Poster Presentation 28th Lorne Cancer Conference 2016

Mechanisms of metastasis and outgrowth from dormancy in bone-metastatic prostate cancer (#297)

Katie Owen 1 , Marek Cmero 2 3 4 , Chris Hovens 2 , Niall Corcoran 2 , Nikola Baschuk 1 , Belinda Parker 1
  1. Department of Biochemistry, Institute for Molecular Science, La Trobe University, Melbourne, VIC, Australia
  2. Department of Surgery, Division of Urology, Royal Melbourne Hospital, Melbourne, VIC, Australia
  3. Department of Computing & Information Systems, University of Melbourne, Melbourne, VIC, Australia
  4. Walter and Eliza Hall Institute, Melbourne, VIC, Australia

Bone metastasis in advanced prostate cancer can occur up to 20 years after primary tumour diagnosis. The latency associated with bone metastasis has been largely attributed to tumour cell dormancy – a state in which tumour cells can survive undetected for prolonged periods. Immune regulation of tumour cells is one mechanism proposed to induce dormancy, while tumour cell evasion of immune surveillance mechanisms may favour metastatic outgrowth. In bone, immune evasion may be facilitated by tumour cell suppression of interferon (IFN), which contributes to antitumour immune surveillance. Here, we aimed to determine the impact of IFN signalling on metastatic progression to bone in prostate cancer. We demonstrated that IFN signalling reduces metastatic burden in bone. Furthermore, it was shown that IFN signalling was significantly downregulated in both human bone metastases derived from prostate cancer patients and in actively proliferating cells from bone in a mouse model of prostate cancer. Through optimisation of a method that enables the isolation and identification of active and dormant tumour cells from bone metastases, we hope to further elucidate how tumour intrinsic IFN pathways shape bone metastasis in prostate cancer.