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Novel, gross chromosomal alterations involving PTEN cooperate with allelic loss in prostate cancer
Alison H M Reid1, Gerhardt Attard, Daniel Brewer
1The Institute of Cancer Research, Sutton, Surrey, UK.
Abstract:
There is increasing evidence that multiple chromosomal rearrangements occur in prostate cancer. PTEN loss is considered to be a key event in prostate carcinogenesis but the mechanisms of loss remain to be fully elucidated. We hypothesised that gross rearrangements may exist that cause disruption of the PTEN gene in the absence of genomic deletion. We therefore designed a novel fluorescence in situ hybridisation (FISH) assay with probes overlying regions 3' and 5' of PTEN and a third probe overlying the gene. We aimed to identify both genomic deletions and gross rearrangements of PTEN that would be overlooked by previously reported single-probe FISH assays. We proceeded to evaluate a tissue microarray with radical prostatectomy and trans-urethral resection of the prostate specimens from 187 patients. We identified PTEN genomic loss in 45/150 (30%) radical prostatectomy patients and 16/37 (43%) trans-urethral resection of the prostate patients. Importantly, our assay detected novel chromosomal alterations in the PTEN gene (characterised by splitting of FISH signals) in 13 tumours (6.9% of all prostate cancers; 21% of PTEN-lost cancers). All PTEN-rearranged tumours had genomic loss at the other allele and had no expression of PTEN by immunohistochemistry. PTEN-rearranged tumours were significantly more likely to have an underlying ERG rearrangement. Our assay differentiated loss of the probe overlying PTEN in isolation or in combination with either one of or both the probes overlying the 3' and 5' regions. This gave an indication of the size of genomic loss and we observed considerable inter-tumoural heterogeneity in the extent of genomic loss in PTEN-lost tumours. In summary, gross rearrangements of the PTEN locus occur in prostate cancer and can be detected by a 'break-apart' FISH assay. This observation could explain the absence of PTEN protein expression in a subgroup of tumours previously classified as having heterozygous genomic loss using single-probe traditional FISH assays.
Insights
Novel fluorescence in situ hybridization (FISH) assays reveal gross rearrangements of the PTEN gene in prostate cancer. This finding explains PTEN loss in some tumors previously thought to have only heterozygous deletion.
Area of Science:
- Genetics and Genomics
- Oncology
- Molecular Biology
Background:
- Prostate cancer involves multiple chromosomal rearrangements.
- PTEN loss is a key event in prostate carcinogenesis, but its mechanisms are not fully understood.
- Previous methods may miss PTEN gene disruptions without complete genomic deletion.
Purpose of the Study:
- To develop and validate a novel fluorescence in situ hybridization (FISH) assay to detect gross rearrangements and deletions of the PTEN gene.
- To investigate the frequency and characteristics of PTEN alterations in prostate cancer specimens.
- To correlate PTEN alterations with PTEN protein expression and other genetic events like ERG rearrangement.
Main Methods:
- Designed a novel FISH assay using three probes: one 5' to PTEN, one 3' to PTEN, and one spanning PTEN.
- Evaluated the assay on a tissue microarray of 187 prostatectomy and trans-urethral resection of the prostate specimens.
- Assessed PTEN protein expression using immunohistochemistry and investigated ERG rearrangement status.
Main Results:
- PTEN genomic loss was identified in 30% of radical prostatectomy and 43% of trans-urethral resection specimens.
- The novel FISH assay detected PTEN gene rearrangements (signal 'break-apart') in 6.9% of all prostate cancers (21% of PTEN-lost cancers).
- All PTEN-rearranged tumors showed loss of the other allele, absent PTEN expression, and were more likely to have ERG rearrangement.
Conclusions:
- Gross rearrangements disrupting the PTEN gene occur in prostate cancer and can be detected by a 'break-apart' FISH assay.
- These rearrangements can lead to PTEN loss and protein expression absence, explaining cases previously misclassified.
- The findings highlight the heterogeneity of PTEN alterations in prostate cancer and their potential link to ERG rearrangements.
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