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TGFβ pathway inhibition in the treatment of non-small cell lung cancer
1Lowe Center for Thoracic Oncology, Dana-Farber Cancer Institute, Boston, MA, United States; Department of Medical Oncology, Dana-Farber Cancer Institute, Boston, MA, United States; Department of Medicine, Brigham and Women's Hospital and Harvard Medical School, Boston, MA, United States; Program in Biological and Biomedical Sciences, Harvard Medical School, Boston, MA, United States.
Abstract:
Advanced non-small cell lung cancer (NSCLC) continues to be an incurable family of thoracic malignancies that is chronically managed with chemotherapy, targeted therapy, and immunotherapy. While the discovery of driver oncogenes and the advent of targeted and immunotherapies in the last decade have vastly improved clinical disease management for patients harboring druggable mutations, the mainstay treatment for the majority of NSCLC patients remains cytotoxic chemotherapy. The clinical efficacy of targeted, immune, and cytotoxic therapies is limited by the development of drug resistance. Transforming growth factor beta (TGFβ) signaling, a crucial mediator of embryonic development and peripheral immune tolerance, may be dysregulated in some malignant contexts, including lung cancer, and has been correlated with poor prognosis in advanced cancers. Aberrant upregulation of TGFβ expression in the tumor microenvironment has also been implicated in promoting NSCLC progression and metastasis, as well as driving the development of resistance to cytotoxic, targeted, and immunomodulatory therapeutic interventions. Here, we examine the mechanisms underlying TGFβ-mediated drug resistance in NSCLC, and consider TGFβ as a combinatorial therapeutic intervention to circumvent or delay the development of NSCLC treatment resistance.
Insights
Transforming growth factor beta (TGFβ) signaling promotes drug resistance in advanced non-small cell lung cancer (NSCLC). Targeting TGFβ may help overcome treatment resistance in NSCLC patients.
Area of Science:
- Oncology
- Molecular Biology
- Cancer Research
Background:
- Advanced non-small cell lung cancer (NSCLC) remains largely incurable, with cytotoxic chemotherapy as the primary treatment for most patients.
- While targeted therapies and immunotherapies have improved outcomes for some, drug resistance remains a significant clinical challenge.
- Transforming growth factor beta (TGFβ) signaling is implicated in cancer progression and poor prognosis.
Purpose of the Study:
- To investigate the mechanisms by which TGFβ signaling contributes to drug resistance in NSCLC.
- To explore the potential of TGFβ as a therapeutic target to overcome treatment resistance in NSCLC.
Main Methods:
- Review of current literature on TGFβ signaling pathways in NSCLC.
- Analysis of the role of TGFβ in the tumor microenvironment.
- Examination of TGFβ's impact on resistance to various cancer therapies.
Main Results:
- Aberrant TGFβ signaling is upregulated in the tumor microenvironment of advanced NSCLC.
- TGFβ promotes NSCLC progression, metastasis, and resistance to chemotherapy, targeted therapy, and immunotherapy.
- Dysregulated TGFβ signaling is correlated with poor patient prognosis.
Conclusions:
- TGFβ signaling is a key mediator of therapeutic resistance in NSCLC.
- Targeting TGFβ may offer a novel strategy to circumvent or delay treatment resistance, improving outcomes for NSCLC patients.
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