Temozolomide ARLTS1 belongs to the ADP-ribosylation factor -ARF-like family of the Ras protein superfamily. ARFs are guanine-nucleotide-binding proteins which are critical components of several different eukaryotic vesicle trafficking pathways. As with other members of the Ras superfamily, ARFs function as molecular switches by cycling between inactive GDP- and active GTP-bound conformations. ARLTS1 has been characterized as an intracellular protein having tissue specific expression in the lung and leucocytes. ARLTS1 variants, such as the nonsense polymorphism Trp149Stop have been suggested to have a role in different cancers. Prostate cancer is the most frequently diagnosed cancer in males in many countries, including Finland. Aging and improved diagnostics most evidently increase the number of new cases, but the incidence is influenced also by some unknown factors. Growing number of new cases create pressure to health care system and new tools for PCa diagnostics, prognostics and treatment are required, especially to avoid over treatment and unnecessary biopsies. During the last several years there has been extensive research in PCa etiology and genome-wide association studies have revealed several common low penetrance genetic alterations. The association of these variants with clinicopathologic features and prognosis remains unclear and results are lacking clinical implications. We recently showed a significant association withCys148Arg variant and the risk of PCa. Further evaluation of this variant is warranted to increase the power of the association and study the functional role of the variant in PCa. More samples are also needed to evaluate the implication of this variant to clinical outcome and a potential role in predictive biomarker of PCa. Besides the genetic variants, DNA copy number aberrations are one of the most frequently observed genetic changes in familial and sporadic PCa. In most of the cases target genes for the aberrations are not fully identified. Interestingly, allelic imbalance has been detected at 13q14.2-13q14.3, and it is an important event in the progression of localized PCa. Differences of 13q14 loss of heterozygosity in different PCa groups could also be used to distinguish clinically insignificant PCa. In this study we analyzed the role of ARLTS1 in more detail, especially the role of Cys148Arg in PCa risk. Chromosomal aberration in 13q14.3 was analyzed with aCGH to evaluate the ARLTS1 copy number changes in PCa xenografts and cell lines. The expression of ARLTS1 was studied in clinical tumor samples, BPH samples and also co-expression data form previously published data was analyzed. The ARLTS1 gene and ARLTS1 polymorphisms have been shown to have a role in the pathogenesis of many cancers. The nonsense polymorphism at the end of the coding region has been revealed to predispose to familial cancer. Functional analyses of the truncated protein have indicated that the Trp149Stop variant might affect apoptosis and tumor suppression. Another ARLTS1 variant, the missense polymorphism Cys148Arg, and especially the CC genotype, has been found to be significantly associated with high-risk familial breast cancer.