Erratum: Frequent overexpression of ETS-related gene-1 (ERG1) in prostate cancer transcriptome

Petrovics, G; Liu, A; Shaheduzzaman, S; Furusato, Bungo; Sun, C; Nau, M; Ravindranath, L; Chen, Y; Dobi, A; Srikantan, V; Sesterhenn, I A; McLeod, D G; Vahey, M; Moul, J W; Srivastava, S

doi:10.1038/sj.onc.1210745

Cited by 42 publications

(71 citation statements)

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“…Interestingly, high ERG expression was seen as protective in the only other prostate cancer study (Petrovics et al, 2005) examining ERG, where high levels of ERG transcription were associated with a lower incidence of prostate-specific antigen (PSA) biochemical failure. The findings by Petrovics need to be viewed with caution, as biochemical failure is a poor surrogate end point for clinically meaningful end points, including clinical relapse and death as demonstrated by three recent studies.…”

Section: Tmprss2:erg F Demichelis Et Almentioning

confidence: 99%

TMPRSS2:ERG gene fusion associated with lethal prostate cancer in a watchful waiting cohort

et al. 2007

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The identification of the TMPRSS2:ERG fusion in prostate cancer suggests that distinct molecular subtypes may define risk for disease progression. In surgical series, TMPRSS2:ERG fusion was identified in 50% of the tumors. Here, we report on a population-based cohort of men with localized prostate cancers followed by expectant (watchful waiting) therapy with 15% (17/111) TMPRSS2:ERG fusion. We identified a statistically significant association between TMPRSS2:ERG fusion and prostate cancer specific death (cumulative incidence ratio ¼ 2.7, Po0.01, 95% confidence interval ¼ 1.3-5.8).Quantitative reverse-transcription-polymerase chain reaction demonstrated high estrogen-regulated gene (ERG) expression to be associated with TMPRSS2:ERG fusion (Po0.005). These data suggest that TMPRSS2:ERG fusion prostate cancers may have a more aggressive phenotype, possibly mediated through increased ERG expression.

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Section: Tmprss2:erg F Demichelis Et Almentioning

confidence: 99%

TMPRSS2:ERG gene fusion associated with lethal prostate cancer in a watchful waiting cohort

et al. 2007

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“…Specimen processing and geneexpression analysis were performed as described. 20,21 Briefly, benign and neoplastic prostate epithelial cells were collected by a pathologist from frozen prostatectomy specimens using laser capture micro-dissection technique. Total RNA was extracted from the dissected specimens using the MicroRNA kit (Stratagene, La Jolla, CA, USA).…”

Section: Methodsmentioning

confidence: 99%

“…Pearson's or Spearman's correlation analyses were used to evaluate the correlation between C-MYC and other gene-expression levels (PTEN, ERG, AR, PSA/KLK3, PCA3, PMEPA1, PSGR, TMPRSS2, AMACR and LTF) in tumor tissue. 20,21,23 The prognostic significance of established clinical variables (race, pathologic stage and Gleason's score, margin status and PSA level at time of diagnosis) and C-MYC expression level were assessed by constructing univariate and multivariate Cox proportional hazards models. Disease progression-free survival curves across different C-MYC expression levels (categorized to quartile groups) were constructed with use of KaplanMeier survival method with log-rank test.…”

Section: Methodsmentioning

confidence: 99%

“…19 Considering sensitivity and quantitative accuracy of the real-time reverse transcription polymerase chain reaction (RT-PCR) assay (TaqMan, Applied Biosystems, Foster City, CA, USA) to quantify C-MYC mRNA levels in RNA samples prepared from laser capture micro-dissected primary CaP specimens, we carefully evaluated overall frequency of C-MYC overexpression in CaP cells, prognostic features of C-MYC expression and its relationship to other previously studied gene-expression alterations (PTEN, ERG, AR, PSA/KLK3, PCA3, PMEPA1, PSGR, TMPRSS2, AMACR and LTF) in our laboratory. 20,21 To our knowledge this is the first comprehensive and quantitative evaluation of C-MYC mRNA expression in microdissected benign and CaP specimens from patients linked to longitudinal post-treatment follow-up.…”

