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      CANCER THERAPEUTICS, NHMRC

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          Abstract

          As head of the Cancer Therapeutics Group Professor Ross Hannan's work focuses on the molecular analysis of major pro-malignant transcription factor networks that operate in cancer cells using an integrated approach that combines cell biology, genomics, proteomics, biochemistry, genetics, bioinformatics and strong interactions with oncologists in the clinic. Through this molecular understanding, he hopes to identify key therapeutic nodes to impede the progression of aggressive cancers. The availability of ribosomes is a fundamental rate-limiting step for tumour cell proliferation. He is examining the genetic and epigenetic processes by which ribosomal RNA gene transcription, is regulated by RNA Polymerase I, and how this process is dysregulated during cancer.Professor Hannan and his group has progressed this fundamental research a step closer to treating patients and changing clinical practice. His group developed the world’s first selective inhibitors of Pol I transcription (Bywater et al. Cancer Cell 2012; Bywater et al., Nature Reviews Cancer 2013), which are a new class of therapeutic. This inhibitor is currently in Phase I clinical trials at Peter Mac for the treatment of haematological malignancies. His lab is also involved in the development of second generation drugs and evaluating their efficiency in other cancers such as ovarian and prostate.A second area of research focus for Professor Hannan is ribosomopathies, a group of inherited diseases including Diamond Blackfan Anaemia (DBA) and myelodysplastic (5q-) syndrome. Such patients are also predisposed to developing haematological malignancies such as acute myeloid leukemia (AML). Ribosomopathies are caused by dysregulated ribosome biogenesis. Thus understanding the mechanisms mediating these diseases may identify novel approaches for their treatment, which at this time is palliative only.Professor Hannan’s group has utilized genome wide and chemical screening to identify potential candidates, which underlie the genetic and/or functional cause of various ribosomopathies. Expanding from this understanding the mechanisms underlying the increased predisposition for patients with ribosomopathies to develop cancers such as AML is also being evaluated.

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          Author and article information

          Journal
          Impact
          impact
          Science Impact, Ltd.
          2398-7073
          May 08 2017
          May 08 2017
          : 2017
          : 4
          : 29-31
          Article
          10.21820/23987073.2017.4.29
          © 2017

          This work is licensed under a Creative Commons Attribution 4.0 Unported License. To view a copy of this license, visit http://creativecommons.org/licenses/by/4.0/

          Earth & Environmental sciences, Medicine, Computer science, Agriculture, Engineering

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