Cargando…

Genomic Rearrangements of PTEN in Prostate Cancer

The phosphatase and tensin homolog gene (PTEN) on chromosome 10q23.3 is a negative regulator of the PIK3/Akt survival pathway and is the most frequently deleted tumor suppressor gene in prostate cancer. Monoallelic loss of PTEN is present in up to 60% of localized prostate cancers and complete loss...

Descripción completa

Detalles Bibliográficos
Autores principales: Phin, Sopheap, Moore, Mathew W., Cotter, Philip D.
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Frontiers Media S.A. 2013
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3775430/
https://www.ncbi.nlm.nih.gov/pubmed/24062990
http://dx.doi.org/10.3389/fonc.2013.00240
_version_ 1782477379713630208
author Phin, Sopheap
Moore, Mathew W.
Cotter, Philip D.
author_facet Phin, Sopheap
Moore, Mathew W.
Cotter, Philip D.
author_sort Phin, Sopheap
collection PubMed
description The phosphatase and tensin homolog gene (PTEN) on chromosome 10q23.3 is a negative regulator of the PIK3/Akt survival pathway and is the most frequently deleted tumor suppressor gene in prostate cancer. Monoallelic loss of PTEN is present in up to 60% of localized prostate cancers and complete loss of PTEN in prostate cancer is linked to metastasis and androgen-independent progression. Studies on the genomic status of PTEN in prostate cancer initially used a two-color fluorescence in situ hybridization (FISH) assay for PTEN copy number detection in formalin fixed paraffin embedded tissue preparations. More recently, a four-color FISH assay containing two additional control probes flanking the PTEN locus with a lower false-positive rate was reported. Combined with the detection of other critical genomic biomarkers for prostate cancer such as ERG, androgen receptor, and MYC, the evaluation of PTEN genomic status has proven to be invaluable for patient stratification and management. Although less frequent than allelic deletions, point mutations in the gene and epigenetic silencing are also known to contribute to loss of PTEN function, and ultimately to prostate cancer initiation. Overall, it is clear that PTEN is a powerful biomarker for prostate cancer. Used as a companion diagnostic for emerging therapeutic drugs, FISH analysis of PTEN is promisingly moving human prostate cancer closer to more effective cancer management and therapies.
format Online
Article
Text
id pubmed-3775430
institution National Center for Biotechnology Information
language English
publishDate 2013
publisher Frontiers Media S.A.
record_format MEDLINE/PubMed
spelling pubmed-37754302013-09-23 Genomic Rearrangements of PTEN in Prostate Cancer Phin, Sopheap Moore, Mathew W. Cotter, Philip D. Front Oncol Oncology The phosphatase and tensin homolog gene (PTEN) on chromosome 10q23.3 is a negative regulator of the PIK3/Akt survival pathway and is the most frequently deleted tumor suppressor gene in prostate cancer. Monoallelic loss of PTEN is present in up to 60% of localized prostate cancers and complete loss of PTEN in prostate cancer is linked to metastasis and androgen-independent progression. Studies on the genomic status of PTEN in prostate cancer initially used a two-color fluorescence in situ hybridization (FISH) assay for PTEN copy number detection in formalin fixed paraffin embedded tissue preparations. More recently, a four-color FISH assay containing two additional control probes flanking the PTEN locus with a lower false-positive rate was reported. Combined with the detection of other critical genomic biomarkers for prostate cancer such as ERG, androgen receptor, and MYC, the evaluation of PTEN genomic status has proven to be invaluable for patient stratification and management. Although less frequent than allelic deletions, point mutations in the gene and epigenetic silencing are also known to contribute to loss of PTEN function, and ultimately to prostate cancer initiation. Overall, it is clear that PTEN is a powerful biomarker for prostate cancer. Used as a companion diagnostic for emerging therapeutic drugs, FISH analysis of PTEN is promisingly moving human prostate cancer closer to more effective cancer management and therapies. Frontiers Media S.A. 2013-09-17 /pmc/articles/PMC3775430/ /pubmed/24062990 http://dx.doi.org/10.3389/fonc.2013.00240 Text en Copyright © 2013 Phin, Moore and Cotter. http://creativecommons.org/licenses/by/3.0/ This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY). The use, distribution or reproduction in other forums is permitted, provided the original author(s) or licensor are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms.
spellingShingle Oncology
Phin, Sopheap
Moore, Mathew W.
Cotter, Philip D.
Genomic Rearrangements of PTEN in Prostate Cancer
title Genomic Rearrangements of PTEN in Prostate Cancer
title_full Genomic Rearrangements of PTEN in Prostate Cancer
title_fullStr Genomic Rearrangements of PTEN in Prostate Cancer
title_full_unstemmed Genomic Rearrangements of PTEN in Prostate Cancer
title_short Genomic Rearrangements of PTEN in Prostate Cancer
title_sort genomic rearrangements of pten in prostate cancer
topic Oncology
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3775430/
https://www.ncbi.nlm.nih.gov/pubmed/24062990
http://dx.doi.org/10.3389/fonc.2013.00240
work_keys_str_mv AT phinsopheap genomicrearrangementsofpteninprostatecancer
AT moorematheww genomicrearrangementsofpteninprostatecancer
AT cotterphilipd genomicrearrangementsofpteninprostatecancer