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Related Experiment Video

Updated: Nov 21, 2025

Multiplexed Immunofluorescence Analysis and Quantification of Intratumoral PD-1+ Tim-3+ CD8+ T Cells
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CD73, Tumor Plasticity and Immune Evasion in Solid Cancers.

Haitang Yang1, Feng Yao1, Paul F Davis2

  • 1Department of Thoracic Surgery, Shanghai Chest Hospital, Shanghai Jiao Tong University, Shanghai 200030, China.

Cancers
|January 12, 2021
PubMed
Summary

Cluster of differentiation 73 (CD73) promotes tumor growth and treatment resistance by enabling cellular plasticity and immune evasion. Targeting CD73 may offer a new strategy for treating solid cancers.

Keywords:
CD73cancer stemnessdrug repurposingimmunotherapymetastasistargeted therapytreatment resistancetumor differentiationtumor plasticity

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Area of Science:

  • Biochemistry
  • Immunology
  • Oncology

Background:

  • Cellular plasticity regulatory networks, crucial in development, can reactivate in disease states like cancer.
  • Ecto-5'-nucleotidase (NT5E), also known as cluster of differentiation 73 (CD73), is a cell surface enzyme.
  • CD73 hydrolyzes extracellular adenosine monophosphate to adenosine (eADO), influencing cell growth, survival, and immune responses.

Purpose of the Study:

  • To review the pro-tumorigenic roles of CD73 and adenosine signaling.
  • To discuss the link between CD73 expression, tumor plasticity, and treatment resistance.
  • To highlight CD73 as a potential therapeutic target in solid cancers.

Main Methods:

  • Literature review of existing research on CD73, adenosine signaling, and cancer.
  • Analysis of data linking CD73 expression to clinical outcomes and tumor behavior.
  • Synthesis of evidence regarding CD73's role in immune evasion and therapeutic resistance.

Main Results:

  • CD73 upregulation in tumor cells correlates with poor clinical outcomes.
  • Tumors exploit CD73-mediated adenosine production for immune evasion and resistance to therapies.
  • CD73 expression is associated with tumor cell stemness and plasticity, facilitating dissemination.

Conclusions:

  • CD73 and adenosine signaling play significant pro-tumorigenic roles.
  • Targeting CD73 presents a promising novel therapeutic strategy for solid tumors.
  • Understanding CD73's contribution to tumor plasticity and immune evasion is critical for developing effective cancer treatments.