Frequent polymorphism in BCR exon b2 identified in BCR-ABL positive and negative individuals using fluorescent hybridization probes

Leukemia. 2000 Nov;14(11):2006-10. doi: 10.1038/sj.leu.2401929.

Abstract

Recently, a polymorphic base in exon 13 of the BCR gene (exon b2 of the major breakpoint cluster region) has been identified in the eighth position before the junctional region of BCR-ABL cDNA. Cytosine replaces thymidine; the corresponding triplets are AAT (T allele) and AAC (C allele), respectively, both coding for asparagine. Therefore, this polymorphism has no implication in the primary structure of BCR and BCR-ABL proteins. However, since the alteration is located close to the fusion region it may have a significant influence on the annealing of PCR primers, probes for real time PCR, and antisense oligonucleotides. We have developed a RT-PCR-based screening method to easily identify polymorphic BCR and BCR-ABL alleles in CML patients and normal individuals in order to estimate their frequency. After amplification from cDNA, a melting curve of a specific fluorogenic probe mapping to the 3' end of BCR exon b2 and spanning the polymorphism readily discriminates between normal and polymorphic BCR and BCR-ABL alleles. This reporter probe is 3' labeled with fluorescein and placed next to 5' LC Red640-labeled anchor probes mapping to the 5' ends of BCR exon b3 or ABL exon a2 so that resonance energy transfer occurs when the probes are hybridized (LightCycler technology). T and C alleles were discriminated by a melting temperature difference of the reporter probe of 3.2 K. We have investigated cDNAs derived from leukocytes from seven cell lines and a total of 229 individuals: normal donors, n = 15; BCR-ABL negative chronic myeloproliferative disorders, n=30; BCR-ABL negative acute leukemias, n= 11; b2a2BCR-ABL positive CML, n = 93; and b3a2BCR-ABL positive CML, n= 80. The frequency of the C allele was 33.0% in BCR-ABL negative individuals, 30.6% in b2a2BCR-ABL, and 23.8% in b3a2BCR-ABL positive CML. In CML patients, 27.7% of BCR-ABL and 27.2% of BCR alleles had the C allele (NS). In total, 132 of 458 (28.8%) exons b2 of BCR or BCR-ABL alleles demonstrated this polymorphism. We conclude that a thymidine/cytosine replacement occurs frequently in BCR exon b2. Probes for real time quantitative RT-PCR should be designed not to map to the critical region in order to avoid underestimation of the number of BCR-ABL transcripts.

Publication types

  • Comparative Study

MeSH terms

  • Acute Disease
  • Alleles
  • Amino Acid Substitution*
  • Chromosomes, Human, Pair 22 / genetics*
  • DNA Mutational Analysis
  • DNA, Complementary / genetics
  • Exons / genetics*
  • False Negative Reactions
  • Fluorescent Dyes
  • Fusion Proteins, bcr-abl / analysis
  • Fusion Proteins, bcr-abl / genetics*
  • Humans
  • Leukemia / genetics
  • Leukemia, Myelogenous, Chronic, BCR-ABL Positive / genetics
  • Myeloproliferative Disorders / genetics
  • Neoplasm Proteins / genetics
  • Nucleic Acid Denaturation
  • Nucleic Acid Hybridization
  • Oligonucleotide Probes
  • Point Mutation*
  • Polymorphism, Genetic*
  • Protein-Tyrosine Kinases*
  • Proto-Oncogene Proteins / genetics*
  • Proto-Oncogene Proteins c-bcr
  • Reference Values
  • Reverse Transcriptase Polymerase Chain Reaction
  • Tumor Cells, Cultured

Substances

  • DNA, Complementary
  • Fluorescent Dyes
  • Neoplasm Proteins
  • Oligonucleotide Probes
  • Proto-Oncogene Proteins
  • Protein-Tyrosine Kinases
  • Fusion Proteins, bcr-abl
  • BCR protein, human
  • Proto-Oncogene Proteins c-bcr