Switching off CD73: a way to boost the activity of conventional and targeted antineoplastic therapies

L Antonioli, SV Novitskiy, KF Sachsenmeier… - Drug discovery today, 2017 - Elsevier
Drug discovery today, 2017Elsevier
Highlights•CD73 supports cancer onset and progression via an 'adenosine halo'.•Preclinical
studies highlighted CD73 as a useful target for cancer management.•CD73 blockade
reduces cancer growth and proliferation and restrains cell spreading.•A synergy is emerging
between CD73 blockade and conventional anticancer therapies.Over the past few years,
several preclinical studies have highlighted the value of CD73 (ecto-5′-nucleotidase) as a
potential therapeutic target for cancer therapy. Indeed, the pharmacological blockade of …
Highlights
  • CD73 supports cancer onset and progression via an ‘adenosine halo’.
  • Preclinical studies highlighted CD73 as a useful target for cancer management.
  • CD73 blockade reduces cancer growth and proliferation and restrains cell spreading.
  • A synergy is emerging between CD73 blockade and conventional anticancer therapies.
Over the past few years, several preclinical studies have highlighted the value of CD73 (ecto-5′-nucleotidase) as a potential therapeutic target for cancer therapy. Indeed, the pharmacological blockade of CD73, via monoclonal antibodies or small molecules, has promise in counteracting cancer development, growth and spread. Synergistic combinations of anti-CD73 drugs with conventional cancer treatments (ie, chemotherapy, radiation therapy, immunotherapy, targeted therapy) have increased therapeutic potential. In this review, we discuss the potential synergistic effects of CD73 blockers and conventional antineoplastic therapies in the treatment of cancer.
Elsevier