Jieun Son, PhD, (Jieun_Son@dfci.harvard.edu) focuses on characterizing rare HER2 mutations found in NSCLC patients. In collaboration with other DFCI investigators, she also aims to provide novel targeted therapies for EGFR/HER2 lung cancers. She is currently working on developing patient-derived ex vivo screening tools for precision medicine.
Seshiru Nakazawa, MD, PhD, (Seshiru_Nakazawa@dfci.harvard.edu) is studying the mechanisms of MET dysregulation and small cell transformation based on patient-derived models and clinical data. He also aims to modulate metabolic pathways to overcome treatment resistance to current molecular-targeted therapies.
Marie-Anais Locquet, PhD, (Marie-anais_Locquet@dfci.harvard.edu) focuses on preventing and reverting acquired resistance to EGFR-targeting therapies in NSCLC. She is working on therapeutic strategies to directly degrade EGFR by the ubiquitin proteasome pathway, as well as identifying potentially targetable vulnerabilities in EGFR-TKI resistant cells. Marie also develops in vitro 3D models of NSCLC from both patients samples and PDX.
Jens Köhler, MD, (Jens_Kohler@dfci.harvard.edu) studies KRAS-driven NSCLC using commercially available cancer cell lines and patient-derived tumors to recapitulate the extremely diverse tumor landscape. His research aims to answer the question of why inhibitors targeting the MAPK pathway can be effective in some patients while they fail in others, with an emphasis on microenvironment circuitries.
Antja-Voy Hartley, PhD (Antja-Voy_Hartley@dfci.harvard.edu) focuses on designing rational and novel combination treatments to overcome resistance to EGFR-targeted therapies in EGFR-mutant lung cancers. Additionally, she explores options for targeted therapies for the treatment of mesotheliomas by linking the tumors’ genomic landscape to potential therapeutic vulnerabilities.
Heidi Haikala, PhD, (heidiM_haikala@dfci.harvard.edu) is studying how to prevent or revert resistance to the current EGFR-targeting therapies. This includes therapeutic strategies to directly degrade the EGFR receptor by using the ubiquitin-proteasome pathway, as well as studying new ways to vertically or in parallel block the EGFR survival signaling by using combination strategies. The research utilizes cutting-edge research models, such as 3D-culture platforms and patient-derived xenograft (PDX) models.
Simon Baldacci, MD, PhD, (Simon_Baldacci@dfci.harvard.edu) is studying the minimal residual disease population following drug treatment in EGFR mutant cell lines and PDX models. The overall goal is to identify novel drug therapies which may target these residual tumor cells, leading to successful translation into a clinical trial protocol.