A variant of DNA polymerase β is not cancer specific

Dawei Bu, Leslie R. Cler, Cheryl M. Lewis, David M. Euhus

Research output: Contribution to journalArticlepeer-review

4 Scopus citations


DNA Polymerase β (Pol β) carries out base-excision repair (BER) required for DNA maintenance, replication, and recombination in eukaryotic cells. A variant characterized by a deletion of exon 11, an 87-bp region in the catalytic domain (pol βΔ208-236), was previously described as a possible cause of genomic instability in cancer. The variant form was hypothesized to act in a dominant negative fashion, due to the fact that the variant inhibits the gap filling and DNA binding activities of the wild-type pol β protein. DNA polymerase β transcripts were analyzed in 8 breast cancer cell lines, snap-frozen benign breast tissues from 10 women, and lymphocytes from 10 normal controls, using reverse-transcription polymerase chain reaction (RT-PCR) and three separate primer pairs. The exon 10-12 splice site (variant) was identified using a primer designed to span the spliced exons and by sequencing RT-PCR products that included exon 10, exon 11 (if present), and exon 12. In all of the samples tested, we found both the wild-type and exon 11 87-bp deleted variant mRNAs expressed. We conclude that expression of the DNA polymerase β variant (pol βΔ208-236) is ubiquitous and not breast cancer specific.

Original languageEnglish (US)
Pages (from-to)327-331
Number of pages5
JournalJournal of Investigative Surgery
Issue number6
StatePublished - Nov 2004
Externally publishedYes


  • Breast cancer
  • DNA polymerase β
  • Polymerase β δ208-236

ASJC Scopus subject areas

  • Surgery


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