Burkitt-like mutations in the c-myc gene locus in prolymphocytic leukemia

Leukemia. 1994 May;8(5):897-902.

Abstract

The c-myc oncogene recently shown to act as a transcription factor, is involved in cellular proliferation. Deregulation of this gene can be one step in malignant transformation. In Burkitt's lymphoma (BL) the c-myc gene is consistently involved in chromosomal translocations and the first exon of the gene has been found to be a frequent target of somatic mutations. These mutations are believed to interfere with normal transcriptional regulation of the gene. We demonstrate a case of the rare prolymphocytic leukemia (PLL), a variant of chronic lymphocytic leukemia (CLL), that shows multiple Burkitt-like mutations in the first exon of c-myc and one nonconservative point mutation in the coding exon 2. Cytogenetic analysis revealed involvement of both chromosomes 8 in chromosomal translocations. Both chromosomes 8 are broken at (q23), the c-myc gene locus. Since the patient's leukemia cells exhibited high expression levels of the mutated allele of the c-myc mRNA, the point mutations alone may have accounted for transcriptional deregulation.

Publication types

  • Case Reports

MeSH terms

  • Amino Acid Sequence
  • Base Sequence
  • Burkitt Lymphoma / genetics*
  • Chromosome Fragility
  • Chromosomes, Human, Pair 8
  • Chronic Disease
  • Exons
  • Genes, myc / genetics*
  • Humans
  • Karyotyping
  • Leukemia, Prolymphocytic / genetics*
  • Male
  • Middle Aged
  • Molecular Sequence Data
  • Point Mutation*
  • Polymerase Chain Reaction

Associated data

  • GENBANK/S70385
  • GENBANK/S70386