Other Publications (1)
Articles by Andrea Marcadis in JoVE
В естественных условиях мышиных седалищного нерва модель рассасывании вторжения Sylvie Deborde*1, Yasong Yu*1, Andrea Marcadis1, Chun-Hao Chen1, Ning Fan2, Richard L. Bakst3, Richard J. Wong1 1Department of Surgery, Memorial Sloan Kettering Cancer Center, 2Molecular Cytology Core Facility, Memorial Sloan Kettering Cancer Center, 3Department of Radiation Oncology, Mount Sinai Hospital Мы описываем в vivo мышиных модель рассасывании вторжения путем введения сингенных поджелудочных клеток рака в седалищный нерв. Модель позволяет для количественной оценки степени нерва вторжения и поддерживает исследование молекулярных и клеточных механизмов рассасывании вторжения.
Other articles by Andrea Marcadis on PubMed
Inflammatory Monocytes Promote Perineural Invasion Via CCL2-Mediated Recruitment and Cathepsin B Expression Cancer Research. | Pubmed ID: 28951461 Perineural invasion (PNI) is an ominous event strongly linked to poor clinical outcome. Cells residing within peripheral nerves collaborate with cancer cells to enable PNI, but the contributing conditions within the tumor microenvironment are not well understood. Here, we show that CCR2-expressing inflammatory monocytes (IM) are preferentially recruited to sites of PNI, where they differentiate into macrophages and potentiate nerve invasion through a cathepsin B-mediated process. A series of adoptive transfer experiments with genetically engineered donors and recipients demonstrated that IM recruitment to nerves was driven by CCL2 released from Schwann cells at the site of PNI, but not CCL7, an alternate ligand for CCR2. Interruption of either CCL2-CCR2 signaling or cathepsin B function significantly impaired PNI Correlative studies in human specimens demonstrated that cathepsin B-producing macrophages were enriched in invaded nerves, which was associated with increased local tumor recurrence. These findings deepen our understanding of PNI pathogenesis and illuminate how PNI is driven in part by corruption of a nerve repair program. Further, they support the exploration of inhibiting IM recruitment and function as a targeted therapy for PNI. .