Dr Elizabeth Algar

contact details

Elizabeth Algar1  Dr Elizabeth Algar
  Cancer
  Murdoch Childrens Research Institute
  Royal Children's Hospital
  Flemington Road
  Parkville Victoria 3052


  T +61 3 9345 4355
  F +61 3 9345 4993
  E elizabeth.algar@rch.org.au

biography

Elizabeth Algar is a graduate of the University of Melbourne and has a PhD in Biochemical Genetics from Griffith University. She started working on paediatric cancer genetics and molecular pathology while at the University of Queensland in 1991. In 1996 she relocated to Melbourne and established a research group at the Murdoch Childrens Research Institute. She is internationally recognized for her work on the Wilms tumour gene, WT1, and the imprinting disorder, Beckwith Wiedemann syndrome.

Her current research focus is on understanding the genetic and epigenetic pathways of cancers occurring in early childhood. Her laboratory is NATA accredited to provide clinical diagnostic molecular tests for paediatric cancers and syndromes and receives samples for testing Australia-wide. She is a regular reviewer for national and international cancer funding organizations and journals, and a member of several scientific societies including the European Association for Cancer Research and the American Society for Human Genetics.

achievements

2010 Founding Fellow Faculty of Science, Royal College of Pathologists Australia (RCPA)
2007 Outstanding achievement award 12th World Congress on Advances in Oncology, Crete. "Epigenetic therapies in cancer-Insights into their effects on imprinted genes"
1998 Lorne Cancer poster prize "Molecular analysis of genes on 11p15.5 in Beckwith Syndrome".
1992-1994 University of Queensland Post-doctoral Fellowship
1986-1989 Griffith University post-graduate scholarship (PhD)
1980-1982 Commonwealth post-graduate research award (MSc)

research focus & interest

Elizabeths key research interest is in understanding the genetic and epigenetic basis for cancer in childhood. Cancers that arise at a very early age, present ideal opportunities for the identification of key genes and pathways important in cell transformation, as they arise from cells that have not yet been exposed to a life-long accumulation of genetic and epigenetic damage. Identification of the early events in cancer initiation has potential for revealing novel biological targets and processes that may be exploited for therapeutic intervention.

Inherited forms of childhood cancer as well as childhood cancer predisposition syndromes are ideal models in which to investigate the critical initiating steps in oncogenesis. Our research involves the genetic analysis of families with a history of childhood cancer, and of children who present with features of a cancer predisposition syndrome. We use a variety of genomics tools to identify constitutional pathological genetic changes linked to cancer.

Genomic imprinting is a process through which gene dosage from the parental chromosomes can be controlled in early development by epigenetic modification of locus control regions. Several genes important in childhood cancer are imprinted, with accumulating evidence that disruption to the imprinting process is a critical step in the initiation of certain childhood cancers.

A focus of our current research is to identify the genetic and environmental factors that control and disrupt the imprinting process. To address these questions we use the following approaches: (1) candidate gene analysis in patient subgroups with identifiable imprinting abnormalities, (2) whole genome analysis on patient subgroups and (3) collection of clinical data related to infertility and use of assisted reproductive technologies within patient subgroups with imprinting anomalies.

publications

Diane K Birks, Andrew M. Donson, Purvi R. Patel, Christopher Dunham, Andrea Muscat, Elizabeth M. Algar, David M. Ashley, B. K. Kleinschmidt-DeMasters, Rajeev Vibhakar, Michael H. Handler, Nicholas K. Foreman. (2011). High expression of BMP pathway genes distinguishes a subset of Atypical Teratoid / Rhabdoid Tumors associated with shorter survival. Neuro-oncology; doi: 10.1093/neuonc/nor140 IF 5.76, IS 1.81

Hui K. Gan, Mark A. Rosenthal, Anthony Dowling, Renate Kalnins, Elizabeth Algar, Angela Benson, Anne-Marie Woods, Lawrence Cher. (2010). A Phase II trial of primary temozolomide in patients with Grade III oligodendroglial brain tumors. Neuro-oncology 2010 May;12(5):500-7. Epub 2010 Feb 8. IF 5.76, IS 1.81.

Dagar V., Chow CW, Ashley DM and Algar EM. Rapid screening for SMARCB1 mutations in rhabdoid tumor using high-resolution melting. (2009). BMC Cancer 9 : 437. IF 3.07, IS 0.98 (online publication-no page numbers)

Elizabeth Algar, Andrea Muscat, Vinod Dagar, Christian Rickert, CW Chow, Jacqueline Biegel, Paul Ekert, Ricky Johnstone and David Ashley. (2009). Imprinted CDKN1C is activated by histone deacetylase inhibitors and restoration of SMARCB1 in rhabdoid tumor.PLoS ONE 4(2): e4482. doi:10.1371/journal.pone.0004482. IF 4.6, IS 1.92 (online publication-no page numbers).

John KC Chan, Laurence Lamant, Elizabeth Algar, Goerges Delsol, William YW Tsang, King Chung Lee, Karin Tiedemann, Chung Wo Chow. (2008). ALK+ histiocytosis: a novel type of systemic histiocytic proliferative disorder of early infancy. Blood. Vol. 112, p. 2965-2968. IF 10.89, IS 3.26.

Tomasz K. Wojdacz, Alexander Dobrovic and Elizabeth M. Algar. (2008) Rapid detection of methylation change at H19 in human imprinting disorders using methylation sensitive high resolution melting. Human Mutation Vol. 29, p1255-1260. IF 6.91, IS= 2.87.

Meredith Wilson, Gregory Peters, Bruce Bennetts, George McGillivray, Zan He Wu, Christopher Poon, Elizabeth Algar. (2008). The Clinical Phenotype of Mosaicism for Genome-wide Paternal Uniparental Disomy: Two New Reports. American J. Med Genetics. Part A. Vol. 146A p137-148. IF2.44, IS=0.785.

Elizabeth M.Algar, Luke St Heaps, Artur Darmanian, Vinod Dagar, Dirk Prawitt, Greg B. Peters and Felicity Collins. (2007). Paternally inherited submicroscopic duplication at 11p15.5 implicates IGF2 in Wilms tumorigenesis. Cancer Research, Vol. 67, pp. 2360-2365. IF=8.04, IS=2.85.