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Inflammation and Myeloid Cells in Cancer Progression and Metastasis
Jenying Deng1, Jason B Fleming2
1Department of Surgical Oncology, The University of Texas MD Anderson Cancer Center, Houston, TX, United States.
Abstract:
To date, the most immunotherapy drugs act upon T cell surface proteins to promote tumoricidal T cell activity. However, this approach has to date been unsuccessful in certain solid tumor types including pancreatic, prostate cancer and glioblastoma. Myeloid-related innate immunity can promote tumor progression through direct and indirect effects on T cell activity; improved understanding of this field may provide another therapeutic avenue for patients with these tumors. Myeloid cells can differentiate into both pro-inflammatory and anti-inflammatory mature form depending upon the microenvironment. Most cancer type exhibit oncogenic activating point mutations (ex. P53 and KRAS) that trigger cytokines production. In addition, tumor environment (ex. Collagen, Hypoxia, and adenosine) also regulated inflammatory signaling cascade. Both the intrinsic and extrinsic factor driving the tumor immune microenvironment and regulating the differentiation and function of myeloid cells, T cells activity and tumor progression. In this review, we will discuss the relationship between cancer cells and myeloid cells-mediated tumor immune microenvironment to promote cancer progression and immunotherapeutic resistance. Furthermore, we will describe how cytokines and chemokines produced by cancer cells influence myeloid cells within immunosuppressive environment. Finally, we will comment on the development of immunotherapeutic strategies with respect to myeloid-related innate immunity.
Insights
Immunotherapy targeting T cells fails in some cancers. Understanding myeloid cells
Area of Science:
- Immunology
- Oncology
- Cancer Research
Background:
- Current immunotherapies primarily target T cell surface proteins, showing limited success in solid tumors like pancreatic cancer, prostate cancer, and glioblastoma.
- Myeloid cells play a dual role in cancer, potentially promoting tumor progression and influencing T cell activity.
- The tumor immune microenvironment, shaped by cancer cell mutations and tumor microenvironment factors, critically regulates myeloid and T cell functions.
Purpose of the Study:
- To review the intricate relationship between cancer cells and myeloid cells in shaping the tumor immune microenvironment.
- To explore how myeloid-related innate immunity contributes to cancer progression and resistance to immunotherapy.
- To discuss the influence of cytokines and chemokines on myeloid cell function within immunosuppressive tumor environments.
Main Methods:
- Literature review of existing research on myeloid cells, tumor immune microenvironment, and cancer progression.
- Analysis of intrinsic (cancer cell mutations) and extrinsic (tumor microenvironment) factors influencing immune cells.
- Discussion of current and potential immunotherapeutic strategies targeting myeloid-related innate immunity.
Main Results:
- Myeloid cells can differentiate into pro- or anti-inflammatory phenotypes based on the microenvironment.
- Cancer cell-intrinsic factors (e.g., P53, KRAS mutations) and extrinsic factors (e.g., collagen, hypoxia, adenosine) drive immune cell behavior.
- Cytokines and chemokines produced by cancer cells significantly impact myeloid cell function and contribute to an immunosuppressive environment.
Conclusions:
- Targeting myeloid-related innate immunity offers a promising therapeutic avenue for difficult-to-treat solid tumors.
- A deeper understanding of the myeloid cell-tumor cell crosstalk is crucial for overcoming immunotherapeutic resistance.
- Future immunotherapeutic strategies should consider modulating myeloid cell functions to enhance anti-tumor responses.
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