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http://dx.doi.org/10.1111/bjh.14533 | DOI Listing |
Br J Haematol
April 2017
Department of Hematology/Oncology, University of Pittsburgh Medical Center, Pittsburgh, PA, USA.
Cancer Res
December 2011
Georgia Health Sciences University School of Medicine, Augusta, Georgia, USA.
Chromosomal translocations and activation of the fibroblast growth factor (FGF) receptor 1 (FGFR1) are a feature of stem cell leukemia-lymphoma syndrome (SCLL), an aggressive malignancy characterized by rapid transformation to acute myeloid leukemia and lymphoblastic lymphoma. It has been suggested that FGFR1 proteins lose their ability to recruit Src kinase, an important mediator of FGFR1 signaling, as a result of the translocations that delete the extended FGFR substrate-2 (FRS2) interacting domain that Src binds. In this study, we report evidence that refutes this hypothesis and reinforces the notion that Src is a critical mediator of signaling from the FGFR1 chimeric fusion genes generated by translocation in SCLL.
View Article and Find Full Text PDFInt J Hematol
March 2010
Dana-Farber Cancer Institute, Harvard Medical School, 44 Binney Street, Boston, MA 02115, USA.
The myeloproliferative neoplasms (MPNs) were first recognized by William Dameshek in 1951. The classic MPNs were polycythemia vera (PV), essential thrombocythemia (ET), primary myelofibrosis (PMF) and chronic myelogenous leukemia. They were originally grouped together based on their shared phenotype of myeloproliferation.
View Article and Find Full Text PDFAm J Hematol
April 2010
Division of Hematology, Mayo Clinic, Rochester, MN, USA.
Chromosome 8p11.2 translocations result in diverse oncogenic fusion genes involving FGFR1 or MYST3. Among 24,262 unique patient cytogenetic studies performed at the Mayo Clinic, 8p11.
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