Genetic Determinants of Prostate Cancer: A Review

Král, Milan; Rosinska, Vlasta; Študent, Vladimír; Grepl, Michal; Hrabec, Martin; Bouchal, Jan

doi:10.5507/bp.155.2011.001

Cited by 23 publications

(23 citation statements)

References 60 publications

(50 reference statements)

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“…Amplifications in chromosome 8q and losses in 3p, 8p, 10q, 13q, and 17p are some examples. Key regulatory genes have been mapped within these chromosome regions, including the homeobox protein Nkx3.1, the phosphatase and tensin homolog deleted on chromosome 10 (PTEN), c-Myc, and cytochrome P450 family 17 (CYP17) 9,15,28,29. Mutations in the breast cancer antigens 1 and 2 (BRCA-1 and -2) are associated with a higher risk of hereditary prostate cancer with earlier onset 9,30.…”

Section: Molecular Alterations In Prostate Cancer and Current Therapiesmentioning

confidence: 99%

“…Key regulatory genes have been mapped within these chromosome regions, including the homeobox protein Nkx3.1, the phosphatase and tensin homolog deleted on chromosome 10 (PTEN), c-Myc, and cytochrome P450 family 17 (CYP17) 9,15,28,29. Mutations in the breast cancer antigens 1 and 2 (BRCA-1 and -2) are associated with a higher risk of hereditary prostate cancer with earlier onset 9,30. A major chromosomal rearrangement is the generation of the fusion gene transmembrane protease, serine 2:v-ets erythroblastosis virus E26 oncogene homolog ( TMPRSS2-ERG ), detected in 15% of high-grade PIN lesions and 50% of localized prostate cases 31,32.…”

Section: Molecular Alterations In Prostate Cancer and Current Therapiesmentioning

confidence: 99%

“…While the incidence rate is highest in Northern European countries and the US and lowest in Asia, the mortality rate is highest in less developed countries 4,5. Susceptibility to develop prostate cancer has been associated with environmental factors, dietary and hormonal agents, abdominal adiposity, diabetes, smoking, prostatitis, and genetic predisposition 6–9. An established risk factor is advanced age with >60% of all diagnosed cases in men older than 70 years 3.…”

Section: Introductionmentioning

confidence: 99%

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Oncolytic adenovirus-mediated therapy for prostate cancer

Sweeney

Halldén

2016

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Prostate cancer is a leading cause of cancer-related death and morbidity in men in the Western world. Tumor progression is dependent on functioning androgen receptor signaling, and initial administration of antiandrogens and hormone therapy (androgen-deprivation therapy) prevent growth and spread. Tumors frequently develop escape mechanisms to androgen-deprivation therapy and progress to castration-resistant late-stage metastatic disease that, in turn, inevitably leads to resistance to all current therapeutics, including chemotherapy. In spite of the recent development of more effective inhibitors of androgen–androgen receptor signaling such as enzalutamide and abiraterone, patient survival benefits are still limited. Oncolytic adenoviruses have proven efficacy in prostate cancer cells and cause regression of tumors in preclinical models of numerous drug-resistant cancers. Data from clinical trials demonstrate that adenoviral mutants have limited toxicity to normal tissues and are safe when administered to patients with various solid cancers, including prostate cancer. While efficacy in response to adenovirus administration alone is marginal, findings from early-phase trials targeting local-ized and metastatic prostate cancer suggest improved efficacy in combination with cytotoxic drugs and radiation therapy. Here, we review recent progress in the development of multimodal oncolytic adenoviruses as biological therapeutics to improve on tumor elimination in prostate cancer patients. These optimized mutants target cancer cells by several mechanisms including viral lysis and by expression of cytotoxic transgenes and immune-stimulatory factors that activate the host immune system to destroy both infected and noninfected prostate cancer cells. Additional modifications of the viral capsid proteins may support future systemic delivery of oncolytic adenoviruses.

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Section: Molecular Alterations In Prostate Cancer and Current Therapiesmentioning

confidence: 99%

Section: Molecular Alterations In Prostate Cancer and Current Therapiesmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

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Oncolytic adenovirus-mediated therapy for prostate cancer

Sweeney

Halldén

2016

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“…Men who have first-degree relatives with prostate cancer are twice more at risk compared with men without a family history (4). Also, people with two first-degree relatives with prostate cancer are fivefold at risk of developing the disease (5).…”

Section: Introductionmentioning

confidence: 96%

Association between the Asp327Asn Polymorphism of Sex Hormone-Binding Globulin Gene and Prostate Cancer

et al. 2016

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Background: By binding SHBG hormone to sex hormones, in addition to carrying them in the blood, they regulate the amount of tissue availability. The genetic changes in the structure of globulin affect its binding to hormones, so in this study the effects of single nucleotide change in exon 8 or rs 6259 in the incidence of prostate cancer was evaluated. Materials and Methods:The study population included 120 patients with prostate cancer and 120 control subjects. After collecting blood samples, DNA was extracted by salting out procedure in order to determine the genotype of individuals by RFLP-PCR method. According to Hardy-Weinberg equilibrium genotypes the allele frequencies were calculated and a relationship between this variation and prostate cancer were evaluated using SPSS V.23.Also, the relationship between variations was investigated. P-values smaller than or equal to 0.05 were considered significant. Results: Results indicated that homozygous mutant genotype AA 2.58 (p value= 0.007, OR: 2.58, CI95%: 1.52-4.38) and heterozygous AG increase the risk of prostate cancer in carriers by 1.18 times (p-value =0.5, OR: 1.18, CI95%: 0.38-3.61). But homozygous of wild genotype GG have a protective role against prostate cancer (p-value =0.005, OR: 0.385, CI95%: 0.23-0.65). Conclusion: Asn allele is one of the main factors in prostate cancer, therefore, it could be used as the non-invasive and suitable marker for early detection in susceptible individuals.

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“…[1314] However, low penetrance and disease heterogeneity have precluded the validation of CaP susceptibility genes. Recent genome wide association studies (GWAS) have identified multiple CaP risk alleles towards defining genetic determinants of CaP risk.…”

Section: Introductionmentioning

confidence: 99%

Oncogenic activation ofERG:A predominant mechanism in prostate cancer

Sreenath¹,

Dobi²,

Petrovics³

et al. 2011

J Carcinog

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Prevalent gene fusions involving regulatory sequences of the androgen receptor (AR) regulated genes (primarily TMPRSS2) and protein coding sequences of nuclear transcription factors of the ETS gene family (predominantly ERG) result in unscheduled androgen dependent ERG expression in prostate cancer (CaP).Cumulative data from a large number of studies in the past six years accentuate ERG alterations in more than half of all CaP patients in Western countries. Studies underscore that ERG functions are involved in the biology of CaP. ERG expression in normal context is selective to endothelial cells, specific hematopoetic cells and pre-cartilage cells. Normal functions of ERG are highlighted in hematopoetic stem cells. Emerging data continues to unravel molecular and cellular mechanisms by which ERG may contribute to CaP. Herein, we focus on biological and clinical aspects of ERG oncogenic alterations, potential of ERG-based stratification of CaP and the possibilities of targeting the ERG network in developing new therapeutic strategies for the disease.

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Genetic Determinants of Prostate Cancer: A Review

Cited by 23 publications

References 60 publications

Oncolytic adenovirus-mediated therapy for prostate cancer

Oncolytic adenovirus-mediated therapy for prostate cancer

Association between the Asp327Asn Polymorphism of Sex Hormone-Binding Globulin Gene and Prostate Cancer

Oncogenic activation ofERG:A predominant mechanism in prostate cancer

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