Author

T. Sconocchia

Listed by name: these papers carry no ORCID for this author, so different people with the same name may be mixed together.

Biology Disciplines

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Immunology· 4

Signature Assays, Organisms & Methods

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Approach:experimental assay· 4 Organism:human· 3 Research Focus:cancer & tumor microenvironment· 2 Research Focus:cell type annotation· 2 Organism:mouse· 2 Assay:proteomics· 2 Assay:bulk RNA-seq· 1 Research Focus:cell-cell communication· 1

Frequent Co-Authors

A. Ottaviani· 3 shared C. Cenciarelli· 3 shared G. Lanzilli· 3 shared G. Sconocchia· 3 shared R. Arriga· 3 shared S. Caratelli· 3 shared A. Venditti· 2 shared D. Lauro· 2 shared

Activity by Year

2019-2021 · peak 2/yr

Co-Author Collaboration Network

10 top collaborators · 45 mutual co-author links

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3 shared papersImmunology

A. Ottaviani

Mutual co-authors in cluster

Author profile →

4 papers

Recent·Most cited

ANTIBODY-INDEPENDENT ANTITUMOR EFFECTS OF CD32A-CHIMERIC RECEPTOR T CELLS: IMPLICATIONS FOR BREAST CANCER PROGNOSIS AND TREATMENT.

G. Sconocchia, G. Lanzilli, V. Cesarini, D. A. Sivestris, R. Arriga, K. Rezvani, S. Caratelli, K. Chen, J. Dou, C. Cenciarelli, G. Toietta, S. Baldari, T. Sconocchia, F. De Paolis, A. Aureli, , G. C. Spagnoli

This study shows CD32A-chimeric receptor T cells can identify CD32A ligands, predict breast cancer sensitivity, and improve prognosis without antibodies.

bioRxiv · Dec 22, 2021 · PreprintImmunology

miR-424(322) is a molecular switch controlling pro-inflammatory vs anti-inflammatory skin DC subset differentiation by modulating TGF-β signaling

V. Zyulina, K.-K. Yan, B. Ju, C. Passegger, C. Tam-Amersdorfer, Q. Pan, T. Sconocchia, C. Pollack, B. Shaner, A. Zebisch, J. Easton, J. Yu, J. Silva, H. Strobl

This study identifies miR-424(322) as a molecular switch that controls the differentiation of pro-inflammatory monocyte-derived DCs (moDCs) versus anti-inflammatory Langerhans cells (LCs) by modulating TGF-β signaling.

bioRxiv · Sep 7, 2020 · PreprintImmunology

CD16-158-VALINE CHIMERIC RECEPTOR T CELLS OVERCOME THE RESISTANCE OF KRAS-MUTATED COLORECTAL CARCINOMA CELLS TO CETUXIMAB

R. Arriga, S. Caratelli, G. Lanzilli, A. Ottaviani, C. Cenciarelli, T. Sconocchia, G. C. Spagnoli, G. Iezzi, M. Roselli, D. Lauro, G. Dotti, S. Ferrone, G. Sconocchia

This study evaluates CD16-158-VALINE chimeric receptor T cells for overcoming cetuximab resistance in KRAS-mutated colorectal cancer, finding they enhance IFNγ and TNF release and control tumor growth in mice.

bioRxiv · Mar 26, 2019Immunology

ELIMINATION OF EGFR-OVEREXPRESSING CANCER CELLS BY CD32 CHIMERIC RECEPTOR T CELLS IN COMBINATION WITH CETUXIMAB OR PANITUMUMAB

S. Caratelli, R. Arriga, T. Sconocchia, A. Ottaviani, G. Lanzilli, D. Pastore, C. Cenciarelli, A. Venditti, M. I. Del Principe, D. Lauro, E. Landoni, H. Du, B. Savoldo, S. Ferrone, G. Dotti, G. Sconocchia

This study shows CD32131R-CR T cells can eliminate EGFR-overexpressing cancer cells when combined with cetuximab or panitumumab, outperforming CD16158F-CR T cells.

bioRxiv · Mar 18, 2019 · PreprintImmunology