The CSF3R T618I mutation causes a lethal neutrophilic neoplasia in Mice that is responsive to therapeutic JAK inhibition

Blood

Volumn 122, Issue 22, 2013, Pages 3628-3631

  Fleischman, Angela G ^a,b   Maxson, Julia E ^a,b   Luty, Samuel B ^a,b   Agarwal, Anupriya ^a   Royer, Lacey R ^a,b   Abel, Melissa L ^a,b   Macmaniman, Jason D ^a,b   Loriaux, Marc M ^a,b   Druker, Brian J ^a,b   Tyner, Jeffrey W ^a,b  

^a OREGON HEALTH AND SCIENCE UNIVERSITY   (United States)

^b OREGON HEALTH AND SCIENCE UNIVERSITY   (United States)

Author keywords

[No Author keywords available]

Indexed keywords

COLONY STIMULATING FACTOR 3 RECEPTOR; JANUS KINASE; RUXOLITINIB; TUMOR MARKER; UNCLASSIFIED DRUG;

ANIMAL EXPERIMENT; ANIMAL MODEL; ARTICLE; ATYPICAL CHRONIC MYELOID LEUKEMIA; BONE MARROW TRANSPLANTATION; CELL INFILTRATION; CHRONIC NEUTROPHILIC LEUKEMIA; CONTROLLED STUDY; DRUG SENSITIVITY; ENZYME INHIBITION; FATALITY; GENE MUTATION; GRANULOCYTE; HEMATOPOIETIC CELL; LEUKOCYTE COUNT; LIVER; MOUSE; NONHUMAN; NUCLEOTIDE SEQUENCE; PRIORITY JOURNAL; SPLEEN; SPLEEN SIZE; SPLEEN WEIGHT; SPLENOMEGALY; TREATMENT RESPONSE;

EID: 84888252332     PISSN: 00064971     EISSN: 15280020     Source Type: Journal    
DOI: 10.1182/blood-2013-06-509976     Document Type: Article

References (13)

1. Maxson JE, Gotlib J, Pollyea DA, et al. Oncogenic CSF3R mutations in chronic neutrophilic leukemia and atypical CML. N Engl J Med. 2013;368(19):1781-1790.
2. Pardanani A, Lasho TL, Laborde RR, et al. CSF3R T618I is a highly prevalent and specific mutation in chronic neutrophilic leukemia. Leukemia. 2013;27(9):1870-1873.
3. Beekman R, Valkhof MG, Sanders MA, et al. Sequential gain of mutations in severe congenital neutropenia progressing to acute myeloid leukemia. Blood. 2012;119(22):5071-5077.
4. Dong F, Brynes RK, Tidow N, Welte K, Löwenberg B, Touw IP. Mutations in the gene for the granulocyte colony-stimulating-factor receptor in patients with acute myeloid leukemia preceded by severe congenital neutropenia. N Engl J Med. 1995;333(8):487-493.
5. Ward AC, van Aesch YM, Schelen AM, Touw IP. Defective internalization and sustained activation of truncated granulocyte colony-stimulating factor receptor found in severe congenital neutropenia/acute myeloid leukemia. Blood. 1999;93(2):447-458.
6. Mitsui T, Watanabe S, Taniguchi Y, et al. Impaired neutrophil maturation in truncated murine G-CSF receptor-transgenic mice. Blood. 2003;101(8):2990- 2995.
7. Kunter G, Woloszynek JR, Link DC. A truncation mutant of Csf3r cooperates with PML-RARa to induce acute myeloid leukemia in mice. Exp Hematol. 2011;39(12):1136-1143.
8. Bumm TG, Elsea C, Corbin AS, et al. Characterization of murine JAK2V617F-positive myeloproliferative disease. Cancer Res. 2006;66(23):11156- 11165.
9. Quintás-Cardama A, Vaddi K, Liu P, et al. Preclinical characterization of the selective JAK1/2 inhibitor INCB018424: therapeutic implications for the treatment of myeloproliferative neoplasms. Blood. 2010;115(15):3109-3117.
10. Beekman R, Touw IP. G-CSF and its receptor in myeloid malignancy. Blood. 2010;115(25):5131-5136.
11. Liu F, Wu HY, Wesselschmidt R, Kornaga T, Link DC. Impaired production and increased apoptosis of neutrophils in granulocyte colony-stimulating factor receptor-deficient mice. Immunity. 1996;5(5):491-501.
12. Verstovsek S, Mesa RA, Gotlib J, et al. A doubleblind, placebo-controlled trial of ruxolitinib for myelofibrosis. N Engl J Med. 2012;366(9):799-807.
13. Harrison C, Kiladjian JJ, Al-Ali HK, et al. JAK inhibition with ruxolitinib versus best available therapy for myelofibrosis. N Engl J Med. 2012;366(9):787-798.