Xiangshu Xiao
Oregon Health & Science University, OR·Pharmacology
Triple negative breast cancer (TNBC) is a breast cancer type that lacks the estrogen receptor, the progesterone receptor and extra copies of HER2, a growth signal receptor. Because it lacks these three targets, it does not respond to drugs aimed at them.
- Fields
Pharmacology
Chemistry
Medicine & Clinical Research
- Topics
triple negative breast cancer
RuvBL1
RuvBL2
- Grants
- 1 known grant, through Jun 2028
What they work on
- Determine the mechanism by which a new small-molecule lead compound targets the RuvBL1/L2 protein complex to block DNA double-strand break repair in triple negative breast cancer cells.
- Optimize the RuvBL1/L2-targeting lead compound using medicinal chemistry strategies to produce improved inhibitors.
- Test the anti-tumor efficacy of optimized RuvBL1/L2 inhibitors in preclinical TNBC models, both alone and combined with PARP inhibitors.
More about the research
TNBC cells are under constant stress from rapid DNA copying and reactive oxygen species, so they keep breaking both strands of their DNA. To survive, they rely heavily on efficient repair of these double-strand breaks. Blocking that repair could therefore kill cancer cells selectively while sparing normal cells, which face far fewer such breaks.
Why it matters
Patients with triple negative breast cancer lack targeted treatment options. Inhibitors of the RuvBL1/L2 complex could become new therapeutic agents that exploit these tumors' dependence on DNA repair. Pairing them with PARP inhibitors may also prove useful.
Known grants
From NIH and NSF research grants. Labs often have other funding we can't see.
Closest labs
Herman Sintim
University of Notre Dame, IN·Chemistry
Biochemically characterize second-generation 3H-pyrazolo[4,3-f]quinoline kinase inhibitors and use new chemistry to make third-generation compounds with better drug-like properties that target FLT3, CDK2, CDK12/13 or CDK18.
Shiaw-Yih Lin
University of Texas MD Anderson Cancer Center, TX·Medicine & Clinical Research
Test whether scarce DNA building blocks (dNTPs) cause RNA to be misinserted into TNBC genomes, and whether blocking RNase H2 leaves these errors in place, causing lethal replication stress. Also identify how tumors resist the inhibitor.
Xinbin Chen
University of California-Davis, CA·Biochemistry
Determine how CDK4/6 enzymes, the RNA-binding protein RBM38 and the protein-synthesis factor eIF4G together boost mutant p53 production, and whether CDK4/6 inhibitors suppress triple-negative breast cancers partly by lowering mutant p53.
The school
Oregon Health & Science University: 24 labs on PI Pages, $545M a year on research, 54 research doctorates a year.
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