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Immune Response to Cancer: From Tumor Onset to Therapeutic Approach
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Immune Response to Cancer: From Tumor Onset to Therapeutic Approach

A special issue of International Journal of Molecular Sciences (ISSN 1422-0067). This special issue belongs to the section "Molecular Immunology".

Deadline for manuscript submissions: closed (26 March 2021) | Viewed by 18733

Special Issue Editors

Dr. Marco Erreni

E-Mail Website
Guest Editor
Unit of Advanced Optical Microscopy, Humanitas Clinical and Research Center – IRCCS, Via Manzoni 56, 20089 Rozzano, Milan, Italy
Interests: tumor microenvironment; tumor-associated macrophages; colorectal cancer; inflammatory bowel diseases; cancer-related inflammation; innate immunity; optical imaging; intravital microscopy
Special Issues, Collections and Topics in MDPI journals
Dr. Diletta Di Mitri

E-Mail Website
Guest Editor
Unit of Advanced Optical Microscopy, Humanitas Clinical and Research Center – IRCCS, Via Manzoni 56, 20089 Rozzano, Milan, Italy
Interests: innate immunity; tumor immunology; tumor microenvironment; tumor-associated macrophages; prostate cancer; immunotherapy; resistance to cancer therapy; high-dimensional profiling of immune subsets
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleague,

Cancer represents a major leading cause of death worldwide. In recent decades, the contribution of the immune system to tumor development has gained growing interest, and inflammation is definitively considered a hallmark of cancer progression. Cancer immune-editing is a complex process by which components of the immune system can either protect the host against cancer development or promote tumor escape by sculpting tumor immunogenicity and modulating antitumor immune response. Efforts have focused on investigating the impact that immune cells have in the different stages of cancer progression, from the early onset of neoplastic transformation and the establishment of a growing tumor to the metastatic dissemination and therapeutic intervention. Accordingly, immunotherapy has today firmly been recognized as a novel pillar of cancer care: The administration of checkpoint inhibitors, cancer vaccines, and specific cytokines has been promisingly used to stimulate the immune system to effectively recognize and eliminate cancer cells.

Although a number of studies deeply investigate the interaction between cancer and the immune system, several aspects still need to be addressed.

The aim of this Special Issue is to provide an overview of recent advances in the field of “Immune Response to Cancer”. We therefore invite researchers to submit original papers and reviews to shed further light on the complex interaction between the immune system and neoplastic progression.

Potential topics include (but are not limited to):

  • The role of the immune system in the establishment and progression of tumor
  • Immunotherapy and immuno-oncology interventions
  • High dimensional profiling of the tumor immune microenvironment
  • Mechanisms of immune-mediated resistance to cancer therapy
  • Imaging the immune system in cancer

Dr. Marco Erreni
Dr. Diletta Di Mitri
Guest Editors

Manuscript Submission Information

Manuscripts should be submitted online at www.mdpi.com by registering and logging in to this website. Once you are registered, click here to go to the submission form. Manuscripts can be submitted until the deadline. All submissions that pass pre-check are peer-reviewed. Accepted papers will be published continuously in the journal (as soon as accepted) and will be listed together on the special issue website. Research articles, review articles as well as short communications are invited. For planned papers, a title and short abstract (about 100 words) can be sent to the Editorial Office for announcement on this website.

Submitted manuscripts should not have been published previously, nor be under consideration for publication elsewhere (except conference proceedings papers). All manuscripts are thoroughly refereed through a single-blind peer-review process. A guide for authors and other relevant information for submission of manuscripts is available on the Instructions for Authors page. International Journal of Molecular Sciences is an international peer-reviewed open access semimonthly journal published by MDPI.

Please visit the Instructions for Authors page before submitting a manuscript. There is an Article Processing Charge (APC) for publication in this open access journal. For details about the APC please see here. Submitted papers should be well formatted and use good English. Authors may use MDPI's English editing service prior to publication or during author revisions.

Keywords

  • tumor immunology
  • tumor microenvironment
  • cancer immuno-editing
  • cancer-related inflammation
  • immunotherapy
  • cancer imaging

Published Papers (5 papers)

