Targeting immunosuppression by TGF-β1 for cancer immunotherapy
Biochemical Pharmacology, ISSN: 0006-2952, Vol: 192, Page: 114697
2021
- 62Citations
- 47Captures
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Example: if you select the 1-year option for an article published in 2019 and a metric category shows 90%, that means that the article or review is performing better than 90% of the other articles/reviews published in that journal in 2019. If you select the 3-year option for the same article published in 2019 and the metric category shows 90%, that means that the article or review is performing better than 90% of the other articles/reviews published in that journal in 2019, 2018 and 2017.
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Metrics Details
- Citations62
- Citation Indexes60
- 60
- CrossRef35
- Patent Family Citations2
- Patent Families2
- Captures47
- Readers47
- 47
Review Description
The TGF-β1 cytokine is a key mediator of many biological processes. Complex regulatory mechanisms are in place that allow one single molecule to exert so many distinct indispensable activities. The complexity of TGF-β1 biology is further illustrated by the opposing dual roles it plays during cancer progression. Risks of toxicities combined with lack of convincing therapeutical efficacy explain at least in part why therapies targeting TGF-β1 have lagged behind in past decades. However, recent successes of immunostimulatory antibodies for the immunotherapy of cancer and findings that TGF-β1 activity associates with resistance to immunotherapeutic drugs have revived the field. In this review, we discuss the biology of TGF-β1 with a special focus on its roles in regulating immune responses in the context of cancer. We describe the various therapeutic approaches available to inhibit TGF-β signalling, and more recent findings that allow selective targeting of specific sources of TGF-β activity, which may prove relevant to increase the efficacy and reduce the toxicity of cancer immunotherapy.
Bibliographic Details
http://www.sciencedirect.com/science/article/pii/S0006295221003105; http://dx.doi.org/10.1016/j.bcp.2021.114697; http://www.scopus.com/inward/record.url?partnerID=HzOxMe3b&scp=85113293141&origin=inward; http://www.ncbi.nlm.nih.gov/pubmed/34302795; https://linkinghub.elsevier.com/retrieve/pii/S0006295221003105; https://dx.doi.org/10.1016/j.bcp.2021.114697
Elsevier BV
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