Section: Introductionmentioning

confidence: 99%

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Overexpression of C-MYC oncogene in prostate cancer predicts biochemical recurrence

Hawksworth

Ravindranath

Chen

et al. 2010

Prostate Cancer Prostatic Dis

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145

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Alterations of chromosome 8, including amplification at 8q24 harboring the C-MYC oncogene, have been noted as one of the most common chromosomal abnormalities in prostate cancer (CaP) progression. However, the frequency of C-MYC alterations in CaP has remained uncertain. A recent study, using a new anti-MYC antibody, described prevalent upregulation of nuclear C-MYC protein expression as an early oncogenic alteration in CaP. Further, we have recently reported regulation of C-MYC expression by ERG and a significant correlation between C-MYC overexpression and TMPRSS2-ERG fusion in early stage CaP. These emerging data suggest that increased C-MYC expression may be a critical and early oncogenic event driving CaP progression. In this study, we assessed whether C-MYC mRNA overexpression in primary prostate tumors was predictive of more aggressive tumor or disease progression. Our approach was to quantitatively determine C-MYC mRNA expression levels in laser capture micro-dissected tumor cells and matched benign epithelial cells in a radical prostatectomy cohort with long follow-up data available. On the basis of our results, we conclude that elevated C-MYC expression in primary prostate tumor is biologically relevant and may be a predictor of future biochemical recurrence.

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“…The identification of high expression of ERG, an ETS-family transcription factor led to the identification of DNA deletions that result in the activation by gene fusion of ERG in many prostate tumors. 41,42 While the most common lesion is a nearly 3-MB deletion of chromosome 21 resulting in the fusion of TMPRSS2 and ERG, other deletions and translocations have been described resulting in fusions of ERG or other ETS-family genes (ETV1, ETV4 and ETV5) resulting in overexpression of a hybrid ETS-family protein (reviewed in Clark and Cooper 43 ). These lesions can be found in up to half of all PCas in people of European descent; however, there has been little advance in using these lesions as biomarkers for PCa therapy or recurrence, and the function of the ERG protein in the tumor is poorly understood (reviewed in Rosen et al 44 ).…”

Section: Somatic Alterations In Tumorsmentioning

confidence: 99%

Genetics and genomics of prostate cancer

Dean¹,

Li²

2013

Asian J Androl

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Prostate cancer (PCa) is one of the most common malignancies in the world with over 890 000 cases and over 258 000 deaths worldwide each year. Nearly all mortalities from PCa are due to metastatic disease, typically through tumors that evolve to be hormone-refractory or castrate-resistant. Despite intensive epidemiological study, there are few known environmental risk factors, and age and family history are the major determinants. However, there is extreme heterogeneity in PCa incidence worldwide, suggesting that major determining factors have not been described. Genome-wide association studies have been performed and a considerable number of significant, but low-risk loci have been identified. In addition, several groups have analyzed PCa by determination of genomic copy number, fusion gene generation and targeted resequencing of candidate genes, as well as exome and whole genome sequencing. These initial studies have examined both primary and metastatic tumors as well as murine xenografts and identified somatic alterations in TP53 and other potential driver genes, and the disturbance of androgen response and cell cycle pathways. It is hoped that continued characterization of risk factors as well as gene mutation and misregulation in tumors will aid in understanding, diagnosing and better treating PCa.

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Erratum: Frequent overexpression of ETS-related gene-1 (ERG1) in prostate cancer transcriptome

Cited by 42 publications

References 0 publications

TMPRSS2:ERG gene fusion associated with lethal prostate cancer in a watchful waiting cohort

TMPRSS2:ERG gene fusion associated with lethal prostate cancer in a watchful waiting cohort

Overexpression of C-MYC oncogene in prostate cancer predicts biochemical recurrence

Genetics and genomics of prostate cancer

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