Resistance Mechanisms to Immune-Checkpoint Blockade in Cancer: Tumor-Intrinsic and -Extrinsic Factors.

By J. Pitt, Marie Vetizou, Romain Daillère, M. Roberti, T. Yamazaki, B. Routy, P. Lepage, I. Boneca, M. Chamaillard, Guido Kroemer and 1 more. Immunity, 2016

952 citations recorded by the source corpus.

Subfields: Immunology, Oncology, Psychiatry and Mental health

View Paper: https://www.semanticscholar.org/paper/ad3597dbce28ea449338a35ce28544d910056150

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In Immunology

1. K. Flaherty
2. D. Barbie
3. Russell W. Jenkins

In Oncology

1. K. Flaherty
2. D. Barbie
3. Russell W. Jenkins

Citations in the corpus

• Natural killer cells in cancer biology and therapy (2020, background): “An example of such approach is immunecheckpoint blockade, with blocking of receptors or ligands that inhibit the activation of CTLs, including programmed cell death protein 1 (PD-1), its main ligand PD-L1, cytotoxic T-lymphocyte antigen 4 (CTLA-4) and lymphocyte-activation gene-3 (LAG-3), by monoclo”
• Targeting autophagy in cancer (2018, background): “The absence of an appropriate response to autophagy induction in tumor cells potentially could predict resistance to immune-checkpoint blocker therapies in human cancers.(92) Michaud et al demonstrated that autophagy was dispensable for chemotherapy-induced cell death but was required for its immuno”
• Generation of tumor-reactive T cells by co-culture of peripheral blood lymphocytes and tumor organoids (2018, neutral): “Treatment failure may be explained at many different levels that include a low number of immunogenic antigens, defective antigen presentation, and/or the expression of alternative immune checkpoint molecules (Blank et al., 2016; Dijkstra et al., 2016; Pitt et al., 2016; Sharma et al., 2017).”
• Regulatory mechanisms of PD-1/PD-L1 in cancers (2024, background): “…antigen mutations and presentation processes, interactions among multiple immune checkpoints, suppressive tumor micro-environment (tumor intrinsic factors, inflammatory environment), oncogenic pathways in tumors, epigenetic changes in key tumor proteins, accumulation of metabolites, etc [452].”
• Mechanisms of resistance to immune checkpoint inhibitors (2018, background): “…presentation by stimulating innate immune responses and dendritic cell function (e.g., type I IFN, TLR ligands, LIGHT, and oncolytic viruses) may promote formation or presentation of suitable neoantigens in tumours with a non-inflamed, immune cell poor TME (Pitt et al, 2016; O’Donnell et al, 2017).”