Role of chromosomal loss in the progression of prostate cancers

Ichikawa, Tomohiko; Suzuki, H.; Itô, Haruo

doi:10.1007/pl00012062

Cited by 8 publications

(6 citation statements)

References 72 publications

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“…Another possible explanation for our observations relates to its role in the development of advanced disease; the ACE gene is linked to other important genes in the process of progression. Many studies have demonstrated genetic alterations that may affect the progression of prostate cancer 54–60. This is consistent with the multigenic model that has been proposed for prostate cancer development and progression 61–64.…”

Section: Discussionsupporting

confidence: 77%

Linkage of angiotensin I‐converting enzyme gene insertion/deletion polymorphism to the progression of human prostate cancer

Medeiros

Vasconcelos

Costa

et al. 2004

The Journal of Pathology

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Angiotensin-converting enzyme (ACE) degrades vasodilator kinins and generates angiotensin II (Ang II). It has been reported that ACE is synthesized by the prostate and that the AT-1 receptor subtype is the predominant prostatic Ang II receptor. A polymorphism in the human ACE gene has been described and the highest levels of circulating and tissue ACE activity are found in carriers of the DD genotype. In the present study, ACE genotypes were determined in 170 patients with prostate cancer and their association with disease progression was analysed. It was found that the DD genotype was present in 31 of 78 (39.8%) patients with advanced disease and in 19 of 82 (23.2%) with localized disease: this difference was statistically significant (OR = 2.18, 95% CI = 1.11-4.03; p = 0.024). Step-wise logistic regression analysis was used to identify predictive parameters of advanced disease and it was observed that the DD genotype (p = 0.002, OR = 5.4, 95% CI = 1.84-16.06), high-grade tumour (p < 0.001, OR = 8.04, 95% CI = 3.03-21.33), and high serum PSA (p < 0.001, OR = 10.87, 95% CI = 4.06-29.13) were significantly associated with advanced disease. The results of this study support the hypothesis that genetic factors related to ACE may influence the behaviour of human prostate cancer.

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Section: Discussionsupporting

confidence: 77%

Linkage of angiotensin I‐converting enzyme gene insertion/deletion polymorphism to the progression of human prostate cancer

Medeiros

Vasconcelos

Costa

et al. 2004

The Journal of Pathology

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“…Although the exact mechanism of ectopic hormonal production is still obscure, it is suggested that genetic abnormalities of hormone and/or pro‐hormone in tumor cells might cause inappropriate secretion of the hormones. Since advanced prostate cancer contains an accumulation of genetic changes, 8 poorly differentiated cases may be more likely to cause abnormal hormonal secretion.…”

Section: Discussionmentioning

confidence: 99%

Prostate adenocarcinoma producing syndrome of inappropriate secretion of antidiuretic hormone

et al. 2001

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The syndrome of inappropriate secretion of antidiuretic hormone (ADH) was recognized in a 68-year-old man with a poorly differentiated metastatic adenocarcinoma of the prostate. Elevated levels of ADH were found in the tissues of the primary tumor and lymph node metastasis. The patient's clinical course is detailed and the pathophysiology of this syndrome is discussed. To our knowledge, this case is the ninth reported case of syndrome of inappropriate secretion of ADH with adenocarcinoma of the prostate. Antidiuretic hormone activity was proven in only three cases including this case.

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“…5,6 LOH analyses have also demonstrated several distinct commonly deleted regions on 13q. 4 Mckie et al 21 have recently reported epigenetic inactivation of the human sprouty2 (hSPRY2) homologue, maps to 13q31.1, in prostate cancer. Sprouty2 is Genetic changes in pT2 and pT3 prostate cancer S Fukasawa et al a key antagonistic regulator of receptor tyrosine kinases signaling and suppression of its expression or function may facilitate proliferation and angiogenesis.…”

Section: Chromosomal Lossesmentioning

confidence: 99%

“…[4][5][6] We have investigated several regions of chromosomal loss in prostate cancer using LOH analysis. [7][8][9][10][11][12][13][14][15] CGH is a molecular technique that allows screening of the whole genome for DNA sequence copy number alterations.…”

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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Role of chromosomal loss in the progression of prostate cancers

Cited by 8 publications

References 72 publications

Linkage of angiotensin I‐converting enzyme gene insertion/deletion polymorphism to the progression of human prostate cancer

Linkage of angiotensin I‐converting enzyme gene insertion/deletion polymorphism to the progression of human prostate cancer

Prostate adenocarcinoma producing syndrome of inappropriate secretion of antidiuretic hormone

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

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