Related Experiment Video
Updated: Jul 10, 2026

Microarray-based Identification of Individual HERV Loci Expression: Application to Biomarker Discovery in Prostate Cancer
Published on: November 2, 2013
Prostate cancer risk and ESR1 TA, ESR2 CA repeat polymorphisms
Matthew H McIntyre1, Philip W Kantoff, Meir J Stampfer
1Channing Laboratory, Department of Medicine, Brigham and Women's Hospital and Harvard Medical School, 181 Longwood Avenue, Boston, MA 02115, USA. mmcintyr@mail.ucf.edu
Specific variations in the estrogen receptor alpha (ESR1) gene, specifically the TA repeat polymorphism, may increase prostate cancer risk. The estrogen receptor beta (ESR2) gene showed no association with risk.
Area of Science:
- Genetics
- Oncology
- Molecular Biology
Background:
- Estrogen receptor alpha (ESR1) gene variants are hypothesized to elevate prostate cancer risk.
- Estrogen receptor beta (ESR2) gene variants are hypothesized to decrease prostate cancer risk.
Purpose of the Study:
- To investigate the association between TA repeat polymorphism in the ESR1 gene (ESR1 (TA)(n)) and prostate cancer risk.
- To investigate the association between CA repeat polymorphism in the ESR2 gene (ESR2 (CA)(n)) and prostate cancer risk.
Main Methods:
- A case-control study was conducted within the Physicians' Health Study, including 545 cases and 674 controls.
- Genotyping focused on the ESR1 (TA)(n) and ESR2 (CA)(n) polymorphisms.
Main Results:
- Carriers of ESR1 (TA)(24) and ESR1 (TA)(25) exhibited the highest prostate cancer risk.
- An increased risk of prostate cancer was observed with specific ESR1 (TA)(n) alleles (OR=1.42 for TA(24), OR=2.10 for TA(25)).
- No significant association was found between ESR2 (CA)(n) polymorphism and prostate cancer risk.
Conclusions:
- The ESR1 (TA)(n) polymorphism may influence an individual's susceptibility to prostate cancer.
- ESR2 (CA)(n) polymorphism does not appear to affect prostate cancer risk.
Related Concept Videos
Non-LTR Retrotransposons
Pharmacogenetics of Drug Targets: β₂-Adrenergic Receptors, Apo E, Thymidylate Synthase
Nucleotide Excision Repair
Cells are regularly exposed to mutagens—factors in the environment that can damage DNA and generate mutations. UV radiation is one of the most common mutagens and is estimated to introduce a significant number of changes in DNA. These include bends or kinks in the structure, which can block DNA replication or transcription. If these errors are not fixed, the damage can cause mutations, which in turn can result in cancer or disease depending on which sequences are...

