Epidemiology of Prostate Cancer

Dijkman, G.A.; Debruyne, F.M.J.

doi:10.1159/000474185

Cited by 82 publications

(47 citation statements)

References 67 publications

(109 reference statements)

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“…1 In Japan, the morbidity and mortality of this disease is increasing year by year. Increased use of serum prostate-specific antigen (PSA) in screening has led to a remarkable increase in the number of newly detected prostate cancer cases.…”

Section: Introductionmentioning

confidence: 99%

Genetic changes in pT2 and pT3 prostate cancer detected by comparative genomic hybridization

Fukasawa

Kino

Kobayashi

et al. 2007

Prostate Cancer Prostatic Dis

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Prostate-specific antigen (PSA) screening has led to a remarkable increase in prostate cancer cases undergoing operative therapy. Over half of patients with locally advanced cancer (^pT3) develop rising PSA levels (biochemical failure) within 10 years. It is very difficult to predict which patients will progress rapidly to advanced disease following biochemical failure (BF). Therefore, a more useful prognostic factor is needed to suggest the most appropriate therapies for each patient. To determine chromosomal aberrations, we examined 30 patients with stage pT2 or pT3 primary prostate adenocarcinomas and no metastases (pN0M0) by comparative genomic hybridization (CGH). Laser capture microdissection (LCM) was used to gather cancer cells from frozen prostate specimens. Common chromosomal alterations included losses on 2q23-24, 4q26-28, 6q14-22, 8p12-22 and 13q21-31, as well as gains on 1p32-36, 6p21 and 17q21-22. Losses at 8p12-22 and 13q21-31 were observed more frequently in pT3 than pT2 tumors (Po0.05 and Po0.01, respectively). Losses at 8p12-22 were more frequent in tumors with BF (Po0.05), and those at 13q12-21 were more frequent in tumors with Gleason score (GS) 7 or more than lower GS (Po0.05). These findings suggest that losses of 8p12-22 and 13q21-31 are important determinants of prostate cancer progression.

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Section: Introductionmentioning

confidence: 99%

Genetic changes in pT2 and pT3 prostate cancer detected by comparative genomic hybridization

Fukasawa

Kino

Kobayashi

et al. 2007

Prostate Cancer Prostatic Dis

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“…Prostate cancer is the most common form of male cancer in the Western world (Dijkman and Debruyne, 1996). It is thought that most elderly men have foci of prostate cancer but most of these tumours are latent and only a few patients will develop life-threatening disease.…”

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confidence: 99%

In vitro modelling of epithelial and stromal interactions in non-malignant and malignant prostates

2000

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SummaryTo study the effects of stromal epithelial cell interactions on prostate cancer metastasis, we have used primary human prostatic stromal cells derived from malignant and non-malignant tissues and established epithelial cell lines from normal (PNT1a and PNT2-C2) and tumour (PC-3, DU145 and LNCaP) origins. The effects of stromal cells on epithelial cell growth were studied in direct and indirect (using culture inserts) co-culture and by exposure to stromal cell-conditioned medium (assessed by MTT assay). The influence of stromal cells on epithelial cell invasion was measured using matrigel invasion chambers and on epithelial cell motility using time lapse microscopy. Results indicated that epithelial cell line growth was similarly unaffected or inhibited by stromal cells derived from malignant (n = 8) or non-malignant tissue (n = 8). In contrast, PNT2-C2 and PC-3 cells were found to be the least and the most invasive and motile epithelia respectively. Stromal cultures enhanced the invasion of both epithelial cells, but no differences were observed between the use of malignant and non-malignant tissues. All stromal cultures modestly stimulated PNT2-C2 motility but displayed a greater stimulation of PC-3 cell motility, while stromal cells derived from malignant tissue stimulated PNT2-C2 and PC-3 cell motility more than stromal cultures from non-malignant tissues.

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“…Family history is the best characterized risk factor for prostate cancer together with age and race (Dijkman and Debruyne, 1996). In many families, aggregation of prostate cancer is caused by autosomal dominantly inherited susceptibility genes with high penetrance (Carter et al, 1992).…”

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confidence: 99%

CAG repeat length in the androgen receptor gene is related to age at diagnosis of prostate cancer and response to endocrine therapy, but not to prostate cancer risk

et al. 1999

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SummaryThe length of the polymorphic CAG repeat in the N-terminal of the androgen receptor (AR) gene is inversely correlated with the transactivation function of the AR. Some studies have indicated that short CAG repeats are related to higher risk of prostate cancer. We performed a case-control study to investigate relations between CAG repeat length and prostate cancer risk, tumour grade, tumour stage, age at diagnosis and response to endocrine therapy. The study included 190 AR alleles from prostate cancer patients and 186 AR alleles from female control subjects. All were whites from southern Sweden. The frequency distribution of CAG repeat length was strikingly similar for cases and controls, and no significant correlation between CAG repeat length and prostate cancer risk was detected. However, for men with non-hereditary prostate cancer (n = 160), shorter CAG repeats correlated with younger age at diagnosis (P = 0.03). There were also trends toward associations between short CAG repeats and high grade (P = 0.07) and high stage (P = 0.07) disease. Furthermore, we found that patients with long CAG repeats responded better to endocrine therapy, even after adjusting for pretreatment level of prostate-specific antigen and tumour grade and stage (P = 0.05). We conclude that short CAG repeats in the AR gene correlate with young age at diagnosis of prostate cancer, but not with higher risk of the disease. Selection of patients with early onset prostate cancer in case-control studies could therefore lead to an over-estimation of the risk of prostate cancer for men with short CAG repeats. An association between long CAG repeats and good response to endocrine therapy was also found, but the mechanism and clinical relevance are unclear.

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Epidemiology of Prostate Cancer

Cited by 82 publications

References 67 publications

Genetic changes in pT2 and pT3 prostate cancer detected by comparative genomic hybridization

Genetic changes in pT2 and pT3 prostate cancer detected by comparative genomic hybridization

In vitro modelling of epithelial and stromal interactions in non-malignant and malignant prostates

CAG repeat length in the androgen receptor gene is related to age at diagnosis of prostate cancer and response to endocrine therapy, but not to prostate cancer risk

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