Leif William Ellisen

In metastatic breast cancer on TROP2- or HER2-targeting antibody-drug conjugates, early CTC disappearance or steep decline tracked response, while CTC epitope levels neither predicted benefit nor vanished at resistance.

This study identifies SIRT5-induced metabolic changes as a driver of chemoresistance in TNBC and reveals ATR checkpoint dependence as a therapeutic vulnerability.

This study identifies TROP2 as a regulator of tight junction-mediated immune exclusion in TNBC, showing that targeting TROP2 enhances anti-PD1 therapy response.

The paper shows that therapy-induced stress increases METTL3 translation, altering gene expression to promote tumor survival.

The paper analyzes rare germline variation in cancer predisposing genes across cancer patients and controls to identify shared mutation properties and candidate susceptibility genes.

The paper predicts cancer cell-of-origin from DNA sequences by matching mutational landscapes to chromatin modification patterns in normal tissues.