVATED PROTEIN KINASE; MITOGEN ACTIVATED PROTEIN KINASE KINASE; ONCOPROTEIN; PROTEIN; STEM CELL FACTOR; STEM CELL FACTOR RECEPTOR; TRANSCRIPTION FACTOR RUNX1; AML1-ETO FUSION PROTEIN, HUMAN; KRAS PROTEIN, HUMAN; PROTEIN P21;

ACUTE GRANULOCYTIC LEUKEMIA; ANIMAL EXPERIMENT; ANIMAL MODEL; ARTICLE; BLOOD; BONE MARROW CELL; CELL POPULATION; CELL TRANSPLANTATION; CENTRAL NERVOUS SYSTEM; CONTROLLED STUDY; CYTOLOGY; ENZYME PHOSPHORYLATION; GENE MUTATION; GENETIC TRANSFECTION; HISTOLOGY; IMMUNOPHENOTYPING; INFANT; LEUKEMOGENESIS; LYMPH NODE; MALE; MORTALITY; MOUSE; MYELOID PROGENITOR CELL; NONHUMAN; NUCLEOTIDE SEQUENCE; PRIORITY JOURNAL; PROTEIN EXPRESSION; PROTEIN FUNCTION; SPLEEN; TERMINAL DISEASE; THYMUS; UPREGULATION; ACUTE MONOCYTIC LEUKEMIA; BONE MARROW TRANSPLANTATION; CANCER MORTALITY; CANCER STAGING; GENETIC TRANSDUCTION; HISTOPATHOLOGY; LEUKEMIC INFILTRATION; MOUSE MODEL; ONCOGENE N RAS; TISSUE STRUCTURE; ACUTE MYELOBLASTIC LEUKEMIA; ANIMAL; C57BL MOUSE; DISEASE MODEL; GENE VECTOR; GENETICS; HUMAN; METABOLISM; MUTATION; ONCOGENE; PATHOLOGY; RETROVIRIDAE;

MUS;

ANIMALS; CORE BINDING FACTOR ALPHA 2 SUBUNIT; DISEASE MODELS, ANIMAL; GENETIC VECTORS; HUMANS; LEUKEMIA, MYELOID, ACUTE; MALE; MICE, INBRED C57BL; MUTATION; ONCOGENE PROTEINS, FUSION; ONCOGENES; PROTO-ONCOGENE PROTEINS P21(RAS); RETROVIRIDAE; TRANSDUCTION, GENETIC;

EID: 84893163032     PISSN: 10158987     EISSN: 14219778     Source Type: Journal    
DOI: 10.1159/000356651     Document Type: Article

References (35)

