Validation of ITD mutations in FLT3 as a therapeutic target in human acute myeloid leukaemia-Reference-Cited by-同舟云学术

Validation of ITD mutations in FLT3 as a therapeutic target in human acute myeloid leukaemia

Published:2012-04-15 Issue:7397 Volume:485 Page:260-263
ISSN:0028-0836
Container-title:Nature
language:en
Short-container-title:Nature

Author:

Smith Catherine C.,Wang Qi,Chin Chen-Shan,Salerno Sara,Damon Lauren E.,Levis Mark J.,Perl Alexander E.,Travers Kevin J.,Wang Susana,Hunt Jeremy P.,Zarrinkar Patrick P.,Schadt Eric E.,Kasarskis Andrew,Kuriyan John,Shah Neil P.

Publisher

Springer Science and Business Media LLC

Subject

Multidisciplinary

Link

http://www.nature.com/articles/nature11016.pdf

Reference33 articles.

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2. Lee, B. H. et al. FLT3 internal tandem duplication mutations induce myeloproliferative or lymphoid disease in a transgenic mouse model. Oncogene 24, 7882–7892 (2005)

3. Shih, L. Y. et al. Acquisition of FLT3 or N-ras mutations is frequently associated with progression of myelodysplastic syndrome to acute myeloid leukemia. Leukemia 18, 466–475 (2004)

4. Knapper, S. et al. A phase 2 trial of the FLT3 inhibitor lestaurtinib (CEP701) as first-line treatment for older patients with acute myeloid leukemia not considered fit for intensive chemotherapy. Blood 108, 3262–3270 (2006)

5. Fischer, T. et al. Phase IIB trial of oral Midostaurin (PKC412), the FMS-like tyrosine kinase 3 receptor (FLT3) and multi-targeted kinase inhibitor, in patients with acute myeloid leukemia and high-risk myelodysplastic syndrome with either wild-type or mutated FLT3. J. Clin. Oncol. 28, 4339–4345 (2010)

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