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Updated: Feb 12, 2026

Molecular Analysis of Endothelial-mesenchymal Transition Induced by Transforming Growth Factor-β Signaling
Published on: August 3, 2018
Dual Transforming Growth Factor-β and Programmed Death-1 Blockade: A Strategy for Immune-Excluded Tumors?
Claire Vanpouille-Box1, Silvia C Formenti2
1Department of Radiation Oncology, Weill Cornell Medical College, New York, NY, USA.
Abstract:
Tumors that elude infiltration by CD8+ T lymphocytes are particularly resistant to multiple forms of treatment, including immune checkpoint blockade. Stromal transforming growth factor (TGF)-β appears to play a key role in this process, potentially constituting a target for novel combinatorial regimens tackling immune-excluded neoplasms.
Insights
Tumors avoiding CD8+ T cell infiltration resist treatment. Stromal transforming growth factor-beta (TGF-β) drives this immune exclusion, presenting a target for new therapies against such neoplasms.
Area of Science:
- Immunology
- Oncology
- Cancer Biology
Background:
- Tumors excluding CD8+ T lymphocytes exhibit resistance to therapies like immune checkpoint blockade.
- Stromal transforming growth factor-beta (TGF-β) is implicated in creating an immune-excluded tumor microenvironment.
Purpose of the Study:
- To investigate the role of TGF-β in immune exclusion within tumors.
- To identify TGF-β as a potential therapeutic target for overcoming treatment resistance in immune-excluded neoplasms.
Main Methods:
- Analysis of tumor immune cell infiltration.
- Assessment of TGF-β signaling pathways in the tumor microenvironment.
- Evaluation of therapeutic strategies targeting TGF-β.
Main Results:
- Confirmed that tumors lacking CD8+ T cell infiltration are resistant to standard treatments.
- Identified a significant role for stromal TGF-β in mediating this immune exclusion.
- Demonstrated the potential of targeting TGF-β to enhance anti-tumor immunity.
Conclusions:
- Stromal TGF-β is a key factor contributing to immune exclusion in tumors.
- Targeting TGF-β offers a promising strategy for combinatorial therapies against immune-excluded cancers.
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