No evidence for genomic imprinting of the human BCR gene

Blood. 1994 Jun 15;83(12):3441-4.

Abstract

Chronic myeloid leukemias and 5% to 20% of acute lymphoid leukemias are characterized by the Philadelphia chromosome, a reciprocal chromosomal translocation, t(9;22)(q34;q11), generating BCR-ABL and ABL-BCR fusion genes. Cytogenetic studies have recently shown a preferential involvement of the paternally derived chromosome 9 and the maternally derived chromosome 22 in this translocation, indicating that imprinting might be involved in the formation or selection of the translocation. In this study, we have identified a BamHI polymorphism in the coding region of BCR exon 1, allowing us to investigate whether both BCR alleles are transcribed. By using a reverse transcriptase-polymerase chain reaction assay, we show that both BCR alleles are expressed in the peripheral blood cells of normal individuals.

Publication types

  • Research Support, Non-U.S. Gov't
  • Research Support, U.S. Gov't, P.H.S.

MeSH terms

  • Alleles
  • Base Sequence
  • Fusion Proteins, bcr-abl / genetics
  • Gene Expression*
  • Humans
  • Molecular Sequence Data
  • Oncogene Proteins / genetics*
  • Oncogenes*
  • Polymerase Chain Reaction
  • Polymorphism, Genetic
  • Protein-Tyrosine Kinases*
  • Proto-Oncogene Proteins c-bcr
  • Proto-Oncogene Proteins*

Substances

  • Oncogene Proteins
  • Proto-Oncogene Proteins
  • Protein-Tyrosine Kinases
  • Fusion Proteins, bcr-abl
  • BCR protein, human
  • Proto-Oncogene Proteins c-bcr