Bioinformatics Approaches to Studying Cancer Genetics and Tumour Evolution

Grant number: 1052904 | Funding period: 2013 - 2017

Completed

Abstract

Chemotherapy often fails because some of the cells in tumour evolve resistance to the drugs the patient is given, causing relapse. We study how a tumour’s unstable genome and high rate of mutation drives its evolution by observing tumour cells in the laboratory as they evolve resistance to drugs and the genetic differences between resistant and sensitive cells. This work will help develop therapeutic strategies to prevent tumours from evolving resistance to chemotherapy.

Related publications (6)

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Patient-derived Models of Abiraterone- and Enzalutamide-resistant Prostate Cancer Reveal Sensitivity to Ribosome-directed Therapy

MG Lawrence, D Obinata, S Sandhu, LA Selth, SQ Wong, LH Porter, N Lister, D Pook, CJ Pezaro, DL Goode, RJ Rebello, AK Clark, M Papargiris, J Van Gramberg, AR Hanson, P Banks, H Wang, B Niranjan, S Keerthikumar, S Hedwards

2018-11-01

Background: The intractability of castration-resistant prostate cancer (CRPC) is exacerbated by tumour heterogeneity, including di..

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Somatic mutations in early metazoan genes disrupt regulatory links between unicellular and multicellular genes in cancer

Anna Trigos, Rick Pearson, Anthony Papenfuss, David Goode

2018-08-09

Extensive transcriptional alterations are observed in cancer, many of which activate core biological processes established in unic..

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How the evolution of multicellularity set the stage for cancer

AS Trigos, RB Pearson, AT Papenfuss, DL Goode

2018-01-01

Neoplastic growth and many of the hallmark properties of cancer are driven by the disruption of molecular networks established dur..

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Altered interactions between unicellular and multicellular genes drive hallmarks of transformation in a diverse range of solid tumors

AS Trigos, RB Pearson, AT Papenfuss, DL Goode

2017-06-13

Tumors of distinct tissues of origin and genetic makeup display common hallmark cellular phenotypes, including sustained prolifera..

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Copy number analysis by low coverage whole genome sequencing using ultra low-input DNA from formalin-fixed paraffin embedded tumor tissue

T Kader, DL Goode, SQ Wong, J Connaughton, SM Rowley, L Devereux, D Byrne, SB Fox, G Mir Arnau, RW Tothill, IG Campbell, KL Gorringe

2016-11-15

Unlocking clinically translatable genomic information, including copy number alterations (CNA), from formalin-fixed paraffin-embed..

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Monogenic and polygenic determinants of sarcoma risk: an international genetic study

ML Ballinger, DL Goode, I Ray-Coquard, PA James, G Mitchell, E Niedermayr, A Puri, JD Schiffman, GS Dite, A Cipponi, RG Maki, AS Brohl, O Myklebost, EW Stratford, S Lorenz, SM Ahn, JH Ahn, JE Kim, S Shanley, V Beshay

2016-09-01

Background Sarcomas are rare, phenotypically heterogeneous cancers that disproportionately affect the young. Outside rare syndrome..

University of Melbourne Researchers