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Tumor progression is a phenomenon where the pre-formed tumor acquires successive mutations to become clinically more aggressive and malignant. In the 1950s, Foulds first described the stepwise progression of cancer cells through successive stages.
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The mammalian target of rapamycin or mTOR protein was discovered in 1994 due to its direct interaction with rapamycin. The protein gets its name from a yeast homolog called TOR. The mTOR protein complex in mammalian cells plays a major role in balancing anabolic processes such as the synthesis of proteins, lipids, and nucleotides and catabolic processes, such as autophagy in response to environmental cues, such as availability of nutrients and growth factors.
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Cancer cells accumulate genetic changes at an abnormally rapid rate due to the defects in the DNA repair mechanisms. From an evolutionary perspective, such genetic instability is advantageous for cancer development. Mutant cell lines accumulate a series of beneficial mutations that contribute to their progression into cancer.
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IFN-γ and CD38 in Hyperprogressive Cancer Development.

Stefania Angelicola1, Francesca Ruzzi1, Lorena Landuzzi2

  • 1Laboratory of Immunology and Biology of Metastasis, Department of Experimental, Diagnostic and Specialty Medicine (DIMES), University of Bologna, 40126 Bologna, Italy.

Cancers
|January 20, 2021
PubMed
Summary
This summary is machine-generated.

Immune checkpoint inhibitors (ICIs) can paradoxically accelerate tumor growth, leading to hyperprogressive disease (HPD). This review explores the potential roles of IFN-γ and CD38 in HPD mechanisms, offering new insights into this challenging clinical problem.

Keywords:
CD38IFN-γcancerhyperprogressionhyperprogressive diseaseimmune checkpoint inhibitorsimmunotherapymacrophagetumor microenvironment

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Area of Science:

  • Immunology
  • Oncology
  • Cancer Research

Background:

  • Immune checkpoint inhibitors (ICIs) have improved cancer patient survival but face limitations due to low response rates and atypical responses.
  • Hyperprogressive disease (HPD), a paradoxical acceleration of tumor growth post-ICI treatment, presents a significant clinical challenge.
  • The underlying mechanisms of HPD remain unclear and debated, necessitating further investigation into contributing factors.

Purpose of the Study:

  • To explore the potential involvement of IFN-γ and CD38 in the pathogenesis of hyperprogressive disease (HPD) following immune checkpoint inhibitor (ICI) therapy.
  • To propose novel hypotheses regarding the mechanisms by which IFN-γ and CD38 may contribute to HPD.
  • To highlight key pathways and cellular processes potentially linking these factors to HPD.

Main Methods:

  • This review synthesizes existing literature on immune checkpoint inhibitors, hyperprogressive disease, IFN-γ, and CD38.
  • It analyzes the known functions and associations of IFN-γ and CD38 with cancer immunity and ICI resistance.
  • The review proposes hypothetical mechanisms for HPD involvement based on current immunological and molecular understanding.

Main Results:

  • Interferon-gamma (IFN-γ) may promote HPD through inflammasome activation, indoleamine 2,3-dioxygenase 1 (IDO1) activity, and activation-induced cell death (AICD) in T cells.
  • CD38 might contribute to HPD by activating adenosine receptors, influencing hypoxia pathways, and mediating AICD-dependent T-cell depletion.
  • Both IFN-γ and CD38 are implicated in resistance to ICI therapy, suggesting a potential link to HPD.

Conclusions:

  • IFN-γ activation of the inflammasome pathway, IDO1, and AICD may drive HPD.
  • CD38's role in HPD could involve adenosine receptor and hypoxia pathway activation, alongside AICD-driven T-cell loss.
  • Further research into IFN-γ and CD38 is crucial for understanding and potentially mitigating HPD in cancer patients treated with ICIs.