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Steven M. Albelda
Researcher at University of Pennsylvania
Publications - 412
Citations - 45881
Steven M. Albelda is an academic researcher from University of Pennsylvania. The author has contributed to research in topics: Cell adhesion molecule & Immunotherapy. The author has an hindex of 103, co-authored 398 publications receiving 41200 citations. Previous affiliations of Steven M. Albelda include Yale University & Gulf Coast Regional Blood Center.
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Journal ArticleDOI
Polarization of Tumor-Associated Neutrophil Phenotype by TGF-β: “N1” versus “N2” TAN
Zvi G. Fridlender,Jing Sun,Samuel Kim,Veena Kapoor,Guanjun Cheng,Leona E. Ling,G. Scott Worthen,Steven M. Albelda +7 more
TL;DR: It is suggested that TGF-beta within the tumor microenvironment induces a population of TAN with a protumor phenotype, and depletion of these neutrophils significantly blunts antitumor effects of treatment and reduces CD8(+) T cell activation.
Journal ArticleDOI
Integrins and other cell adhesion molecules.
TL;DR: Recent data describing the structure and function of some of these cell adhesion molecules are summarized and the possible role of these molecules in development, inflammation, wound healing, coagulation, and tumor metastasis is discussed.
Journal Article
BRAF and RAS mutations in human lung cancer and melanoma
Marcia S. Brose,Patricia Volpe,Michael Feldman,Madhu S. Kumar,Irum Rishi,Renee M. Gerrero,Eugene Einhorn,Meenhard Herlyn,John D. Minna,Andrew G. Nicholson,Jack A. Roth,Steven M. Albelda,Helen Davies,Charles Cox,Graham Brignell,Philip J. Stephens,P. Andrew Futreal,Richard Wooster,Michael R. Stratton,Barbara L. Weber +19 more
TL;DR: Three BRAF mutations identified in this study are novel, altering residues important in AKT-mediated BRAF phosphorylation and suggesting that disruption ofAKT-induced BRAF inhibition can play a role in malignant transformation, first report of mutations documenting this interaction in human cancers.
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Adhesion molecules and inflammatory injury.
TL;DR: These studies demonstrate that CAM blockade can effectively inhibit inflammation; however, there appear to be clear differences in the adhesion requirements for particular types of inflammation.
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Gemcitabine Selectively Eliminates Splenic Gr-1 + /CD11b + Myeloid Suppressor Cells in Tumor-Bearing Animals and Enhances Antitumor Immune Activity
TL;DR: The results suggest that gemcitabine may be a practical strategy for the reduction of myeloid suppressor cells and should be evaluated in conjunction with a variety of immunotherapy approaches.