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.

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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