Jonathan Coloff
University of Illinois Chicago, IL·Biochemistry
Many breast cancers come back years after treatment. Two strategies could help: finding nutrients that some tumors cannot make for themselves, and finding the cells that survive hormone-blocking drugs.
- Fields
Biochemistry
Medicine & Clinical Research
Pharmacology
- Topics
breast cancer
estrogen receptor
endocrine therapy
- Grants
- 2 known grants, through Feb 2028
What they work on
- Determine whether luminal breast tumors, which cannot make the amino acid serine, shrink or stop growing when mice are fed a serine-free diet.
- Define how the serine-making enzyme gene PSAT1 is silenced in luminal breast cancer cells, testing the role of lineage-specific DNA methylation that turns the gene off.
- Identify and characterize the serine transporters that luminal breast cancer cells rely on to import serine, as potential drug targets.
- Define the endocrine therapy-tolerant cell populations in ER+ breast cancer models using single-cell RNA sequencing over time, and validate them in human primary and metastatic tumors.
- Determine how NF-κB, a stress- and survival-signaling protein, is activated in therapy-tolerant cells, and test whether it protects them from treatment-induced stress.
- Test whether blocking NF-κB or its key regulators prevents relapse after endocrine therapy, using patient-derived tumors in immunocompromised mice and an immunocompetent mouse model.
More about the research
The work centers on estrogen receptor-positive (ER+) or "luminal" breast cancer. This is the most common type of breast cancer, and it causes over half of all breast cancer deaths. One project looks at a metabolic weak spot in these tumors. The other looks at a survival signal that lets some tumor cells outlast endocrine therapy, the drugs that block estrogen signaling.
Why it matters
Over half of women with luminal breast cancer eventually stop responding to endocrine therapy, and this disease accounts for most breast cancer deaths. Blocking serine uptake could offer a new treatment option for advanced luminal tumors that cannot make their own serine. Combination treatments that also target NF-κB-driven, therapy-tolerant cells before resistance develops could lower relapse risk for patients with ER+ breast cancer.
Known grants
From NIH and NSF research grants. Labs often have other funding we can't see.
Closest labs
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.
Sean Fanning
Loyola University Chicago, IL·Pharmacology
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.
Steffi Oesterreich
University of Pittsburgh, PA·Medicine & Clinical Research
Compare ILC cell lines, patient-derived organoids, xenografts, homografts and genetically engineered mice with human ILC tumors using histopathology plus genomic, epigenomic and transcriptomic profiling.
The school
University of Illinois Chicago: 42 labs on PI Pages, $532M a year on research, 359 research doctorates a year.
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