Cancer
Cancer isn't one disease. It's a group of diseases where cells grow when they shouldn't, in places they shouldn't, in numbers they shouldn't. Around 20 million people are diagnosed every year. Roughly 10 million die.
Most cancers trace back to broken cellular signaling. Some failures are in kinases — molecular switches that tell cells when to divide; stuck "on," they keep the signal going. Others are in GTPases like KRAS that pass the signal along, or in DNA-repair proteins like BRCA1 that should catch damage but can't. EGFR and Abl are kinases gone wrong in dozens of cancers; KRAS and BRCA1 are different proteins, but all four drive cells to grow when they shouldn't.
The Chodera lab and partner labs simulate how these proteins move, millisecond by millisecond, hunting for the moments where a treatment could grab on.
With collaborators at the University of Washington, we're going further: reading patients' own kinase mutations and predicting which treatments will work for them. Personalized cancer care, built from each patient's own proteins.
Focus areas
Breast Cancer
BRCA1 mutations and DNA-repair failure.
Epigenetics
Histone methyltransferases and gene regulation.
Kidney Cancer
mTOR signaling and growth control.
p53
Tumor suppressor and "guardian of the genome."
Selected posts
Catching KRAS in the act
Simulations reveal new paths for targeted protein degradation of one of the most-mutated cancer drivers.
BRCA1 in breast cancer
How DNA-repair failure drives roughly 70,000 hereditary breast cancers a year.
Drugging the undruggable
The Chodera lab's KRAS simulations look for the moments where a drug could grip on.
mTOR mutants in kidney cancer
Sorting cancer-associated mTOR mutants into clusters with different responses to rapamycin.
Histone methyltransferases
NSD1, NSD2, NSD3 — epigenetic "writers" that drive several cancers when miswired.
FDA-approved kinase inhibitors
Mapping how cancer drugs bind to their kinase targets across the family.
Abl kinase and CML
Drug-resistant conformations of Abl — the target of imatinib in chronic myelogenous leukemia.