CD73: A novel target for cancer immunotherapy

Bin Zhang*

*Corresponding author for this work

Research output: Contribution to journalReview articlepeer-review

193 Scopus citations


The promise of cancer immunotherapy has not been translated into clinical successes, in large part because of tumor-associated immune suppression that blocks effective antitumor immunity. Recent findings show a tumor-induced immunosuppressive mechanism, whereby tumor-derived CD73 functions as an ecto-enzyme to produce extracellular adenosine, which promotes tumor growth by limiting antitumor T-cell immunity via adenosine receptor signaling. Results with small molecule inhibitors, or monoclonal antibodies targeting CD73 in murine tumor models, suggest that targeted CD73 therapy is an important alternative and realistic approach to effective control of tumor growth. In particular, it helps T-cell-based therapy by enhancing the adaptive immune response machinery, which may increase the function of tumor-infiltrating T lymphocytes, and subsequently lead to improved survival in cancer patients.

Original languageEnglish (US)
Pages (from-to)6407-6411
Number of pages5
JournalCancer Research
Issue number16
StatePublished - Aug 15 2010

ASJC Scopus subject areas

  • Oncology
  • Cancer Research


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