3p21.3 tumor suppressor cluster: Prospects for translational applications

Lin Ji, John D. Minna, Jack A. Roth

Research output: Contribution to journalArticle

Abstract

Chromosomal abnormalities at the 3p21.3 region, including homozygous deletions and loss of heterozygosity and expressional deficiencies in 3p21.3 genes including transcriptional silences by promoter hypermethylation, altered mRNA splicing and aberrant transcripts, and lost or defect protein translation and post-translational modifications, are frequently found in most human cancers. Inactivation of 3p21.3 genes in primary tumors affects a wide spectrum of key biological processes such as cell proliferation, cell cycle kinetics, signaling transduction, ion exchange and transportation, apoptosis and cell death, and demonstrates the molecular signatures of carcinogenesis. Restoration of defective 3p21.3 genes with several wild-type 3p21.3 genes suppresses tumor cell growth both in vitro and in vivo. These findings suggest several 3p21.3 genes as potential tumor suppressors and implicates these 3p21.3 genes for future development as biomarkers for the early detection and diagnosis of cancer, and as prognostic and therapeutic tools for cancer prevention and molecular cancer therapy.

Original languageEnglish (US)
Pages (from-to)79-92
Number of pages14
JournalFuture Oncology
Volume1
Issue number1
DOIs
StatePublished - Feb 2005

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Neoplasms
Genes
Early Detection of Cancer
Biological Phenomena
Loss of Heterozygosity
Ion Exchange
Protein Biosynthesis
Gene Silencing
Post Translational Protein Processing
Chromosome Aberrations
Cell Cycle
Carcinogenesis
Cell Death
Biomarkers
Cell Proliferation
Apoptosis
Messenger RNA
Therapeutics
Growth
In Vitro Techniques

Keywords

  • 3p21.3 region
  • Human cancers
  • Molecular cancer therapy
  • Tumor suppressor genes

ASJC Scopus subject areas

  • Oncology
  • Cancer Research

Cite this

3p21.3 tumor suppressor cluster : Prospects for translational applications. / Ji, Lin; Minna, John D.; Roth, Jack A.

In: Future Oncology, Vol. 1, No. 1, 02.2005, p. 79-92.

Research output: Contribution to journalArticle

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