Sabine Brouxhon
University of Rochester, NY·Pharmacology
Targeted breast cancer drugs such as trastuzumab, an antibody against the HER2 growth receptor, and the hormone therapy tamoxifen have improved survival, but most patients with metastatic disease stop responding within about a year. One common escape route is the insulin-like growth factor 1 receptor (IGF-1R), a growth-signaling receptor on the cell surface that, when overexpressed or overactive, keeps tumor cells growing through downstream survival pathways.
- Fields
Pharmacology
Biochemistry
Medicine & Clinical Research
- Topics
breast cancer
soluble E-cadherin
sEcad
- Grants
- 1 known grant, last ended Aug 2026
What they work on
- Characterize how soluble E-cadherin (sEcad) binds and activates the IGF-1R growth receptor, using purified IGF-1R holoreceptor and biochemical and biophysical binding and phosphorylation measurements, including synergy with the natural ligands IGF-1 and EGF.
- Test whether antibodies targeting sEcad suppress IGF-1R-expressing breast cancers, in hormone-receptor-positive and trastuzumab-resistant cell lines and in xenograft and MMTV-PyMT mouse tumor models.
- Define how anti-sEcad antibodies down-regulate the IGF-1R, HER, and MAPK-PI3K/Akt/mTOR-IAP signaling axis and whether this drives apoptosis and necrosis in tumor but not normal cells.
- Evaluate anti-sEcad antibodies in rodents for efficacy, pharmacokinetics and pharmacodynamics, and off-target effects, to assess suitability for further therapeutic development.
More about the research
Antibodies aimed directly at IGF-1R have given mixed clinical results, so this project pursues a different point of attack.
Why it matters
Breast cancer is the most common cancer in women, and resistance to HER2- and hormone-directed therapy limits how long current treatments work. If soluble E-cadherin really acts as a growth-receptor ligand, antibodies against it could become a distinct class of IGF-1R inhibitor for patients whose tumors no longer respond to trastuzumab or hormone therapy, and sEcad levels may also help flag tumors likely to be resistant.
Known grants
From NIH and NSF research grants. Labs often have other funding we can't see.
Closest labs
Jonathan Coloff
University of Illinois Chicago, IL·Biochemistry
Determine whether luminal breast tumors, which cannot make the amino acid serine, shrink or stop growing when mice are fed a serine-free diet.
John Fowlkes
University of Kentucky, KY·Physiology
Determine how deficiencies of insulin and insulin-like growth factor 1 (IGF-1) each contribute to diabetic bone disease at the tissue, cellular and molecular levels in models of type 1 diabetes.
Cornelia Peterson
Tufts University, MA·Medicine & Clinical Research·Early-career
Test how turning the insulin/insulin-like growth factor signaling (IIS) pathway up or down with drugs and genetic tools changes MYC levels, behavior and gene activity in cultured normal and tumor meibocytes, the oil-producing eyelid gland cells.
The school
University of Rochester: 38 labs on PI Pages, $492M a year on research, 308 research doctorates a year.
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