Neoantigens in cancer immunotherapy

By Ton N. Schumacher, Robert Schreiber. Science, 2015

4,352 citations recorded by the source corpus.

View Paper: https://www.semanticscholar.org/paper/c1d1cddf475cdde1cd0499a1e2027f6a36eb5032

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Citations in the corpus

Advances in immunotherapy for hepatocellular carcinoma (2021, background): “I.M. receives funding from MINECO SAF2014-52361-R and SAF 2017- 83267-C2-1R; Worldwide Cancer Research Grant (15-1146); the Asociacion Española Contra el Cancer (AECC) Foundation under grant GCB15152947MELE; and the European Union’s Horizon 2020 Program (grant agreement no. 635122 PROCROP).”
PD-L1 (B7-H1) and PD-1 Pathway Blockade for Cancer Therapy: Mechanisms, Response Biomarkers and Combinations (2016, background): “Nonetheless, recognizing the intrinsic ability of the immune system to specifically target the unique mutations potentially shared by many cancer types (90) is an important part of understanding the mechanism of cancer immunotherapy (91).”
Mechanisms of resistance to immune checkpoint inhibitors (2018, background): “A unique T-cell receptor recognises MHC-bound tumour antigen providing the first signal for T-cell activation and full T-cell activation follows the engagement of the co-stimulatory CD28 receptor on T cells by B7 on the APC (Schumacher and Schreiber, 2015).”
Clonal neoantigens elicit T cell immunoreactivity and sensitivity to immune checkpoint blockade (2016, background): “ized vaccines and cell therapies targeting cancer mutations (5, 6).”
CDK4/6 Inhibition Augments Anti-Tumor Immunity by Enhancing T Cell Activation (2017, methodology): “As Kras mutant GEMMs are not responsive to checkpoint blockade (3,44), in part due to a low levels of somatic mutations (45), we utilized the murine syngeneic colon adenocarcinoma model MC38.”
Potential Predictive Value of TP53 and KRAS Mutation Status for Response to PD-1 Blockade Immunotherapy in Lung Adenocarcinoma (2016, background): “The underlying biology of such limitations has not been clearly understood until recent studies, which showed that the presence of TILs and mutational burden correlated with T-effector signature and immunogenic features that supported the response to anti–PD-1/PD-L1 therapy (5, 8, 12, 38, 39).”
Tumor evolution of glioma intrinsic gene expression subtype associates with immunological changes in the microenvironment (2017, background): “Missense mutations may generate neoantigens that can be recognized by CD8+ T cells (Schumacher and Schreiber, 2015).”
Allele-Specific HLA Loss and Immune Escape in Lung Cancer Evolution (2017, background): “The majority of cancer immunotherapies, including immune checkpoint blockade therapy, aim to counteract immune evasion by shifting the balance in favor of immune activation, enabling T cell-mediated cancer cell elimination (Schumacher and Schreiber, 2015).”
Neoantigen vaccine generates intratumoral T cell responses in phase Ib glioblastoma trial (2018, methodology): “Next, we defined expression scores, for each cell, for the following genes and signatures, based on the average E of the gene(s) indicated in parenthesis: (1) CD4 (CD4); (2) CD8 (CD8A and CD8B); (3) regulatory T (Treg) cells (FOXP3 and IL2RA); (4) cytotoxic T cells (PRF1, GZMA, GZMK, NKG7 and CST7);”