Affiliation: Peter MacCallum Cancer Centre
Location: Melbourne, Australia
- Association of paediatric mastocytosis with a polymorphism resulting in an amino acid substitution (M541L) in the transmembrane domain of c-KITR Foster
School of Biomedical Sciences, The University of Newcastle, Callaghan, New South Wales 2308, Australia
Br J Dermatol 159:1160-9. 2008..The receptor tyrosine kinase c-KIT plays a key role in normal mast cell development. Point mutations in c-KIT have been associated with sporadic or familial mastocytosis...
- Molecular basis of the constitutive activity and STI571 resistance of Asp816Val mutant KIT receptor tyrosine kinaseRowan Foster
School of Biomedical Sciences, Faculty of Health, University of Newcastle, Callaghan NSW 2308, Australia
J Mol Graph Model 23:139-52. 2004..The reasons for this apparent discrepancy are discussed...
- Overexpression of P-glycoprotein in K562 cells does not confer resistance to the growth inhibitory effects of imatinib (STI571) in vitroPetranel T Ferrao
Rm 511, Medical Sciences Bldg, University of Newcastle, University Dr, Callaghan, New South Wales 2308, Australia
Blood 102:4499-503. 2003..In contrast, overexpression of Bcl-xL, which blocks apoptosis, resulted in partial protection against the drug. We conclude that Pgp up-regulation is not likely to be a significant contributor to imatinib resistance...
- Constitutively active mutant D816VKit induces megakayocyte and mast cell differentiation of early haemopoietic cells from murine foetal liverPetranel T Ferrao
School of Biomedical Sciences, Faculty of Health, University of Newcastle, Room 511, Medical Sciences Building, University Drive, Callaghan 2308, Australia
Leuk Res 27:547-55. 2003..We conclude that constitutive expression of D816VKit in primary haemopoietic cells is not a sufficient transforming stimulus but leads to the survival and maturation of cells whose phenotype is influenced by the presence of SCF...
- Juxtamembrane mutant V560GKit is more sensitive to Imatinib (STI571) compared with wild-type c-kit whereas the kinase domain mutant D816VKit is resistantMichelle J Frost
School of Biomedical Sciences, University of Newcastle, Room 511, Medical Sciences Building, Callaghan, NSW 2308, Australia
Mol Cancer Ther 1:1115-24. 2002..Overall, these findings demonstrate the increased susceptibility of the Kit juxtamembrane mutant, V560G, and the resistance of the kinase domain mutant, D816V, to Imatinib compared with WTKit...
- Phosphatidylinositol 3 kinase contributes to the transformation of hematopoietic cells by the D816V c-Kit mutantR Chian
Basic Research Laboratory and the Laboratory of Immunobiology, Division of Basic Sciences, National Cancer Institute-Frederick, MD 21702, USA
Blood 98:1365-73. 2001....
- Intracellular P-gp contributes to functional drug efflux and resistance in acute myeloid leukaemiaP Ferrao
Division of Haematology, Hanson Centre for Cancer Research, Institute of Medical and Veterinary Science, PO Box 14 Rundle Mall, Frome Road, Adelaide, SA 5000, Australia
Leuk Res 25:395-405. 2001..Therefore, the level of total P-gp protein or mRNA may be a better indicator of MDR than surface P-gp protein. In addition, we provide evidence for a novel mechanism of drug sequestration in K562 myeloid leukaemic cells...
- Effects of mutant c-kit in early myeloid cellsL K Ashman
Division of Haematology, Hanson Centre for Cancer Research, Institute of Medical and Veterinary Science, Adelaide, Australia
Leuk Lymphoma 37:233-43. 2000..Thus the extent to which c-Kit mutations contribute to malignancies of early myeloid phenotype remains unknown, and resolution of this issue is complicated by the heterogeneity of this family of diseases...
- Efficacy of CHK inhibitors as single agents in MYC-driven lymphoma cellsP T Ferrao
Molecular Oncology Laboratory and Cancer Therapeutics Program, Research Division, Peter MacCallum Cancer Centre, St Andrews Place, East Melbourne, Victoria, Australia
Oncogene 31:1661-72. 2012..We propose that inhibitors of CHK can act in a synthetically lethal manner in cancers with replication stress as a result of these cancers being reliant on CHK proteins for an effective DDR and cell survival...