JAK1 mutation analysis in T-cell acute lymphoblastic leukemia cell lines

T-cell acute lymphoblastic leukemia (T-ALL) is a malignancy of T-cell precursors that mainly occurs in children and adolescents. A variety of oncogenic events that are involved in the pathogenesis of T-ALL have been identified, including NOTCH1 and PTEN mutations, overexpression of TAL1 , LYL1 and

[1]  Y. Chung,et al.  Somatic Mutations of JAK1 and JAK3 in Acute Leukemias and Solid Cancers , 2008, Clinical Cancer Research.

[2]  R. Wilson,et al.  Identification of somatic JAK1 mutations in patients with acute myeloid leukemia. , 2008, Blood.

[3]  E. Clappier,et al.  Somatically acquired JAK1 mutations in adult acute lymphoblastic leukemia , 2008, The Journal of experimental medicine.

[4]  P. Marynen,et al.  In vitro validation of γ-secretase inhibitors alone or in combination with other anti-cancer drugs for the treatment of T-cell acute lymphoblastic leukemia , 2008, Haematologica.

[5]  M. Odero,et al.  JAK2-V617F activating mutation in acute myeloid leukemia: prognostic impact and association with other molecular markers , 2007, Leukemia.

[6]  T. Golub,et al.  Identification of driver and passenger mutations of FLT3 by high-throughput DNA sequence analysis and functional assessment of candidate alleles. , 2007, Cancer cell.

[7]  Govind Bhagat,et al.  Mutational loss of PTEN induces resistance to NOTCH1 inhibition in T-cell leukemia , 2007, Nature Medicine.

[8]  D. Gilliland,et al.  TG101209, a small molecule JAK2-selective kinase inhibitor potently inhibits myeloproliferative disorder-associated JAK2V617F and MPLW515L/K mutations , 2007, Leukemia.

[9]  J. Ihle,et al.  Jak2: normal function and role in hematopoietic disorders. , 2007, Current opinion in genetics & development.

[10]  P. Marynen,et al.  The ability of sorafenib to inhibit oncogenic PDGFRbeta and FLT3 mutants and overcome resistance to other small molecule inhibitors. , 2007, Haematologica.

[11]  T. Haferlach,et al.  JAK2 seems to be a typical cooperating mutation in therapy-related t(8;21)/ AML1-ETO-positive AML , 2007, Leukemia.

[12]  G. Ehninger,et al.  Tyrosine kinase mutations of JAK2 are rare events in AML but influence prognosis of patients with CBF-leukemias. , 2007, Haematologica.

[13]  P. Lev,et al.  JAK2V617F mutation in platelets from essential thrombocythemia patients: correlation with clinical features and analysis of STAT5 phosphorylation status , 2006, European journal of haematology.

[14]  W. Hiddemann,et al.  Identification of additional cytogenetic and molecular genetic abnormalities in acute myeloid leukaemia with t(8;21)/AML1‐ETO , 2006, British journal of haematology.

[15]  S. H. Lee,et al.  The JAK2 V617F mutation in de novo acute myelogenous leukemias , 2006, Oncogene.

[16]  T. Brümmendorf,et al.  Prognostic impact of c-KIT mutations in core binding factor leukemias: an Italian retrospective study. , 2004, Blood.

[17]  K. Döhner,et al.  JAK2V617F mutations as cooperative genetic lesions in t(8;21)-positive acute myeloid leukemia. , 2006, Haematologica.

[18]  K. Mitani,et al.  A randomized, postremission comparison of four courses of standard‐dose consolidation therapy without maintenance therapy versus three courses of standard‐dose consolidation with maintenance therapy in adults with acute myeloid leukemia , 2005, Cancer.

[19]  H. Mitsuya,et al.  Mutations in the receptor tyrosine kinase pathway are associated with clinical outcome in patients with acute myeloblastic leukemia harboring t(8;21)(q22;q22) , 2005, Leukemia.

[20]  P. Marynen,et al.  Genetic insights in the pathogenesis of T-cell acute lymphoblastic leukemia. , 2005, Haematologica.

[21]  N. Asou The role of a Runt domain transcription factor AML1/RUNX1 in leukemogenesis and its clinical implications. , 2003, Critical reviews in oncology/hematology.