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Updated: Apr 30, 2026

Studying Triple Negative Breast Cancer Using Orthotopic Breast Cancer Model
Published on: March 20, 2020
Targeting CD73 and downstream adenosine receptor signaling in triple-negative breast cancer
Bertrand Allard1, Martin Turcotte, John Stagg
1Centre de Recherche du Centre Hospitalier de l'Université de Montréal (CRCHUM), Faculté de Pharmacie et Institut du Cancer de Montréal , 900 Rue Saint Denis, 10ième étage, Montréal H2X0X9, QC , Canada +514 890 8000 ext: 25170 ; +514 412 7661 ; john.stagg@umontreal.ca.
Introduction:
Despite significant improvements in diagnosis and therapy over the past 20 years, breast cancer remains a worldwide public health issue. In particular, triple negative breast cancer (TNBC), a subset of very aggressive breast tumors, is associated with a poor prognosis and has very few efficient therapeutic options. The ectonucleotidase CD73 has recently emerged as a promising new target for TNBC in preclinical models. Pharmacological targeting of CD73 and downstream adenosine A2A/A2B receptor signaling is currently an active field of research that could lead to the development of new cancer therapeutics, including options against TNBC.
Areas Covered:
This article reviews the basic structural and molecular features of CD73 and its role in the development of cancer, with a particular focus on CD73's role in the biology of TNBC.
Expert Opinion:
It was recently demonstrated that CD73 expression in TNBC is associated with worse clinical outcomes and increased resistance to anthracycline chemotherapy. Targeted blockade of the CD73/A2A axis has been shown to impair various aspects of tumorigenesis and displays synergism with other anti-cancer treatments in preclinical studies. Hence, we strongly argue for the development of CD73 inhibitors and for the repositioning of A2A antagonists in cancer.
Insights
Targeting CD73, an enzyme linked to poor outcomes in triple-negative breast cancer (TNBC), shows promise. Blocking CD73 and related signaling pathways may offer new therapeutic strategies for TNBC.
Area of Science:
- Oncology
- Molecular Biology
- Cancer Therapeutics
Background:
- Breast cancer remains a global health challenge, with triple-negative breast cancer (TNBC) presenting aggressive characteristics and limited treatment options.
- The ectonucleotidase CD73 is emerging as a significant target in TNBC, showing potential for novel therapeutic interventions.
- Research into pharmacological targeting of CD73 and adenosine receptor signaling is advancing cancer treatment development.
Purpose of the Study:
- To review the structural and molecular characteristics of CD73.
- To elucidate the role of CD73 in cancer development.
- To specifically focus on the involvement of CD73 in the biology of TNBC.
Main Methods:
- Literature review of CD73 structure and function.
- Analysis of CD73's role in cancer biology, particularly TNBC.
- Examination of preclinical data on CD73 targeting and its synergistic effects.
Main Results:
- CD73 expression in TNBC correlates with adverse clinical outcomes and resistance to anthracycline chemotherapy.
- Targeted inhibition of the CD73/A2A pathway effectively hinders tumorigenesis in preclinical models.
- Combined blockade of CD73/A2A demonstrates synergistic effects with other anti-cancer therapies.
Conclusions:
- CD73 is a validated therapeutic target in TNBC.
- Development of CD73 inhibitors is strongly recommended for TNBC treatment.
- Repositioning of A2A antagonists should be considered for cancer therapy.
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