How Can Immune Checkpoint Inhibitors Cause Hyperprogression in Solid Tumors?

Denis, Morgane; Duruisseaux, M.; Brevet, Marie; Dumontet, Charles

doi:10.3389/fimmu.2020.00492

Cited by 47 publications

(43 citation statements)

References 66 publications

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“…This is referred to as “hyperprogression” and has been described in a range of tumors including select cases of melanoma. While not fully defined, hyperprogression is referred to by some studies as a >50% increase in tumor volume at first assessment after treatment as compared with baseline [66–68]. The vast majority of cases of hyperprogression received CPI monotherapy alone.…”

Section: Introductionmentioning

confidence: 99%

Combined anti‐PD‐1 and anti‐CTLA‐4 checkpoint blockade: Treatment of melanoma and immune mechanisms of action

et al. 2021

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Cytotoxic T‐lymphocyte associated protein‐4 (CTLA‐4) and the Programmed Death Receptor 1 (PD‐1) are immune checkpoint molecules that are well‐established targets of antibody immunotherapies for the management of malignant melanoma. The monoclonal antibodies, Ipilimumab, Pembrolizumab, and Nivolumab, designed to interfere with T cell inhibitory signals to activate immune responses against tumors, were originally approved as monotherapy. Treatment with a combination of immune checkpoint inhibitors may improve outcomes compared to monotherapy in certain patient groups and these clinical benefits may be derived from unique immune mechanisms of action. However, treatment with checkpoint inhibitor combinations also present significant clinical challenges and increased rates of immune‐related adverse events. In this review, we discuss the potential mechanisms attributed to single and combined checkpoint inhibitor immunotherapies and clinical experience with their use.

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Section: Introductionmentioning

confidence: 99%

Combined anti‐PD‐1 and anti‐CTLA‐4 checkpoint blockade: Treatment of melanoma and immune mechanisms of action

et al. 2021

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“…Moreover, among the nonresponders, it is possible to identify a population of patients, whose percentage can vary from 4 to 29% according to different studies [ 22 ], who experience an extremely rapid increase in tumor growth and metastatic spread after ICI administration, a dramatic progression of disease that, for this reason, was called hyperprogressive disease (HPD). It is worth mentioning that HPD represents a completely different pattern of progression and is not superimposable with conventional progressive disease or pseudoprogression.…”

Section: Introductionmentioning

confidence: 99%

Mechanisms of hyperprogressive disease after immune checkpoint inhibitor therapy: what we (don’t) know

Camelliti

Noci

Bianchi

et al. 2020

J Exp Clin Cancer Res

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Immune checkpoint inhibitors (ICIs) have made a breakthrough in the treatment of different types of tumors, leading to improvement in survival, even in patients with advanced cancers. Despite the good clinical results, a certain percentage of patients do not respond to this kind of immunotherapy. In addition, in a fraction of nonresponder patients, which can vary from 4 to 29% according to different studies, a paradoxical boost in tumor growth after ICI administration was observed: a completely unpredictable novel pattern of cancer progression defined as hyperprogressive disease. Since this clinical phenomenon has only been recently described, a universally accepted clinical definition is lacking, and major efforts have been made to uncover the biological bases underlying hyperprogressive disease. The lines of research pursued so far have focused their attention on the study of the immune tumor microenvironment or on the analysis of intrinsic genomic characteristics of cancer cells producing data that allowed us to formulate several hypotheses to explain this detrimental effect related to ICI therapy. The aim of this review is to summarize the most important works that, to date, provide important insights that are useful in understanding the mechanistic causes of hyperprogressive disease.

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“…Other limitations of checkpoint inhibitor therapies include hyperprogression following checkpoint inhibition [ 67 ] and heterogeneous determinants of differences in response rates in patients with similar tumors [ 68 ]. Furthermore, utility and efficacy of checkpoint blockade is limited by several mechanisms of resistances through upregulation of additional checkpoint molecules, inherent lack of infiltration of immune effectors in the tumors, immunosuppressive and heterogeneous tumor microenvironments, and disparities in tumor-intrinsic factors such as oncogenic signaling pathways [ 69 , 70 ].…”

Section: Types Of Immunotherapy: Their Combinations and Limitationmentioning

confidence: 99%

Immunotherapies and Combination Strategies for Immuno-Oncology

Barbari

Fontaine

Parajuli

et al. 2020

IJMS

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The advent of novel immunotherapies in the treatment of cancers has dramatically changed the landscape of the oncology field. Recent developments in checkpoint inhibition therapies, tumor-infiltrating lymphocyte therapies, chimeric antigen receptor T cell therapies, and cancer vaccines have shown immense promise for significant advancements in cancer treatments. Immunotherapies act on distinct steps of immune response to augment the body’s natural ability to recognize, target, and destroy cancerous cells. Combination treatments with immunotherapies and other modalities intend to activate immune response, decrease immunosuppression, and target signaling and resistance pathways to offer a more durable, long-lasting treatment compared to traditional therapies and immunotherapies as monotherapies for cancers. This review aims to briefly describe the rationale, mechanisms of action, and clinical efficacy of common immunotherapies and highlight promising combination strategies currently approved or under clinical development. Additionally, we will discuss the benefits and limitations of these immunotherapy approaches as monotherapies as well as in combination with other treatments.

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How Can Immune Checkpoint Inhibitors Cause Hyperprogression in Solid Tumors?

Cited by 47 publications

References 66 publications

Combined anti‐PD‐1 and anti‐CTLA‐4 checkpoint blockade: Treatment of melanoma and immune mechanisms of action

Combined anti‐PD‐1 and anti‐CTLA‐4 checkpoint blockade: Treatment of melanoma and immune mechanisms of action

Mechanisms of hyperprogressive disease after immune checkpoint inhibitor therapy: what we (don’t) know

Immunotherapies and Combination Strategies for Immuno-Oncology

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