A method to better predict the likelihood that endocrine therapy alone after surgical intervention will be sufficient to treat patients with estrogen-receptor-positive breast cancer

Tech ID:
2007.008.HSCS
Description:

The University of Texas Health Science Center at San Antonio seeks to partner with a diagnostic products company to develop and commercialize a clinical diagnostic with the potential to determine if a patient with estrogen receptor (ER) positive breast cancer is suitable for treatment with endocrine therapy (e.g., tamoxifen and/or the aromatase inhibitors anastrozole (Arimidex┬«), letrozole (Femara┬«), and others). 

 

Overall, approximately 60-65% of breast cancers are found to be ER-positive upon biopsy.  Estrogen is a growth hormone, and in patients with ER+ breast cancers, estrogen binds to the estrogen receptors in the patient's breast cancer cells and can be thought of as the "fuel" that drives the breast cancer cells.  ER+ breast cancer patients frequently receive endocrine therapy; medications such as tamoxifen (an estrogen agonist/antagonist) or an aromatase inhibitor (used to block estrogen production) with the goal of eliminating the mitogenic effects of estrogen.  Unfortunately, many cancers eventually select for tumor cells that can survive despite the absence of estrogen.  These so-called estrogen (or hormone) insensitive tumors frequently metastasize and are associated with very poor prognosis.  Recent treatment approaches for hormone-insensitive breast cancers include use of the Signal Transduction Inhibitors (STIs), given with the goal of inhibiting EGFR/HER2 receptor signaling thought to be active in hormone insensitive cancers.  However, this approach has not proven particularly effective in combating endocrine resistance, suggesting the involvement of a novel cell survival pathway.  DBC1, a protein involved in many areas of cancer, may be responsible for mediating this novel prosurvival pathway and thus may be an important therapeutic target.

  

DBC1 is upregulated and complexed with ER2 in hormone independent tumor cells.  Drs. Boyer and Trauernicht have discovered that inhibiting the formation of the DBC-1/ER2 complex by siRNA-mediated depletion of cellular DBC-1 results in rapid apoptosis.  This suggests the complex is at least partially responsible for cancer cell survival in ER+ hormone independent breast cancer cells, and that disrupting the formation of the DBC-1/ER2 complex by siRNA or other means may result in a meaningful improvement in clinical outcomes.  The researchers are developing an assay to identify other complex-formation inhibitors and are available for collaboration to this end.

 

Market Applications:

For patients with ER+ hormone independent breast cancers:

  • Treatment:  chemo/radiation adjuvant for treatment refractory cancers
  • Prevention:  used in conjunction with standard of care estrogen ablation therapies, prevent the progression of hormone sensitive tumors into hormone-independent breast cancers by eliminating the selection of tumor cells able to survive in the absence of estrogen via the DBC-1 pathway

 

Benefits and Advantages:

  • Addresses a great unmet need: another treatment option for patients with advanced ER+ breast cancer
  • Potentially improve overall survival by stopping development of treatment-resistant breast cancers,
  • Decrease overall healthcare system costs associated with the emergence of treatment resistant cancers

IP Status:  U.S. Pat. No. 7,807,383, issued October 5, 2010

Patent Information:
Category(s):
Diagnostics
For information contact:
Daniel Rafferty
Business Development Manager
Office of Technology Commercialization
raffertyde@uthscsa.edu
Inventors:
Amy Trauernicht
Thomas Boyer
Keywords:
Biologics
Drugs