1. Johnson L, Mercer K, Greenbaum D: Somatic activation of the K-ras oncogene causes early onset lung cancer in mice. Nature 2001;410:1111-1116.
2. Bos JL: Ras oncogenes in human cancer: a review. Cancer Res 1989;49:4682-4689.
3. Croce CM: Oncogenes and cancer. N Engl J Med 2008;358:502-511.
4. Rodenhuis S: Ras and human tumors. Semin Cancer Biol 1992;3:241-247.
5. Marchetti A, Milella M, Felicioni L: Clinical implications of KRAS mutations in lung cancer patients treated with tyrosine kinase inhibitors: an important role for mutations in minor clones. Neoplasia 2009;11:1084-1092.
6. Sasaki H, Okuda K, Kawano 0: Nras and Kras mutation in Japanese lung cancer patients: Genotyping analysis using LightCycler. Oncol Rep 2007;18:623-628.
7. Wang Z, Feng Y, Bardessy N, Wong KK, Liu XY, Ji H: Temporal dissection of K-ras(G12D) mutant in vitro and in vivo using a regulatable K-ras(G12D) mouse allele. PLoS One 2012;7:e37308.
8. Zaker F, Darley RL, al Sabah A, Burnett AK: Oncogenic RAS genes impair erythroid differentiation of erythroleukaemia cells. Leuk Res 1997;21:635-640.
9. Sabnis AJ, Cheung LS, Dail M: Oncogenic Kras initiates leukemia in hematopoietic stem cells. PLoS Biol 2009;7:e59.
10. Ahlquist X Bottillo I, Danielsen SA: RAS signaling in colorectal carcinomas through alteration of RAS, RAF, NF1, and/or RASSF1A. Neoplasia 2008;10:680-686, 2 p following 6.
11. Liu L, Zhu S, Gong Z, Low BC: K-ras/PI3K-Akt signaling is essential for zebrafish hematopoiesis and angiogenesis. PLoS One 2008;3:e2850.
12. Wells V, Downward J, Mallucci L: Functional inhibition of PI3K by the betaGBP molecule suppresses Ras-MAPK signalling to block cell proliferation. Oncogene 2007;26:7709-7714.
13. Menges CW, McCance DJ: Constitutive activation of the Raf-MAPK pathway causes negative feedback inhibition of Ras-PI3K-AKT and cellular arrest through the EphA2 receptor. Oncogene 2008;27:2934-2940.
14. Bos JL, Rehmann H, Wittinghofer A: GEFs and GAPs: critical elements in the control of small G proteins. Cell 2007;129:865-877.
15. Jackson EL, Willis N, Mercer K: Analysis of lung tumor initiation and progression using conditional expression of oncogenic K-ras. Genes Dev 2001;15:3243-3248.
16. Tuveson DA, Shaw AT, Willis NA: Endogenous oncogenic K-ras(G12D) stimulates proliferation and widespread neoplastic and developmental defects. Cancer Cell 2004;5:375-387.
17. Fisher GH, Wellen SL, Klimstra D: Induction and apoptotic regression of lung adenocarcinomas by regulation of a K-Ras transgene in the presence and absence of tumor suppressor genes. Genes Dev 2001;15:3249-3262.
18. Gardini A, Cesaroni M, Luzi L: AML1/ETO oncoprotein is directed to AML1 binding regions and co-localizes with AML1 and HEB on its targets. PLoS Genet 2008;4:el000275.
19. Li X, Xu YB, Wang Q: Leukemogenic AML1-ETO fusion protein upregulates expression of connexin 43: the role in AML 1-ETO-induced growth arrest in leukemic cells. J Cell Physiol 2006;208:594-601.
20. Yuan Y, Zhou L, Miyamoto T: AML1-ETO expression is directly involved in the development of acute myeloid leukemia in the presence of additional mutations. Proc Natl Acad Sci USA 2001;98:10398-10403.
21. Zhang DE, Burel S, Zhou L, Hetherington CJ, Yuan Y: AML1 and AML1 fusion protein AML1-ETO in myeloid gene regulation and leukemogenesis. Blood Cells Mol Dis 2001;27:368-376.
22. Steffen B, Knop M, Bergholz U: AML1/ETO induces self-renewal in hematopoietic progenitor cells via the Groucho-related amino-terminal AES protein. Blood 2011;117:4328-4337.
23. Kelly LM, Kutok JL, Williams IR: PML/RARalpha and FLT3-ITD induce an APL-like disease in a mouse model. Proc Natl Acad Sci USA 2002;99:8283-8288.
24. Ono R, Nakajima H, Ozaki K: Dimerization of MLL fusion proteins and FLT3 activation synergize to induce multiple-lineage leukemogenesis. J Clin Invest 2005;115:919-929.
25. Zuber J, Radtke I, Pardee TS: Mouse models of human AML accurately predict chemotherapy response. Genes Dev 2009;23:877-889.
26. Wang YY, Zhao LJ, Wu CF: C-KIT mutation cooperates with full-length AML1-ETO to induce acute myeloid leukemia in mice. Proc Natl Acad Sci USA 2011;108:2450-2455.
27. Kuate S, Stefanou D, Hoffmann D, Wildner O, Uberla K: Production of lentiviral vectors by transient expression of minimal packaging genes from recombinant adenoviruses. J Gene Med 2004;6:1197-1205.
28. Kay MA, Glorioso JC, Naldini L: Viral vectors for gene therapy: the art of turning infectious agents into vehicles of therapeutics. Nat Med 2001;7:33-40.
29. Gilliland DG, Jordan CT, Felix CA: The molecular basis of leukemia. Hematology Am Soc Hematol Educ Program 2004:80-97.
30. Castellano E, Santos E: Functional specificity of ras isoforms: so similar but so different. Genes Cancer 2011;2:216-231.
31. Parikh C, Subrahmanyam R, Ren R: Oncogenic NRAS, KRAS, and HRAS exhibit different leukemogenic potentials in mice. Cancer Res 2007;67:7139-146.
32. Schessl C, Rawat VP, Cusan M: The AML1-ETO fusion gene and the FLT3 length mutation collaborate in inducing acute leukemia in mice. J Clin Invest 2005;115:2159-2168.
33. Wang J, Liu Y, Li Z: Endogenous oncogenic Nras mutation promotes aberrant GM-CSF signaling in granulocytic/monocytic precursors in a murine model of chronic myelomonocytic leukemia. Blood 2010;116:5991-6002.
34. Yan M, Burel SA, Peterson L: Deletion of an AML1-ETO C-terminal NcoR/SMRT-interacting region strongly induces leukemia development. Proc Natl Acad Sci USA 2004;101:17186-17191.
35. Kuo YH, Landrette SF, Heilman SA: Cbf beta-SMMHC induces distinct abnormal myeloid progenitors able to develop acute myeloid leukemia. Cancer Cell 2006;9:57-68.