Poster & Mini-oral COSA 2015 ASM

Intraductal Carcinoma of the Prostate (IDC-P) in Men with High Risk Prostate Cancer (PCa) Survives Androgen Deprivation Therapy.  (#155)

Carmel Pezaro 1 , Kohei Hasimoto 1 , Laura Porter 1 , Mitchell Lawrence 1 , Hong Wang 1 , Melissa Papargiris 1 , Heather Thorne 2 , Mark Frydenberg 1 , Declan Murphy 3 , Andrew Ryan 4 , David Clouston 4 , Damien Bolton 5 , Gail Risbridger 1 , Renea Taylor 6
  1. Department of Anatomy and Developmental Biology, Monash University, Melbourne
  2. kConFab, Familial Cancer Centre and Department of Oncology, Peter MacCallum Cancer Centre, University of Melbourne, Melbourne
  3. Division of Cancer Surgery, Peter MacCallum Cancer Centre, Victoria and Epworth Research Centre, Epworth Healthcare, Melbourne
  4. TissuPath, Melbourne
  5. Department of Urology, University of Melbourne, Melbourne
  6. Department of Physiology, Monash University, Melbourne

Aims:

Risk classification of localised PCa relies on staging and pathological grading criteria that are focused on the appearance of the epithelium. The histological sub-type IDC-P has not been incorporated into grading, but has been associated with poor cancer outcomes. We determined to examine the relevance of IDC-P in a longitudinal model of PCa.

Methods:

With project-specific ethics approval, we developed patient derived xenografts (PDXs) of localised high-risk sporadic or familial PCa using tissue obtained at radical prostatectomy. Eight patient tissues with adenocarcinoma and IDC-P were selected for PDX (N=5 sporadic high-risk by D’Amico criteria; N=3 familial cases). Specimens were established as PDXs in host mice for 4-8 weeks, followed by castration for 4 weeks and then testosterone-restoration for 4 weeks. The primary study endpoints were tumour volume and proliferation assessed by Ki-67 immunohistochemistry.

Results:

At baseline, IDC-P was the predominant phenotype in high-risk patient tissues. IDC-P was present in PDXs of both sporadic and in familial PCa samples. Castration resulted in prominent regression of IDC-P, as with adenocarcinoma. However, following testosterone replacement there was clear regeneration of IDC-P, indicating the presence of castrate-tolerant cells.

Conclusions:

These data demonstrate that IDC-P cells are able to survive castration in a PDX model of high risk PCa, suggesting an ongoing role for IDC-P in the pathogenesis of PCa. The molecular features and key drivers of IDC-P warrant further study.  In men with localized PCa, the presence of IDC-P may identify a high-risk patient cohort likely to benefit from further adjuvant therapies.