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Immune checkpoints linked to the adenosine pathway, specifically CD73 and CD39, play a pivotal role in fostering tumor development by suppressing the antitumor immune response and facilitating angiogenesis. In diverse preclinical murine cancer models, concurrent inhibition of CD73 and CD39 augments their antitumor efficacy, complementing immune checkpoint inhibition, targeted therapies, or conventional treatments. Studies indicate that individuals with advanced solid tumors may experience a favorable therapeutic response through the combined blockade of CD39 and CD73. Furthermore, investigations reveal the involvement of the A3 adenosine receptor (A3AR) and its signaling pathways in various tumor properties, suggesting the potential utility of A3AR agonists across diverse cancer therapeutic modalities. This succinct overview underscores the distinct role of CD39 and CD73 in regulating tumor immunity and carcinogenesis, not only in tumor cells but also in non-tumor cells. The article aims to elucidate the potential immunotherapeutic advantages of synergistically employing CD39 and CD73 inhibitors with A3AR agonists, emphasizing the consideration of an individual’s sleep-wake cycle and circadian rhythm for optimal efficacy.

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Chronobiologically Targeted Anticancer Strategy: Synergistic Inhibition of CD39 and CD73 with Adenosine Receptor Agonists

  • 章节

  • 发表日期：

    2024年

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  • Ismail Celil Haskologlu,
  • Emine Erdag,
  • Damla Ulker,
  • Mecit Orhan Uludag,
  • Ahmet Ozer Sehirli,
  • Nurettin Abacioglu

摘要

Immune checkpoints linked to the adenosine pathway, specifically CD73 and CD39, play a pivotal role in fostering tumor development by suppressing the antitumor immune response and facilitating angiogenesis. In diverse preclinical murine cancer models, concurrent inhibition of CD73 and CD39 augments their antitumor efficacy, complementing immune checkpoint inhibition, targeted therapies, or conventional treatments. Studies indicate that individuals with advanced solid tumors may experience a favorable therapeutic response through the combined blockade of CD39 and CD73. Furthermore, investigations reveal the involvement of the A3 adenosine receptor (A3AR) and its signaling pathways in various tumor properties, suggesting the potential utility of A3AR agonists across diverse cancer therapeutic modalities. This succinct overview underscores the distinct role of CD39 and CD73 in regulating tumor immunity and carcinogenesis, not only in tumor cells but also in non-tumor cells. The article aims to elucidate the potential immunotherapeutic advantages of synergistically employing CD39 and CD73 inhibitors with A3AR agonists, emphasizing the consideration of an individual’s sleep-wake cycle and circadian rhythm for optimal efficacy.