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Pancreatic Neoplasms: HELP
Articles by Andrea R. Marcadis
Based on 2 articles published since 2010
(Why 2 articles?)
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Between 2010 and 2020, Andrea Marcadis wrote the following 2 articles about Pancreatic Neoplasms.
 
+ Citations + Abstracts
1 Article An In Vivo Murine Sciatic Nerve Model of Perineural Invasion. 2018

Deborde, Sylvie / Yu, Yasong / Marcadis, Andrea / Chen, Chun-Hao / Fan, Ning / Bakst, Richard L / Wong, Richard J. ·Department of Surgery, Memorial Sloan Kettering Cancer Center; debordes@mskcc.org. · Department of Surgery, Memorial Sloan Kettering Cancer Center. · Molecular Cytology Core Facility, Memorial Sloan Kettering Cancer Center. · Department of Radiation Oncology, Mount Sinai Hospital. ·J Vis Exp · Pubmed #29733315.

ABSTRACT: Cancer cells invade nerves through a process termed perineural invasion (PNI), in which cancer cells proliferate and migrate in the nerve microenvironment. This type of invasion is exhibited by a variety of cancer types, and very frequently is found in pancreatic cancer. The microscopic size of nerve fibers within mouse pancreas renders the study of PNI difficult in orthotopic murine models. Here, we describe a heterotopic in vivo model of PNI, where we inject syngeneic pancreatic cancer cell line Panc02-H7 into the murine sciatic nerve. In this model, sciatic nerves of anesthetized mice are exposed and injected with cancer cells. The cancer cells invade in the nerves proximally toward the spinal cord from the point of injection. The invaded sciatic nerves are then extracted and processed with OCT for frozen sectioning. H&E and immunofluorescence staining of these sections allow quantification of both the degree of invasion and changes in protein expression. This model can be applied to a variety of studies on PNI given its versatility. Using mice with different genetic modifications and/or different types of cancer cells allows for investigation of the cellular and molecular mechanisms of PNI and for different cancer types. Furthermore, the effects of therapeutic agents on nerve invasion can be studied by applying treatment to these mice.

2 Article Inflammatory Monocytes Promote Perineural Invasion via CCL2-Mediated Recruitment and Cathepsin B Expression. 2017

Bakst, Richard L / Xiong, Huizhong / Chen, Chun-Hao / Deborde, Sylvie / Lyubchik, Anna / Zhou, Yi / He, Shizhi / McNamara, William / Lee, Sei-Young / Olson, Oakley C / Leiner, Ingrid M / Marcadis, Andrea R / Keith, James W / Al-Ahmadie, Hikmat A / Katabi, Nora / Gil, Ziv / Vakiani, Efsevia / Joyce, Johanna A / Pamer, Eric / Wong, Richard J. ·Department of Radiation Oncology, Mount Sinai School of Medicine, New York, New York. · Immunology Program, Memorial Sloan-Kettering Cancer Center, New York, New York. · Department of Surgery, Memorial Sloan-Kettering Cancer Center, New York, New York. · Cancer Biology and Genetics Program, Memorial Sloan Kettering Cancer Center, New York, New York. · Department of Pathology, Memorial Sloan Kettering Cancer Center, New York, New York. · Department of Otolaryngology, Rambam Healthcare Campus, The Technion-Israel Institute of Technology, Haifa, Israel. · Ludwig Institute for Cancer Research, University of Lausanne, Lausanne, Switzerland. · Department of Surgery, Memorial Sloan-Kettering Cancer Center, New York, New York. wongr@mskcc.org. ·Cancer Res · Pubmed #28951461.

ABSTRACT: 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