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Consistent fusion of ZNF198 to the fibroblast growth factor receptor-1 in the t(8;13)(p11;q12) myeloproliferative syndrome.
TLDR
It is hypothesized that this fusion leads to constitutive activation of the FGFR1 tyrosine kinase in a manner analogous to the activation of ABL by BCR in chronic myeloid leukemia. Expand
TEL‐AML1 fusion in acute lymphoblastic leukaemia of adults
TLDR
The TEL‐AML1 fusion gene is found in adult ALL, though less commonly than in children, as well as in chronic myeloid leukaemia in blastic crisis. Expand
Identification of four new translocations involving FGFR1 in myeloid disorders
TLDR
It is concluded that all mRNA fusions in EMS result in splicing to FGFR1 exon 9 but breakpoints in FOP are variable, two‐color FISH can identify patients with EMS, and the t(8;17)(p11;q25), t (8;11)( p11;p15), and ins(12;8)(p 11;p11p21) are novel karyotypic changes that most likely involveFGFR1. Expand
A model of APL with FLT3 mutation is responsive to retinoic acid and a receptor tyrosine kinase inhibitor, SU11657.
TLDR
The results suggest that the acquisition of FLT3 mutations by cells with a pre-existing t(15;17) is a frequent pathway to the development of APL, and indicate that APL patients with FLt3 mutations may benefit from combination therapy with all-trans retinoic acid plus an FLT 3 inhibitor. Expand
Abnormalities of chromosome band 8p11 in leukemia: two clinical syndromes can be distinguished on the basis of MOZ involvement.
TLDR
The 8p11 breakpoint is flanked by YACs 782H11 and 847B12 and is at least 1 Mb telomeric to MOZ and is likely, therefore, that MOZ is fused to a novel gene at 8q13 in this case. Expand
Antagonism of HOX/PBX dimer formation blocks the in vivo proliferation of melanoma.
TLDR
A novel, cell-permeable antagonist of the interaction between HOX proteins and PBX, a second homeodomain-containing transcription factor that modifies HOX activity is described and can block the growth of murine B16 cells and trigger apoptosis both in vitro and in vivo when administered to mice with flank tumors. Expand
Forced retinoic acid receptor alpha homodimers prime mice for APL-like leukemia.
TLDR
It is demonstrated that the dimerization interface of RARalpha fusion partners is a critical element in APL pathogenesis while pointing to other features of PML for enhancing penetrance and progression. Expand
The rate and kinetics of molecular response to donor leucocyte transfusions in chronic myeloid leukaemia patients treated for relapse after allogeneic bone marrow transplantation
TLDR
It is concluded that molecular monitoring is a sensitive indicator of response to DLT; different kinetics of molecular response may reflect disease heterogeneity or differences in the mode of action of DLT. Expand
Forced retinoic acid receptor α homodimers prime mice for APL-like leukemia
TLDR
It is demonstrated that the dimerization interface of RARalpha fusion partners is a critical element in APL pathogenesis while pointing to other features of PML for enhancing penetrance and progression. Expand
Recurring chromosomal abnormalities in leukemia in PML-RARA transgenic mice identify cooperating events and genetic pathways to acute promyelocytic leukemia.
TLDR
These murine leukemias have a defined spectrum of changes that recapitulates, in part, the cytogenetic abnormalities found in human APL, and demonstrate that different cooperating events may generate leukemia via different pathways. Expand
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