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Research

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25 pages, 6794 KiB  
Article
Inhibition of the Histone Methyltransferase EZH2 Enhances Protumor Monocyte Recruitment in Human Mesothelioma Spheroids
by Silvia Mola, Giulia Pinton, Marco Erreni, Marco Corazzari, Marco De Andrea, Ambra A. Grolla, Veronica Martini, Laura Moro and Chiara Porta
Int. J. Mol. Sci. 2021, 22(9), 4391; https://doi.org/10.3390/ijms22094391 - 22 Apr 2021
Cited by 13 | Viewed by 3000
Abstract
Malignant pleural mesothelioma (MPM) is a highly aggressive cancer with a long latency period and dismal prognosis. Recently, tazemetostat (EPZ-6438), an inhibitor of the histone methyltransferase EZH2, has entered clinical trials due to the antiproliferative effects reported on MPM cells. However, the direct [...] Read more.
Malignant pleural mesothelioma (MPM) is a highly aggressive cancer with a long latency period and dismal prognosis. Recently, tazemetostat (EPZ-6438), an inhibitor of the histone methyltransferase EZH2, has entered clinical trials due to the antiproliferative effects reported on MPM cells. However, the direct and indirect effects of epigenetic reprogramming on the tumor microenvironment are hitherto unexplored. To investigate the impact of tumor-associated macrophages (TAMs) on MPM cell responsiveness to tazemetostat, we developed a three-dimensional MPM spheroid model that recapitulates in vitro, both monocytes’ recruitment in tumors and their functional differentiation toward a TAM-like phenotype (Mo-TAMs). Along with an increased expression of genes for monocyte chemoattractants, inhibitory immune checkpoints, immunosuppressive and M2-like molecules, Mo-TAMs promote tumor cell proliferation and spreading. Prolonged treatment of MPM spheroids with tazemetostat enhances both the recruitment of Mo-TAMs and the expression of their protumor phenotype. Therefore, Mo-TAMs profoundly suppress the antiproliferative effects due to EZH2 inhibition in MPM cells. Overall, our findings indicate that TAMs are a driving force for MPM growth, progression, and resistance to tazemetostat; therefore, strategies of TAM depletion might be evaluated to improve the therapeutic efficacy of pharmacological inhibition of EZH2. Full article
(This article belongs to the Special Issue Immune Response to Cancer: From Tumor Onset to Therapeutic Approach)
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15 pages, 5066 KiB  
Communication
STAT6 Is Critical for the Induction of Regulatory T Cells In Vivo Controlling the Initial Steps of Colitis-Associated Cancer
by Yael Delgado-Ramirez, Angel Ocaña-Soriano, Yadira Ledesma-Soto, Jonadab E. Olguín, Joselín Hernandez-Ruiz, Luis I. Terrazas and Sonia Leon-Cabrera
Int. J. Mol. Sci. 2021, 22(8), 4049; https://doi.org/10.3390/ijms22084049 - 14 Apr 2021
Cited by 12 | Viewed by 3106
Abstract
Inflammation is the main driver of the tumor initiation and progression in colitis-associated colorectal cancer (CAC). Recent findings have indicated that the signal transducer and activator of transcription 6 (STAT6) plays a fundamental role in the early stages of CAC, and STAT6 knockout [...] Read more.
Inflammation is the main driver of the tumor initiation and progression in colitis-associated colorectal cancer (CAC). Recent findings have indicated that the signal transducer and activator of transcription 6 (STAT6) plays a fundamental role in the early stages of CAC, and STAT6 knockout (STAT6−/−) mice are highly resistant to CAC development. Regulatory T (Treg) cells play a major role in coordinating immunomodulation in cancer; however, the role of STAT6 in the induction and function of Treg cells is poorly understood. To clarify the contribution of STAT6 to CAC, STAT6−/− and wild type (WT) mice were subjected to an AOM/DSS regimen, and the frequency of peripheral and local Treg cells was determined during the progression of CAC. When STAT6 was lacking, a remarkable reduction in tumor growth was observed, which was associated with decreased inflammation and an increased number of CD4+CD25+Foxp3+ cells in the colon, circulation, and spleen, including an over-expression of TGF-beta, IL-10, and Foxp3, compared to WT mice, during the early stages of CAC development. Conversely, WT mice showed an inverse frequency of Treg cells compared with STAT6−/− mice, which was followed by intestinal tumor formation. Increased mucosal inflammation, histological damage, and tumorigenesis were restored to levels observed in WT mice when an early inhibition/depletion of Treg cells was performed in STAT6−/− mice. Thus, with STAT6 deficiency, an increased number of Treg cells induce resistance against tumorigenesis, arresting tumor-promoting inflammation. We reported a direct role of STAT6 in the induction and function of Treg cells during CAC development and suggest that STAT6 is a potential target for the modulation of immune response in colitis and CAC. Full article
(This article belongs to the Special Issue Immune Response to Cancer: From Tumor Onset to Therapeutic Approach)
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Review

