Background: Phosphatase and tensin homolog (PTEN) gene aberration and trans membrane protease, serine 2 (TMPRSS2)-v-ets avian erythroblastosis virus E26 oncogene homolog (ERG) fusion are the most prevalent genomic events in prostate cancer. In this study we aimed to evaluate the frequency of PTEN alteration and TMPRSS2-ERG fusion and possible link between these two biomarkers in Iranian men.
Methods: We assessed 42 fresh frozen tissue samples of prostate cancer (PCA) obtained by radical prostatectomy, interrogating the TMPRSS2-ERG fusion gene along with PTEN gene status using Real Time PCR and FISH methods.
Results: Using Real Time PCR we identified the TMPRSS2-ERG fusion in 64% (27/42) of tumor samples, which was confirmed by FISH technique, giving 21 positive samples with deletion, suggesting the presence of TMPRSS2-ERG fusion gene. By contrast, PTEN deletion was detected in 52% (11/21) of PCA samples, which all showed low expression in Real Time. Concomitance of PTEN deletion or low expression and TMPRSS2-ERG fusion was present in PCA samples (P=0.005). All of the PTEN deletion samples showed TMPRSS2-ERG fusion, (11/11, 100%) while not all of the TMPRSS2-ERG fusion positive samples showed PTEN deletion. None of 29 cases of BPH and 8 cases of normal zone of tumor tissue showed TMPRSS2-ERG fusion.
Conclusions: These results indicate that PTEN loss occurs in cooperation with TMPRSS2-ERG fusion in PCA. While the majority of PCA samples harbor TMPRSS2-ERG fusion as well as PTEN gene deletion, normal tissues do not show these molecular aberrations.
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http://dx.doi.org/10.1016/j.gene.2015.09.068 | DOI Listing |
Int J Cancer
December 2024
Department of Epidemiology, Harvard T. H. Chan School of Public Health, Boston, MA, USA.
The most common somatic alteration in primary prostate cancer is the TMPRSS2:ERG gene fusion, which may be caused or promoted by distinct etiologic factors. The objective of this systematic review was to assess epidemiologic evidence on etiologic factors for prostate cancer by tumor TMPRSS2:ERG fusion status in human populations. Of 3071 publications identified, 19 cohort or case-control studies from six distinct study populations were included in this systematic review.
View Article and Find Full Text PDFFront Biosci (Landmark Ed)
September 2024
Department of Anesthesiology, Reanimatology and Narcology, Semey Medical University, 071400 Semey, Republic of Kazakhstan.
Chromosomal rearrangements and recurrent gene fusions were previously presumed to be the primary oncogenic mechanisms of hematological malignancies. However, the discovery of gene fusions in different cancers has opened new horizons to comprehensively investigate how cell type-specific fusion oncoproteins modulate signaling cascades. Prostate cancer (PCa) is a multifaceted and therapeutically challenging disease, and functional genomics have helped us develop a better understanding of the mechanisms underlying prostate carcinogenesis, castration-resistant PCa, and metastasis.
View Article and Find Full Text PDFCytojournal
August 2024
Department of Urology, The First Affiliated Hospital of Anhui Medical University, Hefei, Anhui, China.
In the ever-evolving landscape of oncology, the battle against prostate cancer (PCa) stands at a transformative juncture, propelled by the integration of molecular diagnostics into traditional cytopathological frameworks. This synthesis not only heralds a new epoch of precision medicine but also significantly enhances our understanding of the disease's genetic intricacies. Our comprehensive review navigates through the latest advancements in molecular biomarkers and their detection technologies, illuminating the potential these innovations hold for the clinical realm.
View Article and Find Full Text PDFAnticancer Res
October 2024
Molecular Unit, Department of Pathology, Herlev Hospital, Herlev, Denmark.
Background/aim: The emergence of novel DNA damage repair (DDR) pathways in molecular-target therapy drugs (MTTD) has shown promising outcomes in treating patients with metastatic castration-resistant prostate cancer (mCRPC). About 25% of mCRPC patients have actionable deleterious aberrations in DDR genes, primarily in the homologous recombination (HR) pathway. However, the response rate in patients with BRCA1/2 or mutations in HRR-related genes is only 45%-55%, when exposed to poly ADP ribose polymerase (PARP) inhibitor-based therapy (PARPi).
View Article and Find Full Text PDFMod Pathol
September 2024
Department of Pathology and Laboratory Medicine, Memorial Sloan Kettering Cancer Center, New York, New York. Electronic address:
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