Analysis of the Smad2 gene in hematological malignancies

Leukemia. 1998 Jan;12(1):94-5. doi: 10.1038/sj.leu.2400888.

Abstract

A total of 34 leukemia and lymphoma samples (17 clinical samples and 17 cell lines) were analyzed for mutations of the Smad2 gene by reverse transcriptase-polymerase chain reaction single strand conformation polymorphism (RT-PCR-SSCP) analysis. Nine of the 34 samples had 18q chromosomal abnormalities. No shifted bands were detected in any of the hematological malignancies. Our results suggest that resistance to cell growth inhibitory effects of TGF-beta in hematological malignancies is not due to alterations of the Smad2 gene.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Adolescent
  • Adult
  • Aged
  • Aged, 80 and over
  • Burkitt Lymphoma / genetics
  • Burkitt Lymphoma / immunology
  • Chromosome Aberrations*
  • Chromosome Deletion
  • Chromosome Disorders*
  • Chromosome Mapping
  • Chromosomes, Human, Pair 14
  • Chromosomes, Human, Pair 18*
  • DNA-Binding Proteins / genetics*
  • Genes, Tumor Suppressor*
  • Humans
  • Immunophenotyping
  • Leukemia, Myeloid, Acute / classification
  • Leukemia, Myeloid, Acute / genetics*
  • Lymphoma, Non-Hodgkin / genetics*
  • Middle Aged
  • Precursor Cell Lymphoblastic Leukemia-Lymphoma / classification
  • Precursor Cell Lymphoblastic Leukemia-Lymphoma / genetics*
  • Precursor Cell Lymphoblastic Leukemia-Lymphoma / immunology
  • Smad2 Protein
  • Trans-Activators*
  • Translocation, Genetic
  • Tumor Cells, Cultured

Substances

  • DNA-Binding Proteins
  • SMAD2 protein, human
  • Smad2 Protein
  • Trans-Activators