About Us

The Molecular Biology of Prostate Cancer Group (MBPCG) studies somatic genetic and epigenetic alterations in prostate cancer with emphasis on alterations associated with disease progression. Finding the common genetic alterations is an important step in the development of better diagnostics and therapeutics. Especially, MBPCG is exploring strategies to therapeutically interfere with androgen signaling.
Research interests and expertise

The goal of the research group is to identify recurrent genetic and epigenetic alterations in prostate cancer using modern genomic tools, such as next generation sequencing. Special emphasis is currently placed on non-coding RNAs (ncRNA). In addition, we have a strong interest towards androgen receptor (AR) gene, amplification of which was first described by the group. We study mechanistic consequences of the overexpression of AR using models we have established, as well as clinical samples of castration-resistant disease. We also identify and characterize downstream genes of AR signaling pathway, to screen for candidate drug targets.


We were first to describe AR amplification as a major alteration in progressed prostate cancer (Visakorpi et al. 1995 Nature Genetics), and have since conducted considerable work in understanding molecular biology and downstream effects of AR in prostate cancer. The group has contributed significantly in understanding of genetic, epigenetic and gene expression changes during prostate cancer development and progression. Of candidate drug targets, especially TMPRSS2:ERG fusion gene, as well as our recently discovered microRNA, miR-32, show promise for utility.


We work in brand new laboratories in the ARVO building in the University of Tampere Kauppi campus. We belong to Prostate Cancer Research Center (PCRC) which integrates multidisciplinary research on prostate cancer in the University of Tampere and the Pirkanmaa Hospital District, the second biggest Hospital District in Finland. We have a unique collection of population-based clinical materials and models with complementary expertise from molecular mechanisms to clinical practice. This provides an exceptionally strong basis to find answers to the most important questions in treatment of prostate cancer: the etiology of the disease, identification of clinically relevant disease, personalized cancer therapy and novel treatment modalities to combat the disease.

Major Publications

Gundem G, Van Loo P, Kremeyer B, Alexandrov L, Tubio J, Papaemmanuil E, Brewer D, Kallio H, Högnäs G, Annala M, Goody V, Latimer C, O’Meara S, Dawson K, Isaacs W, Emmert-Buck M, Nykter M, Foster C, Kote-Jarai Z, Easton D, Whitaker H, Neal D, Cooper C, Eeles R, Visakorpi T, Campbell P, McDermott U1, Wedge D1. Bova GS1. The evolutionary history of lethal metastatic prostate cancer. 1shared correspondence.Nature 520:353-357, 2015.
Khanna A, Rane JK, Kivinummi KK, Urbanucci A, Helenius MA, Tolonen TT, Saramäki OR, Latonen L, Manni V, Pimanda JE, Maitland NJ, Westermarck J, Visakorpi T. CIP2A is a candidate therapeutic target in clinically challenging prostate cancer cell populations. Oncotarget 6:19661-70, 2015.
Ylipää A1, Kivinummi K1, Kohvakka A, Annala M, Latonen L, Scaravilli M, Kartasalo K, Leppänen SP, Karakurt S, Seppälä J, Yli-Harja O, Tammela TLJ, Zhang W, Visakorpi T2, Nykter M2. Transcriptome sequencing reveals PCAT5 as a novel ERG-regulated long non-coding RNA in prostate cancer. 1shared first authors; 2shared correspondence, Cancer Res, 75:4026-4031, 2015.
Bova GS1, Kallio H1, Annala M1, Kivinummi K, Högnäs G, Häyrynen S, Rantapero T, Kivinen V, Isaacs W, Tolonen T, Nykter M, Visakorpi T. Integrated clinical, whole genome, and transcriptome analysis of multisampled lethal metastatic prostate cancer. 1shared first authors. Cold Spring Harb Mol Case Stud 2:a000752, 2016.
Latonen L, Scaravilli M, Gillen A, Zhang F, Ruusuvuori P, Kujala P, Poutanen M, Visakorpi T. In vivo expression of miR-32 induces proliferation in prostate epithelium. Am J Pathol, 187:2546-2557, 2017.