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Updated: Feb 10, 2026
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Isolation of Cancer Stem Cells From Human Prostate Cancer Samples
Published on: March 14, 2014
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Protocols for Studies on TMPRSS2/ERG in Prostate Cancer.
Hubert Pakula1, Douglas E Linn1, Daniel R Schmidt2
1Division of Genetics, Department of Medicine, Brigham and Women's Hospital, Harvard Medical School, Boston, MA, USA.
Methods in Molecular Biology (Clifton, N.J.)
|May 23, 2018
Summary
TMPRSS2/ERG gene fusions are common in prostate cancer, driving early tumor development. These fusions also reveal ETS2 as a prostate tumor suppressor, crucial for cancer progression.
Area of Science:
- Oncology
- Molecular Biology
- Genetics
Background:
- TMPRSS2/ERG gene fusions are the most frequent genetic alterations in human prostate cancer.
- These fusions result in the aberrant expression of ERG (ETS family transcription factor) in prostate cells.
- Approximately 60% of these fusions arise from intrachromosomal deletions between TMPRSS2 and ERG.
Purpose of the Study:
- To create and utilize TMPRSS2/ERG knockin mouse models to study their role in prostate cancer.
- To investigate the early events in prostate tumorigenesis driven by TMPRSS2/ERG.
- To identify potential tumor suppressors within the TMPRSS2-ERG interstitial region.
Main Methods:
- Generation of TMPRSS2/ERG knockin mouse models.
- In vivo and in vitro studies to analyze prostate cancer development.
- Analysis of gene expression and tumor suppressor roles.
Main Results:
- TMPRSS2/ERG acts as an early oncogenic event, sensitizing prostate cells to cooperate with other oncogenic events like PTEN deficiency.
- The interstitial region between TMPRSS2 and ERG contains ETS2, a prostate tumor suppressor.
- Loss of ETS2 contributes to prostate cancer progression.
Conclusions:
- TMPRSS2/ERG knockin mouse models are valuable tools for studying prostate cancer.
- TMPRSS2/ERG is an early driver of prostate cancer, and ETS2 loss contributes to its progression.
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