<i>TMPRSS2–ERG</i> gene fusion prevalence and class are significantly different in prostate cancer of caucasian, african‐american and japanese patients

Magi‐Galluzzi, Cristina; Tsusuki, Toyonori; Elson, Paul; Simmerman, Kelly; LaFargue, Christopher J.; Esgueva, Raquel; Klein, Eric A.; Rubin, Mark A.; Zhou, Ming

doi:10.1002/pros.21265

Cited by 243 publications

(232 citation statements)

References 30 publications

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“…Importantly, the association of PTEN loss with lethal events among ERG fusion-negative tumors was much stronger than that seen for PTEN loss considered without ERG status, and this association remained strong even when considering tumors with heterogeneous PTEN loss. Finally, white men primarily comprise our cohort (97%), so our results may not be generalizable to other racial/ethnic groups, in which ERG expression and PTEN loss may be less frequent (45)(46)(47)(48)(49)(50).…”

Section: Articlementioning

confidence: 99%

A Prospective Investigation of PTEN Loss and ERG Expression in Lethal Prostate Cancer

Ahearn¹,

Pettersson²,

Ebot³

et al. 2015

JNCI.J

164

186

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Section: Articlementioning

confidence: 99%

A Prospective Investigation of PTEN Loss and ERG Expression in Lethal Prostate Cancer

Ahearn¹,

Pettersson²,

Ebot³

et al. 2015

JNCI.J

164

186

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“…[13][14][15] The TMPRSS2-ERG gene fusion is the principle genomic alteration and a characteristic signature in approximately half of all prostate cancers. 14,[16][17][18][19][20][21][22][23] ERG regulates matrix metalloproteinases, thus influencing extracellular matrix remodeling and the invasive potential of malignant cells. [24][25][26][27] PTEN is among the most commonly mutated tumor suppressor genes in human cancer.…”

mentioning

confidence: 99%

PTEN losses exhibit heterogeneity in multifocal prostatic adenocarcinoma and are associated with higher Gleason grade

et al. 2013

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Prostatic adenocarcinoma is an epithelial malignancy characterized by marked histological heterogeneity. It most often has a multifocal distribution within the gland, and different Gleason grades may be present within different foci. Data from our group and others have shown that the genomic deletion of the phosphatase and tensin homolog deleted on chromosome 10 (PTEN) tumor suppressor gene and the disruption of the ETS gene family have a central role in prostate cancer and are likely to be associated with Gleason grade. In this study, prostate cancer samples were systematically analyzed to determine whether there was concordance between PTEN losses and TMPRSS2-ERG fusion rearrangements, within or between foci in multifocal disease, using well-annotated tissue microarrays (TMAs) consisting of 724 cores derived from 142 radical prostatectomy specimens. Three-color fluorescence in situ hybridization analysis of both the PTEN deletion and the TMPRSS2-ERG fusion was used to precisely map genetic heterogeneity, both within and between tumor foci represented on the TMA. PTEN deletion was observed in 56 of 134 (42%) patients (hemizygous ¼ 42 and homozygous ¼ 14). TMPRSS2-ERG fusion was observed in 63 of 139 (45%) patients. When analyzed by Gleason pattern for a given TMA core, PTEN deletions were significantly associated with Gleason grades 4 or 5 over grade 3 (Po0.001). Although TMPRSS2-ERG fusions showed a strong relationship with PTEN deletions (P ¼ 0.007), TMPRSS2-ERG fusions did not show correlation with Gleason grade. The pattern of genetic heterogeneity of PTEN deletion was more diverse than that observed for TMPRSS2-ERG fusions in multifocal disease. However, the marked interfocal discordance for both TMPRSS2-ERG fusions and PTEN deletions was consistent with the concept that multiple foci of prostate cancer arise independently within the same prostate, and that individual tumor foci can have distinct patterns of genetic rearrangements.

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“…13 Such findings are consistent with previous reports on PCa patients in China, 14 as well as those in Japanese and Korean populations. [15][16][17] Two novel gene fusions, CTAGE5-KHDRBS3 and USP9Y-TTTY15, occurred frequently in our patient cohort; 13 further validation in a larger and multicentre population is warranted. These differences may be further utilized in exploring the unique Chinese mechanism upon tumour onset and progression, as a study has confirmed a possible alternative path of carcinogenesis in gene fusion and PTEN inactivation.…”

Section: Gene Fusionmentioning

confidence: 89%

Prostate cancer research in China

Ren¹,

Chen²,

Sun³

2013

Asian J Androl

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Prostate cancer (PCa) research in China has been on a rocketing trend in recent years. The first genome-wide association study (GWAS) in China identified two new PCa risk associated single nucleotide polymorphisms (SNPs). Next generation sequencing is beginning to be used, yielding novel findings: gene fusions, long non-coding RNAs and other variations. Mechanisms of PCa progression have been illustrated while various diagnosis biomarkers have been investigated extensively. Personalized therapy based on genetic factors, nano-medicine and traditional Chinese medicine has been the focus of experimental therapeutic research for PCa. This review intends to shed light upon the recent progress in PCa research in China and points out the possible breakthroughs in the future.

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TMPRSS2–ERG gene fusion prevalence and class are significantly different in prostate cancer of caucasian, african‐american and japanese patients

Cited by 243 publications

References 30 publications

A Prospective Investigation of PTEN Loss and ERG Expression in Lethal Prostate Cancer

A Prospective Investigation of PTEN Loss and ERG Expression in Lethal Prostate Cancer

PTEN losses exhibit heterogeneity in multifocal prostatic adenocarcinoma and are associated with higher Gleason grade

Prostate cancer research in China

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