Sean Fanning
Loyola University Chicago, IL·Pharmacology
Many breast cancers are fueled by estrogen and are treated with hormone therapies that block the estrogen receptor. Estrogen receptor alpha (ERα) is the protein that senses estrogen and switches on growth genes.
- Fields
Pharmacology
Biochemistry
Medicine & Clinical Research
- Topics
breast cancer
estrogen receptor alpha
ERα
- Grants
- 1 known grant, through Apr 2028
What they work on
- Determine how a library of more than 100 SERMs and SERDs bind to and reshape mutant Y537S estrogen receptor alpha, using X-ray co-crystal structures and anti-cancer assays in breast cancer cells.
- Test whether the most effective compounds work by changing Y537S ERα genomic activity, including its protein partners, where it binds the genome, and which genes it switches on.
- Measure anti-tumor and tissue-specific activity of the best SERMs and SERDs in hormone-resistant ER-positive breast cancer models in vivo.
More about the research
Over time, many tumors stop responding to these drugs. In about 40% of progressing ER-positive patients, tumors acquire mutations in ESR1, the gene that encodes ERα. These mutations keep the receptor active even without hormone, help it resist approved drugs, and switch on gene programs that promote spread. Y537S, a single amino-acid change, is among the most common of these mutations and the most drug-resistant. Newer drugs called selective estrogen receptor degraders (SERDs), which push the receptor to be destroyed, work unevenly against it and have side effects.
Why it matters
Resistance to hormone therapy is a leading cause of death from ER-positive breast cancer, the second leading cause of cancer death in the United States. Clarifying which drug-receptor interactions best block the Y537S mutant could guide the design of more effective, better-tolerated antiestrogen drugs for patients whose tumors carry ESR1 mutations.
Known grants
From NIH and NSF research grants. Labs often have other funding we can't see.
Closest labs
Jing Yang
University of California-San Diego, CA·Biochemistry
Determine how the Hippo pathway, through the LATS1/2 kinases, controls transcription of ESR1, the main estrogen receptor gene, in breast cells and what ESR1 contributes to Hippo biology in breast tissue.
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.
Deeann Wallis-Schultz
University of Alabama at Birmingham, AL·Genetics
Track tumor onset, growth, histology and molecular changes in Ras and estrogen signaling over time in Nf1 knockin (p.R1276Q) and knockout rats, comparing findings with human breast tumor samples.
The school
Loyola University Chicago: 8 labs on PI Pages, $61M a year on research, 156 research doctorates a year.
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