Tumor microenvironment and immunotherapy of oral cancer

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Abstract

Oral cancer is one of the most common malignant tumors of the head and neck, not only affects the appearance, but also affects eating and even endangers life. The clinical treatments of oral cancer mainly include surgery, radiotherapy, and chemotherapy. However, unsatisfactory therapeutic effect and toxic side effects are still the main problems in clinical treatment. Tumor microenvironment (TME) is not only closely related to the occurrence, growth, and metastasis of tumor but also works in the diagnosis, prevention, and treatment of tumor and prognosis. Future studies should continue to investigate the relationship of TME and oral cancer therapy. This purpose of this review was to analyze the characteristics of oral cancer microenvironment, summarize the traditional oral cancer therapy and immunotherapy strategies, and finally prospect the development prospects of oral cancer immunotherapy. Immunotherapy targeting tumor microenvironment is expected to provide a new strategy for clinical treatment of oral cancer.

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Primary, Adaptive, and Acquired Resistance to Cancer Immunotherapy.

Padmanee Sharma, Siwen Hu-Lieskovan, Jennifer A. Wargo … (2017)

Cancer immunotherapy can induce long lasting responses in patients with metastatic cancers of a wide range of histologies. Broadening the clinical applicability of these treatments requires an improved understanding of the mechanisms limiting cancer immunotherapy. The interactions between the immune system and cancer cells are continuous, dynamic, and evolving from the initial establishment of a cancer cell to the development of metastatic disease, which is dependent on immune evasion. As the molecular mechanisms of resistance to immunotherapy are elucidated, actionable strategies to prevent or treat them may be derived to improve clinical outcomes for patients.

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Macrophage plasticity, polarization, and function in health and disease.

Fatemeh Mardani, Abbas Shapouri-Moghaddam, Saeed Mohammadian … (2018)

Macrophages are heterogeneous and their phenotype and functions are regulated by the surrounding micro-environment. Macrophages commonly exist in two distinct subsets: 1) Classically activated or M1 macrophages, which are pro-inflammatory and polarized by lipopolysaccharide (LPS) either alone or in association with Th1 cytokines such as IFN-γ, GM-CSF, and produce pro-inflammatory cytokines such as interleukin-1β (IL-1β), IL-6, IL-12, IL-23, and TNF-α; and 2) Alternatively activated or M2 macrophages, which are anti-inflammatory and immunoregulatory and polarized by Th2 cytokines such as IL-4 and IL-13 and produce anti-inflammatory cytokines such as IL-10 and TGF-β. M1 and M2 macrophages have different functions and transcriptional profiles. They have unique abilities by destroying pathogens or repair the inflammation-associated injury. It is known that M1/M2 macrophage balance polarization governs the fate of an organ in inflammation or injury. When the infection or inflammation is severe enough to affect an organ, macrophages first exhibit the M1 phenotype to release TNF-α, IL-1β, IL-12, and IL-23 against the stimulus. But, if M1 phase continues, it can cause tissue damage. Therefore, M2 macrophages secrete high amounts of IL-10 and TGF-β to suppress the inflammation, contribute to tissue repair, remodeling, vasculogenesis, and retain homeostasis. In this review, we first discuss the basic biology of macrophages including origin, differentiation and activation, tissue distribution, plasticity and polarization, migration, antigen presentation capacity, cytokine and chemokine production, metabolism, and involvement of microRNAs in macrophage polarization and function. Secondly, we discuss the protective and pathogenic role of the macrophage subsets in normal and pathological pregnancy, anti-microbial defense, anti-tumor immunity, metabolic disease and obesity, asthma and allergy, atherosclerosis, fibrosis, wound healing, and autoimmunity.

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Is Open Access

A framework for advancing our understanding of cancer-associated fibroblasts

Erik Sahai, Igor Astsaturov, Edna Cukierman … (2020)

Cancer-associated fibroblasts (CAFs) are a key component of the tumour microenvironment with diverse functions, including matrix deposition and remodelling, extensive reciprocal signalling interactions with cancer cells and crosstalk with infiltrating leukocytes. As such, they are a potential target for optimizing therapeutic strategies against cancer. However, many challenges are present in ongoing attempts to modulate CAFs for therapeutic benefit. These include limitations in our understanding of the origin of CAFs and heterogeneity in CAF function, with it being desirable to retain some antitumorigenic functions. On the basis of a meeting of experts in the field of CAF biology, we summarize in this Consensus Statement our current knowledge and present a framework for advancing our understanding of this critical cell type within the tumour microenvironment.

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Author and article information

Contributors

Song Zhu: zhusong@jlu.edu.cn

Jie Chen: chenjie@ciac.ac.cn

Journal

Journal ID (nlm-ta): Eur J Med Res

Journal ID (iso-abbrev): Eur J Med Res

Title: European Journal of Medical Research

Publisher: BioMed Central (London )

ISSN (Print): 0949-2321

ISSN (Electronic): 2047-783X

Publication date (Electronic): 8 October 2022

Publication date PMC-release: 8 October 2022

Publication date Collection: 2022

Volume: 27

Electronic Location Identifier: 198

Affiliations

[1 ]GRID grid.64924.3d, ISNI 0000 0004 1760 5735, Hospital of Stomatology, , Jilin University, ; Changchun, 130021 People’s Republic of China

[2 ]GRID grid.9227.e, ISNI 0000000119573309, Key Laboratory of Polymer Ecomaterials, Changchun Institute of Applied Chemistry, , Chinese Academy of Sciences, ; Changchun, 130022 People’s Republic of China

Article

Publisher ID: 835

DOI: 10.1186/s40001-022-00835-4

PMC ID: 9547678

PubMed ID: 36209263

SO-VID: d7e8c9c0-1dfd-4f80-a771-cbe6994ca4c3

License:

Open AccessThis article is licensed under a Creative Commons Attribution 4.0 International License, which permits use, sharing, adaptation, distribution and reproduction in any medium or format, as long as you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons licence, and indicate if changes were made. The images or other third party material in this article are included in the article's Creative Commons licence, unless indicated otherwise in a credit line to the material. If material is not included in the article's Creative Commons licence and your intended use is not permitted by statutory regulation or exceeds the permitted use, you will need to obtain permission directly from the copyright holder. To view a copy of this licence, visit http://creativecommons.org/licenses/by/4.0/. The Creative Commons Public Domain Dedication waiver ( http://creativecommons.org/publicdomain/zero/1.0/) applies to the data made available in this article, unless otherwise stated in a credit line to the data.

History

Date received : 3 August 2022

Date accepted : 22 September 2022

Funding

Funded by: Science and Technology Research Program of Education Department of Jilin Province

Award ID: JJKH20221097KJ

Award Recipient : Min Wang

Funded by: National Key Research and Development Program of China

Award ID: 2021YFC2400405

Award Recipient : Song Zhu

Funded by: National Natural Science Foundation of China

Award ID: 51973217

Award Recipient : Jie Chen

Funded by: Department of Science and Technology of Jilin Province

Award ID: 20200201075JC

Award Recipient : Jie Chen

Custom metadata

ScienceOpen disciplines: Medicine

Keywords: oral cancer,immunotherapy,tumor microenvironment,immune checkpoint blockade,immune tolerance

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ScienceOpen disciplines: Medicine

Keywords: oral cancer, immunotherapy, tumor microenvironment, immune checkpoint blockade, immune tolerance

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Cancer Immunotherapy

Most cited references 197

Primary, Adaptive, and Acquired Resistance to Cancer Immunotherapy.

Macrophage plasticity, polarization, and function in health and disease.

A framework for advancing our understanding of cancer-associated fibroblasts

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