Petranel Ferrao

Summary

Affiliation: Peter MacCallum Cancer Centre
Location: Melbourne, Australia

Publications

  1. Ferrao P, Macmillan E, Ashman L, Gonda T. Enforced expression of full length c-Myb leads to density-dependent transformation of murine haemopoietic cells. Oncogene. 1995;11:1631-8 pubmed
    ..Moreover, the production of, or sensitivity to, such a factor may be influenced by Myb itself, since CT Myb-infected cells cultured at low densities show higher levels of transformation than WT Myb-infected cells. ..
  2. Gonda T, Favier D, Ferrao P, Macmillan E, Simpson R, Tavner F. The c-myb negative regulatory domain. Curr Top Microbiol Immunol. 1996;211:99-109 pubmed
  3. Ferrao P, Gonda T, Ashman L. Expression of constitutively activated human c-Kit in Myb transformed early myeloid cells leads to factor independence, histiocytic differentiation, and tumorigenicity. Blood. 1997;90:4539-52 pubmed
  4. Ashman L, Ferrao P, Cole S, Cambareri A. Effects of mutant c-kit in early myeloid cells. Leuk Lymphoma. 2000;37:233-43 pubmed
    ..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...
  5. Ferrao P, Sincock P, Cole S, Ashman L. Intracellular P-gp contributes to functional drug efflux and resistance in acute myeloid leukaemia. Leuk Res. 2001;25:395-405 pubmed
    ..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. ..
  6. Chian R, Young S, Danilkovitch Miagkova A, Ronnstrand L, Leonard E, Ferrao P, et al. Phosphatidylinositol 3 kinase contributes to the transformation of hematopoietic cells by the D816V c-Kit mutant. Blood. 2001;98:1365-73 pubmed
  7. Frost M, Ferrao P, Hughes T, Ashman L. Juxtamembrane mutant V560GKit is more sensitive to Imatinib (STI571) compared with wild-type c-kit whereas the kinase domain mutant D816VKit is resistant. Mol Cancer Ther. 2002;1:1115-24 pubmed
    ..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. ..
  8. Ferrao P, Gonda T, Ashman L. Constitutively active mutant D816VKit induces megakayocyte and mast cell differentiation of early haemopoietic cells from murine foetal liver. Leuk Res. 2003;27:547-55 pubmed
    ..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. ..
  9. Ferrao P, Frost M, Siah S, Ashman L. Overexpression of P-glycoprotein in K562 cells does not confer resistance to the growth inhibitory effects of imatinib (STI571) in vitro. Blood. 2003;102:4499-503 pubmed
    ..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. ..

More Information

Publications14

  1. Foster R, Griffith R, Ferrao P, Ashman L. Molecular basis of the constitutive activity and STI571 resistance of Asp816Val mutant KIT receptor tyrosine kinase. J Mol Graph Model. 2004;23:139-52 pubmed
    ..The reasons for this apparent discrepancy are discussed. ..
  2. Foster R, Byrnes E, Meldrum C, Griffith R, Ross G, Upjohn E, et al. Association of paediatric mastocytosis with a polymorphism resulting in an amino acid substitution (M541L) in the transmembrane domain of c-KIT. Br J Dermatol. 2008;159:1160-9 pubmed publisher
    ..The data suggest that the single nucleotide polymorphism resulting in the substitution M541L may predispose to paediatric mastocytosis. ..
  3. Ferrao P, Bukczynska E, Johnstone R, McArthur G. Efficacy of CHK inhibitors as single agents in MYC-driven lymphoma cells. Oncogene. 2012;31:1661-72 pubmed publisher
    ..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. ..
  4. Ramsdale R, Jorissen R, Li F, Al Obaidi S, Ward T, Sheppard K, et al. The transcription cofactor c-JUN mediates phenotype switching and BRAF inhibitor resistance in melanoma. Sci Signal. 2015;8:ra82 pubmed publisher