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Hyperprogressive disease: recognizing a novel pattern to improve patient management.

Stéphane Champiat1,2, Roberto Ferrara3, Christophe Massard1

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Immune checkpoint inhibitors like anti-PD-1/PD-L1 antibodies can paradoxically cause hyperprogression, a worsening of cancer. This review explores evidence, causes, and management challenges of this phenomenon.

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Area of Science:

  • Oncology
  • Immunotherapy
  • Cancer Research

Background:

  • Immune checkpoint inhibitors (ICIs), specifically anti-PD-1/PD-L1 monoclonal antibodies, have revolutionized cancer treatment for many patients with solid tumors.
  • However, a subset of patients experiences disease deterioration, termed hyperprogressive disease (HPD), under these therapies.

Purpose of the Study:

  • To review the current evidence on hyperprogressive disease (HPD) following immune-checkpoint inhibition.
  • To discuss pathophysiological hypotheses explaining HPD.
  • To outline challenges in managing HPD in clinical practice and inform treatment decisions.

Main Methods:

  • Literature review of studies investigating hyperprogressive disease.
  • Analysis of proposed pathophysiological mechanisms.
  • Discussion of clinical management strategies and decision-making.

Main Results:

  • Evidence for hyperprogressive disease (HPD) exists across various solid tumors treated with anti-PD-1/PD-L1 therapies.
  • Several pathophysiological hypotheses are proposed, including T cell exhaustion and altered tumor microenvironment.
  • Current patient management in routine settings faces challenges in identifying and treating HPD.

Conclusions:

  • Hyperprogressive disease (HPD) is a recognized, albeit paradoxical, response to immune checkpoint inhibitors.
  • Understanding the underlying mechanisms is crucial for developing predictive biomarkers and effective management strategies.
  • Risk assessment for HPD should be integrated into clinical decision-making for immunotherapy.