Abstract
The progression of organ-confined prostate cancer to metastatic cancer is inevitably fatal. Consequently, identification of structural changes in the genome and associated transcriptional responses that drive this progression is critical to understanding the disease process and the development of biomarkers and therapeutic targets. In this study, whole genome copy number changes in genomes of hormone-naïve lymph node metastases were profiled using array comparative genomic hybridization, and matched primaries were included for a subset. Matched primaries and lymph node metastases showed very similar copy number profiles that are distinct from primary tumors that fail to metastasize.
| Original language | English (US) |
|---|---|
| Pages (from-to) | 1083-1089 |
| Number of pages | 7 |
| Journal | Neoplasia |
| Volume | 8 |
| Issue number | 12 |
| DOIs | |
| State | Published - Dec 2006 |
Funding
Abbreviations: FABP5, fatty acid –binding protein 5; TPD52, tumor protein D52; NGFR, nerve growth factor receptor; MYC, myelocytomatosis viral oncogene homolog; PIAS3, protein inhibitor of activated STAT protein 3; ARL2, ADP ribosylation factor–like 2; SNX15, sorting nexin 15; MEN1, multiple endocrine neoplasia 1; RPS3, ribosomal protein S3; CBX8, chro-mobox homolog 8; CBX4, chromobox homolog 4 Address all correspondence to: Colin Collins, UCSF Box 0808, San Francisco, CA 94143. E-mail: [email protected] 1This work was supported by the University of California at San Francisco Prostate Cancer SPORE, National Institutes of Health grant P50CA89520. *This article refers to supplementary material, which is designated by W (i.e., Table W1) and is available online at www.bcdecker.com. Received 30 May 2006; Revised 5 September 2006; Accepted 30 October 2006.
Keywords
- Biomarkers
- Lymph nodes
- Metastases
- Prostate cancer
- aCGH
ASJC Scopus subject areas
- Cancer Research
