Constitutive and acquired mechanisms of resistance to immune checkpoint blockade in human cancer

M Bellone, AR Elia

Research output: Contribution to journalArticle

7 Citations (Scopus)

Abstract

Cancer immunotherapy with monoclonal antibodies directed against regulatory pathways in T lymphocytes has been revolutionizing medical oncology, and the clinical success of monoclonal antibodies targeting either cytotoxic T lymphocyte antigen-4 (CTLA-4) or program death-1 (PD-1) in patients affected by melanoma, Hodgkin's lymphoma, Merkel cell carcinoma, and head and neck, bladder, renal cell or non-small cell lung cancer is way beyond the most optimistic expectation. However, immune checkpoint blockade (ICB) has failed to arrest progression in a consistent amount of patients affected by those tumors, and various histological types, including breast, colon and prostate cancer, are less sensitive to this therapeutic approach. Such clinical findings have fueled massive research efforts in the attempt to identify pre-existing and acquired mechanisms of resistance to ICB. Here we focus on evidences emerging from studies in humans on how tumor cells and the tumor microenvironment contribute to the heterogeneous clinical responses, and we propose strategies stemming from pre-clinical models that might improve clinical outcomes for patients. © 2017 Elsevier Ltd.
Original languageEnglish
Pages (from-to)17-24
Number of pages8
JournalCytokine and Growth Factor Reviews
Volume36
Issue number2
DOIs
Publication statusPublished - 2017

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Tumors
Cells
Monoclonal Antibodies
CTLA-4 Antigen
Merkel Cell Carcinoma
Cellular Microenvironment
Neoplasms
Oncology
Tumor Microenvironment
T-cells
Medical Oncology
Hodgkin Disease
Non-Small Cell Lung Carcinoma
Immunotherapy
Colonic Neoplasms
Melanoma
Prostatic Neoplasms
Urinary Bladder
Neck
Head

Cite this

Constitutive and acquired mechanisms of resistance to immune checkpoint blockade in human cancer. / Bellone, M; Elia, AR.

In: Cytokine and Growth Factor Reviews, Vol. 36, No. 2, 2017, p. 17-24.

Research output: Contribution to journalArticle

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