Skip NavigationSkip to Content
Return Return to Search Results

Expression of candidate chromosome 3p21.3 tumor suppressor genes and down-regulation of BLU in some esophageal squamous cell carcinomas

  1. Author:
    Lo, P. H. Y.
    Leung, A. C. C.
    Xiong, W. J.
    Law, S.
    Duh, F. M.
    Lerman, M. I.
    Stanbridge, E. J.
    Lung, M. L.

  2. Author Address

    Hong Kong Univ Sci & Technol, Dept Biol, Kowloon, Hong Kong, Peoples R China. Univ Hong Kong, Dept Surg, Hong Kong, Hong Kong, Peoples R China. SAIC Frederick Inc, NCI, Basic Res Program, Frederick, MD USA. NCI, Immunobiol Lab, Frederick, MD 21701 USA. Univ Calif Irvine, Coll Med, Dept Microbiol & Mol Genet, Irvine, CA 92717 USA.;Lung, ML, Hong Kong Univ Sci & Technol, Dept Biol, Clear Water Bay, Kowloon, Hong Kong, Peoples R China.;bomaria@ust.hk
    1. Year: 2006
    2. Date: Mar
  2. Journal: Cancer Letters
    1. 234
    2. 2
    3. Pages: 184-192
  4. Type of Article: Article
  5. ISSN: 0304-3835
  1. Abstract:

    dThe expression of six chromosome 3p21.3 candidate tumor suppressor genes (BLU, FUS2, HYAL2, NPRL2, RASSF1A, and SEMA3B) in esophageal squamous cell carcinoma (ESCC) has been investigated. Reduced expression of BLU was detected in some ESCC cell lines and tumor tissues and the difference was quantitated by real-time quantitative polymerase chain reaction. Methylation specific-PCR revealed the down-regulation of BLU by epigenetic inactivation. However, exogeneous expression of BLU did not functionally suppress tumofigenicity in nude mice. These results suggest that over-expression of BLU alone is not sufficient to inhibit tumorigenicity. Further studies on BLU interacting proteins are required to elucidate the possible role of BLU in the development of ESCC. (c) 2005 Elsevier Ireland Ltd. All rights reserved.

    See More

  1. Keywords:

External Sources

  1. View Full Text
  2. DOI: 10.1016/j.canlet.2005.03.036
  3. View record in Web of Science®
  4. WOS: 000236661400009

Library Notes

  1. No notes added.
NCI at Frederick

You are leaving a government website.

This external link provides additional information that is consistent with the intended purpose of this site. The government cannot attest to the accuracy of a non-federal site.

Linking to a non-federal site does not constitute an endorsement by this institution or any of its employees of the sponsors or the information and products presented on the site. You will be subject to the destination site's privacy policy when you follow the link.

ContinueCancel