Area of research
Oncology · Molecular Biology
Research interest
Research interests include PARP inhibition in cancer therapy, HER2/EGFR in Cancer Research, PI3K/AKT/mTOR signaling in cancer, and Advanced Breast Cancer Therapies.
Harnessing STING Signaling and Natural Killer Cells Overcomes PARP Inhibitor Resistance in Homologous Recombination–Deficient Breast Cancer
Data from Preclinical <i>In Vivo</i> Validation of the RAD51 Test for Identification of Homologous Recombination-Deficient Tumors and Patient Stratification
Data from Identification of a Molecularly-Defined Subset of Breast and Ovarian Cancer Models that Respond to WEE1 or ATR Inhibition, Overcoming PARP Inhibitor Resistance
High p16 expression and heterozygous RB1 loss are biomarkers for CDK4/6 inhibitor resistance in ER+ breast cancer
Preclinical <i>In Vivo</i> Validation of the RAD51 Test for Identification of Homologous Recombination-Deficient Tumors and Patient Stratification
Identification of a Molecularly-Defined Subset of Breast and Ovarian Cancer Models that Respond to WEE1 or ATR Inhibition, Overcoming PARP Inhibitor Resistance
Author Correction: High p16 expression and heterozygous RB1 loss are biomarkers for CDK4/6 inhibitor resistance in ER+ breast cancer
PI3K activation promotes resistance to eribulin in HER2-negative breast cancer
Genetic Alterations in the PI3K/AKT Pathway and Baseline AKT Activity Define AKT Inhibitor Sensitivity in Breast Cancer Patient-derived Xenografts
RAD51 foci as a functional biomarker of homologous recombination repair and PARP inhibitor resistance in germline BRCA-mutated breast cancer
A RAD51 assay feasible in routine tumor samples calls PARP inhibitor response beyond BRCA mutation
Abstract 3596: Biomarkers of response to CDK4/6 inhibitor (CDK4/6i) in hormone receptor (HR) positive and HER2-positive breast cancer (BC) patient-derived xenografts (PDX)
Early Adaptation and Acquired Resistance to CDK4/6 Inhibition in Estrogen Receptor–Positive Breast Cancer
PI3K inhibition results in enhanced estrogen receptor function and dependence in hormone receptor–positive breast cancer
PI3K Inhibition Impairs BRCA1/2 Expression and Sensitizes BRCA-Proficient Triple-Negative Breast Cancer to PARP Inhibition