Localization of SMAD5 and its evaluation as a candidate myeloid tumor suppressor

Cancer Res. 1997 Sep 1;57(17):3779-83.

Abstract

Acquired interstitial or complete losses of chromosome 5 are recurring anomalies associated with preleukemic myelodysplasia and acute myelogenous leukemia with a poor prognosis. Previous studies have delineated a potential myeloid tumor suppressor locus to a <2.4-Mb interval between the genes for IL9 and EGR1 on 5q31. In this report, we have localized the SMAD5 gene, a homologue of the tumor suppressor genes SMAD4/DPC-4 and SMAD2/JV18.1, to the minimal myeloid tumor suppressor locus and characterized its open reading frame and genomic organization. SMAD5 transcripts are readily detectable in hematolymphoid tissues and leukemic blasts. Absence of intragenic mutations in the remaining SMAD5 allele of leukemic patients and multiple solid tumor cell lines prescreened for loss of heterozygosity suggests that SMAD5 may not be a common target of somatic inactivation in malignancy.

Publication types

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

MeSH terms

  • Base Sequence
  • Chromosome Mapping*
  • Chromosomes, Human, Pair 5 / genetics*
  • DNA, Complementary / genetics
  • DNA-Binding Proteins*
  • Genes, Tumor Suppressor / genetics*
  • Genetic Markers
  • Humans
  • Leukemia, Myeloid, Acute / genetics*
  • Molecular Sequence Data
  • Myelodysplastic Syndromes / genetics
  • Neoplasm Proteins / genetics*
  • Neoplasm Proteins / metabolism
  • Open Reading Frames / genetics
  • Phosphoproteins / genetics*
  • Phosphoproteins / metabolism
  • Sequence Analysis, DNA
  • Smad5 Protein
  • Trans-Activators*

Substances

  • DNA, Complementary
  • DNA-Binding Proteins
  • Genetic Markers
  • Neoplasm Proteins
  • Phosphoproteins
  • SMAD5 protein, human
  • Smad5 Protein
  • Trans-Activators