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GATA-3 Reporter Plasmids for Revealing Underlying Mechanisms in Breast Cancer

Posted Dec 20 2010 7:00pm

Description of Invention:
Scientists at the National Institutes of Health (NIH) have developed GATA-3 gene reporter plasmids that express a green fluorescent protein (GFP) or luciferase reporter protein under the control of a GATA-3 promoter. Cells expressing this plasmid will glow fluorescent green or emit light energy, respectively, if GATA-3 gene expression is activated in the cells. The reporter construct allows cells where GATA-3 gene expression is activated to be isolated and collected for further analysis or be monitored in the host environment.

GATA-3 is a transcription factor that is highly expressed in several types of cells and is a critical transcription factor for the development of particular lineages of hematopoietic cells and normal mammary luminal epithelium. GATA-3 plays a regulatory role in determining the fate of cells in the hematopoietic systems and the mammary gland. Disruption of GATA-3 expression leads to defects in the development of sub-types of lymphoid cells and luminal mammary epithelial cells. GATA3 expression is highly associated with luminal sub-types of breast cancer, whereas expression of GATA3 is low or undetectable in basal subtypes of breast cancer which often have a poor prognosis. Low or limited GATA-3 expression is correlated with larger tumors, increased likelihood of tumor-positive lymph nodes, and predicts an overall poorer clinical outcome compared to patients with higher mammary GATA-3 expression. Researchers believe that a better understanding of GATA-3 function and its dysregulation during the onset and progression of breast cancer will lead to new strategies in diagnosing and treating the disease.

  • Research tool to help identify factors that modify GATA-3 expression that may serve as potential therapeutic targets for developing drugs to treat breast cancer or hematologic malignancies.
  • Research tool that could be utilized as an important component of a breast cancer diagnostic kit or platform to better understand the most effective treatment options for individual breast cancer patients.
  • Molecular tool to better understand the mechanisms that contribute to hematopoietic and mammary cell/gland development and differentiation in order to identify the critical stages were dysfunction can lead to the onset of breast cancer.
  • Molecular biology laboratory tool for sorting breast cancer positive and negative cells so that further comparative experiments can be performed to understand the cellular properties of the two sets of cells.

  • Useful for in vitro and in vivo assays: Using the GFP or luciferase expression of these reporter plasmids, researchers can identify cells expressing various levels of GATA-3 and isolate these different subsets in vitro. These reporter constructs can also be transfected into cells to measure GATA-3 expression levels in vivo in real time from hematopoietic and breast cancer models.
  • Possible identification of new targets for breast cancer therapy: The reporter plasmids could be utilized to identify factors that serve to activate GATA-3 in normal mammary cells or inhibit GATA-3 expression in breast cancer cells. Such factors could serve as targets for novel breast cancer therapies.

Hosein Kouros-Mehr (NCI)
Jeffrey E Green (NCI)

Patent Status:
HHS, Reference No. E-128-2009/0

Research Tool -- Patent protection is not being pursued for this technology.

Relevant Publication:
  1. H. Kouros-Mehr, et al. GATA-3 and the regulation of the mammary luminal cell fate. Curr Opin Cell Biol. 2008 Apr;20(2):164-170. [ PubMed: 18358709 ]
  2. H. Kouros-Mehr, et al. GATA-3 links tumor differentiation and dissemination in the luminal breast cancer model. Cancer Cell 2008 Feb;13(2):141-152. [ PubMed: 18242514 ]
  3. H. Kouros-Mehr, et al. GATA-3 maintains the differentiation of the luminal cell fate in the mammary gland. Cell 2006 Dec 1;127(5):1041-1055. [ PubMed: 17129787 ]

Licensing Status:
Available for licensing under a Biological Materials License Agreement.

Devices/Instrumentation - Research Tools and Materials
Cancer - Research Materials

For Licensing Information Please Contact:
Samuel Bish Ph.D.
NIH Office of Technology Transfer
6011 Executive Blvd. Suite 325,
Rockville, MD 20852
United States
Phone: 301-435-5282
Fax: 301-402-0220

Ref No: 2207

Updated: 12/2010

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