Screening for prostate cancer

Department of Epidemiology&PreventiveMedicine, School of PublicHealth&PreventiveMedicine,MonashUniversity,Melbourne,Australia. .
Cochrane database of systematic reviews (Online) (Impact Factor: 6.03). 01/2013; 1(1):CD004720. DOI: 10.1002/14651858.CD004720.pub3
Source: PubMed


Any form of screening aims to reduce disease-specific and overall mortality, and to improve a person's future quality of life. Screening for prostate cancer has generated considerable debate within the medical and broader community, as demonstrated by the varying recommendations made by medical organizations and governed by national policies. To better inform individual patient decision-making and health policy decisions, we need to consider the entire body of data from randomised controlled trials (RCTs) on prostate cancer screening summarised in a systematic review. In 2006, our Cochrane review identified insufficient evidence to either support or refute the use of routine mass, selective, or opportunistic screening for prostate cancer. An update of the review in 2010 included three additional trials. Meta-analysis of the five studies included in the 2010 review concluded that screening did not significantly reduce prostate cancer-specific mortality. In the past two years, several updates to studies included in the 2010 review have been published thereby providing the rationale for this update of the 2010 systematic review. To determine whether screening for prostate cancer reduces prostate cancer-specific mortality or all-cause mortality and to assess its impact on quality of life and adverse events.

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    • "For example, a panel of moderate-risk genetic variants (with average OR of 3) that are present in 20% of the population would enable targeted PSA screening of 20% of the population and would detect 60% of all prostate cancers in the population. Currently, PSA screening has not been shown to decrease overall mortality from prostate cancer in the general population, but it might perform better in the high-risk setting (Ilic et al., 2013). To date, we have identified six other founder alleles in three genes (CHEK2, HOXB13, and NBN) that predispose to prostate cancer in Poland, and in combination with rs188140481, these have a combined prevalence of 7.0% in the population (Cybulski et al., 2013b). "
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    ABSTRACT: A number of single nucleotide polymorphisms (SNPs) in the human genome have been associated with increased risk of prostate cancer. Recently, a single SNP in the region of chromosome 8q24 (rs188140481) has been associated with a three-fold increased risk of prostate cancer in Europe and North America. To establish whether rs188140481 is associated with the risk of prostate cancer in Poland, we genotyped 3467 men with prostate cancer and 1958 controls. The A allele of rs188140481 was detected in 44 of 3467 (1.3%) men with prostate cancer and in seven of 1958 (0.4%) controls (odds ratio=3.6; 95% confidence interval 1.6-7.9; P=0.0006). The allele was present in eight of 390 (2.1%) men with familial prostate cancer (odds ratio=5.8; 95% confidence interval 2.1-16.2; P=0.001). A positive family history of cancers at sites other than the prostate was observed in 27% of men who carried the rs188140481 risk allele and in 44% of noncarriers (P=0.04). No cancer at a site other than the prostate was more common in first-degree or second-degree relatives of carriers of the rs188140481 risk allele than relatives of noncarriers. The rs188140481 polymorphism in the 8q24 region confers a moderate increase in the risk of prostate cancer in Polish men. The SNP does not appear to be associated with susceptibility to cancers of other types.
    European journal of cancer prevention: the official journal of the European Cancer Prevention Organisation (ECP) 09/2014; 24(2). DOI:10.1097/CEJ.0000000000000079 · 3.03 Impact Factor
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    • "Prostate cancer is the most common non-cutaneous cancer and the second leading cause of cancer mortality in men in the United States [1]. Despite increased screening for early detection and monitoring, prostate cancer-specific mortality has remained at the same level [2]. This is likely due to both the inability to diagnostically distinguish between the non-invasive, indolent localized prostate cancers and the very aggressive localized cancers with high metastatic potentials, and the poor understanding of the cellular and molecular basis for metastatic prostate cancers [3]. "
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    ABSTRACT: Despite all the blood-based biomarkers used to monitor prostate cancer patients, prostate cancer remains as the second common cause of cancer mortality in men in the United States. This is largely due to a lack of understanding of the molecular pathways that are responsible for the aggressive forms of prostate cancers, the castrate-resistant prostate cancer and the metastatic prostate cancer. Cell signaling pathways activated by the ERBB2 oncogene or the RAS oncogene are frequently found to be altered in metastatic prostate cancers. To evaluate and define the role of the ERBB2/RAS pathway in prostate cancer metastasis, we have evaluated the impact of ERBB2- or RAS-overexpression on the metastatic potentials for four prostate cancer cell lines derived from tumors with different androgen sensitivities. To do so, we transfected the human DU145, LnCaP, and PC3 prostate cancer cells and the murine Myc-CaP prostate cancer cells with the activated form of ERBB2 or H-RAS and assessed their metastatic potentials by three complementary assays, a wound healing assay, a transwell motility assay, and a transwell invasion assay. We showed that while overexpression of ERBB2 increased the metastatic potential of the androgen-insensitive prostate cancer cells (i.e. PC3 and DU145), it did not affect metastatic potentials of the androgen-sensitive prostate cancer cells (i.e. LnCaP and Myc-CaP). In contrast, overexpression of H-RAS only increased the cell motility of Myc-CaP cells, which overexpress the human c-MYC oncogene. Our data suggest that ERBB2 collaborates with androgen signaling to promote prostate cancer metastasis, and that although RAS is one of the critical downstream effectors of ERBB2, it does not phenocopy ERBB2 for its impact on the metastatic potentials of prostate cancer cell lines.
    PLoS ONE 06/2014; 9(6):e99525. DOI:10.1371/journal.pone.0099525 · 3.23 Impact Factor
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    • "PCa is the most frequently diagnosed cancer in males, but very often it is not highly invasive. The wide adoption of PSA screening has been proved to increase diagnosis, to induce over treatment, to cause anxiety, treatment adverse events and to reduce the quality of life of patients [20,21]. For these reasons continuous efforts are made to identify new more reliable markers for the diagnosis and prognosis of PCa other than PSA. "
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    ABSTRACT: Dickoppf-1 (DKK-1) is a negative regulator of bone formation with tumorigenic potential. The up-regulation of DKK-1 is an early event in prostate cancer (PCa) development, thus we investigated its role as a marker in the diagnosis and prognosis of PCa. We retrospectively enrolled 159 patients who underwent prostate biopsy, either for elevated PSA or suspect digital rectal examination, between 2003 and 2010. During the biopsy, one serum sample was collected from all patients; PSA and DKK-1 were measured by ELISA technique. Amongst the biopsy of 159 patients 75 were affected by PCa and 84 were not the mean period of follow-up for these patients was 5 years; a new biopsy was performed in case of PCa suspicion. PSA performed better than DKK-1 in detecting PCa (0.63 vs 0.51 respectively). Differently from PSA DKK-1 was significantly higher in patients who developed PCa during follow-up than in cancer-free ones, thus DKK-1 performed better than PSA in detecting these patients (0.67 vs 0.55). DKK-1 was significantly lower in patients with bone metastases, whereas PSA was not significantly different in patients with different outcomes. DKK-1 might be predictive for patients negative at first biopsy who will develop PCa and in the prognosis of bone metastases. It performed worse than PSA in the early diagnosis of Pca.
    BMC Clinical Pathology 03/2014; 14(1):11. DOI:10.1186/1472-6890-14-11
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