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13 pages, 323 KiB  
Review
Anti-PD1/PD-L1 Immunotherapy for Non-Small Cell Lung Cancer with Actionable Oncogenic Driver Mutations
by Edouard Dantoing, Nicolas Piton, Mathieu Salaün, Luc Thiberville and Florian Guisier
Int. J. Mol. Sci. 2021, 22(12), 6288; https://doi.org/10.3390/ijms22126288 - 11 Jun 2021
Cited by 56 | Viewed by 6367
Abstract
Anti-PD1/PD-L1 immunotherapy has emerged as a standard of care for stage III-IV non-small cell lung cancer (NSCLC) over the past decade. Patient selection is usually based on PD-L1 expression by tumor cells and/or tumor mutational burden. However, mutations in oncogenic drivers such as [...] Read more.
Anti-PD1/PD-L1 immunotherapy has emerged as a standard of care for stage III-IV non-small cell lung cancer (NSCLC) over the past decade. Patient selection is usually based on PD-L1 expression by tumor cells and/or tumor mutational burden. However, mutations in oncogenic drivers such as EGFR, ALK, BRAF, or MET modify the immune tumor microenvironment and may promote anti-PD1/PD-L1 resistance. In this review, we discuss the molecular mechanisms associated with these mutations, which shape the immune tumor microenvironment and may impede anti-PD1/PD-L1 efficacy. We provide an overview of the current clinical data on anti-PD1/PD-L1 efficacy in NSCLC with oncogenic driver mutation. Full article
(This article belongs to the Special Issue Immune Response to Cancer: From Tumor Onset to Therapeutic Approach)
13 pages, 430 KiB  
Review
Immunology and Immunotherapeutic Approaches for Advanced Renal Cell Carcinoma: A Comprehensive Review
by Yoon-Soo Hah and Kyo-Chul Koo
Int. J. Mol. Sci. 2021, 22(9), 4452; https://doi.org/10.3390/ijms22094452 - 24 Apr 2021
Cited by 12 | Viewed by 2716
Abstract
Renal cell carcinoma (RCC) is a malignant tumor associated with various tumor microenvironments (TMEs). The immune system is activated by the development of cancer and drives T cell anti-tumor response. CD8 T cells are known to improve clinical outcomes and sensitivity to immunotherapy, [...] Read more.
Renal cell carcinoma (RCC) is a malignant tumor associated with various tumor microenvironments (TMEs). The immune system is activated by the development of cancer and drives T cell anti-tumor response. CD8 T cells are known to improve clinical outcomes and sensitivity to immunotherapy, and play a crucial role against tumors. In contrast, tumor-associated macrophages (TAMs) suppress immunity against malignancy and lead to tumor progression. TAMs are promoted from damaged TMEs and mount proinflammatory responses to pathogens. Initial immunotherapy consists of interferon-α and interleukin-2. However, response to such therapy is unclear in most patients, and it is associated with high levels of toxicity. Immune checkpoint inhibitors (ICIs), which up-regulate immune responses by blocking the programed cell death protein 1 (PD-1) receptor, the ligand of PD-1, or cytotoxic T-lymphocyte-associated protein 4 T cells, have led to a new era of immunotherapy. Furthermore, combination strategies with ICIs have proven effective through several randomized controlled trials. We expect the next generation of immunotherapy to lead to better outcomes based on ongoing trials and inspire new therapeutic strategies. Full article
(This article belongs to the Special Issue Immune Response to Cancer: From Tumor Onset to Therapeutic Approach)
20 pages, 1504 KiB  
Review
The Dark Side of the Force: When the Immune System Is the Fuel of Tumor Onset
by Elisabeth Digifico, Silvia Balinzo and Cristina Belgiovine
Int. J. Mol. Sci. 2021, 22(3), 1224; https://doi.org/10.3390/ijms22031224 - 27 Jan 2021
Cited by 10 | Viewed by 2953
Abstract
Nowadays, it is well accepted that inflammation is a critical player in cancer, being, in most cases, the main character of the process. Different types of tumor arise from sites of infection or chronic inflammation. This non-resolving inflammation is responsible for tumor development [...] Read more.
Nowadays, it is well accepted that inflammation is a critical player in cancer, being, in most cases, the main character of the process. Different types of tumor arise from sites of infection or chronic inflammation. This non-resolving inflammation is responsible for tumor development at different levels: it promotes tumor initiation, as well as tumor progression, stimulating both tumor growth and metastasis. Environmental factors, lifestyle and infections are the three main triggers of chronic immune activation that promote or increase the risk of many different cancers. In this review, we focus our attention on tumor onset; in particular, we summarize the knowledge about the cause and the mechanisms behind the inflammation-driven cancer development. Full article
(This article belongs to the Special Issue Immune Response to Cancer: From Tumor Onset to Therapeutic Approach)
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