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Gut 2009;58:1546-1554 doi:10.1136/gut.2009.179531
  • Recent advances in basic science

MicroRNAs: tools for cancer diagnostics

  1. T Paranjape1,
  2. F J Slack2,
  3. J B Weidhaas1
  1. 1
    Department of Therapeutic Radiology, Yale University School of Medicine, New Haven, Connecticut, USA
  2. 2
    Department of Molecular, Cellular and Developmental Biology, Yale University, New Haven, Connecticut, USA
  1. Correspondence to Dr F J Slack, Department of Molecular, Cellular and Developmental Biology, Yale University, PO Box 208103, New Haven, CT 06520, USA; frank.slack{at}yale.edu

    Abstract

    Recently, a novel class of global gene regulators called microRNAs (miRNAs), were identified in both plants and animals. MiRNAs can reduce protein levels of their target genes with a minor impact on the target genes’ mRNAs. Accumulating evidence demonstrates the importance of miRNAs in cancer. MiRNAs that are overexpressed in cancer may function as oncogenes, and miRNAs with tumour suppressor activity in normal tissue may be downregulated in cancer. Although major advances have been achieved in our understanding of cancer biology, as well as in the development of new targeted therapies, the progress in developing improved early diagnosis and screening tests has been inadequate. This results in most cancers being diagnosed in advanced stages, delaying timely treatment and leading to poor outcomes. There is intense research seeking specific molecular changes that are able to identify patients with early cancer or precursor lesions. MiRNA expression data in various cancers demonstrate that cancer cells have different miRNA profiles compared with normal cells, thus underscoring the tremendous diagnostic and therapeutic potential of miRNAs in cancer. These unique properties of miRNAs make them extremely useful potential agents for clinical diagnostics as well as in personalised care for individual patients in the future.

    Footnotes

    • Funding TP was supported by a grant from the Yale Center for Clinical Investigation. FS and JW were supported by NIH CA131301-01A1.

    • Competing interests None.

    • Provenance and Peer review Commissioned; externally peer reviewed.

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