P
Peter Pytel
Researcher at University of Chicago
Publications - 149
Citations - 4485
Peter Pytel is an academic researcher from University of Chicago. The author has contributed to research in topics: Medicine & Glioma. The author has an hindex of 32, co-authored 139 publications receiving 3735 citations. Previous affiliations of Peter Pytel include Jagiellonian University & University of Illinois at Chicago.
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CCL2 Produced by the Glioma Microenvironment Is Essential for the Recruitment of Regulatory T Cells and Myeloid-Derived Suppressor Cells
Alan L. Chang,Jason Miska,Derek A. Wainwright,Mahua Dey,Claudia V. Rivetta,Dou Yu,Deepak Kanojia,Katarzyna C. Pituch,Jian Qiao,Peter Pytel,Yu Han,Meijing Wu,Lingjiao Zhang,Craig Horbinski,Atique U. Ahmed,Maciej S. Lesniak +15 more
TL;DR: It is reported that macrophages and microglia within the glioma microenvironment produce CCL2, a chemokine that is critical for recruiting both CCR4+ Treg and CCR2+Ly-6C+ monocytic MDSCs in this disease setting.
CCL2 produced by the glioma microenvironment is essential for the recruitment of regulatory T cells and myeloid-derived suppressor cells
Alan L. Chang,Jason Miska,Derek A. Wainwright,Mahua Dey,Claudia V. Rivetta,Dou Yu,Deepak Kanojia,Katarzyna C. Pituch,Jian Qiao,Peter Pytel,Yu Han,Meijing Wu,Lingjiao Zhang,Craig Horbinski,Atique U. Ahmed,Maciej S. Lesniak +15 more
TL;DR: This paper found that macrophages and microglia within the glioma microenvironment produce CCL2, a chemokine that is critical for recruiting both regulatory T cells (Treg) and myeloid-derived suppressor cells (MDSC).
Journal ArticleDOI
The role of glioma stem cells in chemotherapy resistance and glioblastoma multiforme recurrence
TL;DR: The molecular mechanisms of chemoresistance of G SCs are discussed and the reasons why complete eradication of GSCs is so difficult to achieve are described.
Journal ArticleDOI
Disruption of nesprin-1 produces an Emery Dreifuss muscular dystrophy-like phenotype in mice.
Megan J. Puckelwartz,Eric J Kessler,Yuan Zhang,Didier Hodzic,K. Natalie Randles,Glenn E. Morris,Judy U. Earley,Michele Hadhazy,James M. Holaska,Stephanie K. Mewborn,Peter Pytel,Elizabeth M. McNally +11 more
TL;DR: In this article, the role of the LINC complex, and nesprin-1, in neuromuscular and cardiac disease was demonstrated. But, the NESPRIN-1 protein does not interact with SUN2.
Journal Article
Abstract 1431: Disruption of Nesprin-1 Produces an Emery Dreifuss Muscular Dystrophy-like Phenotype in Mice
Eric J Kessler,Megan J. Puckelwartz,Yuan Zhang,Judy U. Earley,Michele Hadhazy,James M. Holaska,Stephanie K. Mewborn,Peter Pytel,Elizabeth M. McNally +8 more
TL;DR: The role of the LINC complex, and nesprin-1, in neuromuscular and cardiac disease is demonstrated and coimmunoprecipitation experiments with SUN2 and nESprin reveal that mutant nes PRIN-1 protein no longer interacts with SUN 2.