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Special Issue "Immune Microenvironment in Solid and Hematological Malignancies"

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A special issue of Journal of Clinical Medicine (ISSN 2077-0383). This special issue belongs to the section "Hematology".

Deadline for manuscript submissions: 25 May 2023 | Viewed by 6243

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Special Issue Editor

Dr. Antonio G. Solimando

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Guest Editor

Guido Baccelli Unit of Internal Medicine, Department of Biomedical Sciences and Human Oncology, School of Medicine, Aldo Moro University of Bari, Bari, Italy
Interests: internal medicine; oncology; hematological malignancies; multiple myeloma; emergency
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Special Issue Information

Dear Colleagues,

It is my pleasure to invite you to contribute to the upcoming Special Issue of the Journal of Clinical Medicine devoted entitled “Immune Microenvironment in Solid and Hematological Malignancies”. The aim of this issue is to provide an overview of current knowledge on the crucial mechanisms promoting tumor niche interactions and mediating immunosuppression during cancer development and progression.

Despite significant improvements in therapy during the last decade, most cancer patients develop refractory disease over time. Treatment of refractory malignancy is a major challenge, likely due to the still poorly characterized inter- and intratumor heterogeneity and the complex interplay of neoplastic cells with the tumor microenvironment. In particular, there is an urgent need to unravel how these features of the cancer neighborhood are linked to molecular mechanisms of drug resistance and aggressive phenotype. The aim of this issue is to review current knowledge on the crucial mechanisms promoting malignant evolution and mediating immunosuppression during cancer development and progression. As is now well known, tumors grow and evolve through a constant crosstalk with the surrounding milieu, and emerging evidence indicates that several gatekeepers and immune-tolerogenic environments frequently occur simultaneously in response to this crosstalk. Accordingly, strategies combining anti-tumor therapy and immunotherapy seem to hold the promise to tip the balance of the cancer niche and improve patient outcomes.

All manuscripts will be peer-reviewed according to standard journal procedures and policies.

I hope that you will be able to accept this invitation and contribute to the success of this Special Issue. I look forward to collaborating with you.

Sincerely,

Dr. Antonio G. Solimando
Guest Editor

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. Journal of Clinical Medicine is an international peer-reviewed open access semimonthly journal published by MDPI.

Please visit the Instructions for Authors page before submitting a manuscript. The Article Processing Charge (APC) for publication in this open access journal is 2600 CHF (Swiss Francs). 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

immune cells
immune checkpoints
immunotherapy
microenvironment
tumor angiogenesis

Published Papers (5 papers)

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Editorial

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Open AccessEditorial

The Urgent Need for Precision Medicine in Cancer and Its Microenvironment: The Paradigmatic Case of Multiple Myeloma

Antonio Giovanni Solimando

Markus Krebs

Max Bittrich

and

Hermann Einsele

J. Clin. Med. 2022, 11(18), 5461; https://doi.org/10.3390/jcm11185461 - 16 Sep 2022

Viewed by 831

Abstract

Precision medicine is particularly relevant for cancer and microenvironment deconvolution for therapeutic purposes in hematological and non-hematological malignancies [...] Full article

(This article belongs to the Special Issue Immune Microenvironment in Solid and Hematological Malignancies)

Review

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Open AccessReview

Extracellular Vesicles and Their Roles in the Tumor Immune Microenvironment

Antonia Reale

Tiffany Khong

and

Andrew Spencer

J. Clin. Med. 2022, 11(23), 6892; https://doi.org/10.3390/jcm11236892 - 22 Nov 2022

Cited by 1 | Viewed by 718

Abstract

Tumor cells actively incorporate molecules (e.g., proteins, lipids, RNA) into particles named extracellular vesicles (EVs). Several groups have demonstrated that EVs can be transferred to target (recipient) cells, making EVs an important means of intercellular communication. Indeed, EVs are able to modulate the functions of target cells by reprogramming signaling pathways. In a cancer context, EVs promote the formation of a supportive tumor microenvironment (TME) and (pre)metastatic niches. Recent studies have revealed that immune cells, tumor cells and their secretome, including EVs, promote changes in the TME and immunosuppressive functions of immune cells (e.g., natural killer, dendritic cells, T and B cells, monocytes, macrophages) that allow tumor cells to establish and propagate. Despite the growing knowledge on EVs and on their roles in cancer and as modulators of the immune response/escape, the translation into clinical practice remains in its early stages, hence requiring improved translational research in the EVs field. Here, we comprehensively review the current knowledge and most recent research on the roles of EVs in tumor immune evasion and immunosuppression in both solid tumors and hematological malignancies. We also highlight the clinical utility of EV-mediated immunosuppression targeting and EV-engineering. Importantly, we discuss the controversial role of EVs in cancer biology, current limitations and future perspectives to further the EV knowledge into clinical practice. Full article

(This article belongs to the Special Issue Immune Microenvironment in Solid and Hematological Malignancies)

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Open AccessReview

Pathways of Angiogenic and Inflammatory Cytokines in Multiple Myeloma: Role in Plasma Cell Clonal Expansion and Drug Resistance

Maria Antonia Frassanito

Angelo Vacca

and

Roberto Ria

J. Clin. Med. 2022, 11(21), 6491; https://doi.org/10.3390/jcm11216491 - 01 Nov 2022

Cited by 1 | Viewed by 795

Abstract

Multiple myeloma (MM) is the second most common hematological malignancy, and despite the introduction of innovative therapies, remains an incurable disease. Identifying early and minimally or non-invasive biomarkers for predicting clinical outcomes and therapeutic responses is an active field of investigation. Malignant plasma cells (PCs) reside in the bone marrow (BM) microenvironment (BMME) which comprises cells (e.g., tumour, immune, stromal cells), components of the extracellular matrix (ECM) and vesicular and non-vesicular (soluble) molecules, all factors that support PCs’ survival and proliferation. The interaction between PCs and BM stromal cells (BMSCs), a hallmark of MM progression, is based not only on intercellular interactions but also on autocrine and paracrine circuits mediated by soluble or vesicular components. In fact, PCs and BMSCs secrete various cytokines, including angiogenic cytokines, essential for the formation of specialized niches called “osteoblastic and vascular niches”, thus supporting neovascularization and bone disease, vital processes that modulate the pathophysiological PCs–BMME interactions, and ultimately promoting disease progression. Here, we aim to discuss the roles of cytokines and growth factors in pathogenetic pathways in MM and as prognostic and predictive biomarkers. We also discuss the potential of targeted drugs that simultaneously block PCs’ proliferation and survival, PCs–BMSCs interactions and BMSCs activity, which may represent the future goal of MM therapy. Full article

(This article belongs to the Special Issue Immune Microenvironment in Solid and Hematological Malignancies)

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Open AccessReview

The Leading Role of the Immune Microenvironment in Multiple Myeloma: A New Target with a Great Prognostic and Clinical Value

Vanessa Desantis

Francesco Domenico Savino

Antonietta Scaringella

Maria Assunta Potenza

Carmela Nacci

Maria Antonia Frassanito

Angelo Vacca

and

Monica Montagnani

J. Clin. Med. 2022, 11(9), 2513; https://doi.org/10.3390/jcm11092513 - 29 Apr 2022

Cited by 8 | Viewed by 2194

Abstract

Multiple myeloma (MM) is a plasma cell (PC) malignancy whose development flourishes in the bone marrow microenvironment (BMME). The BMME components’ immunoediting may foster MM progression by favoring initial immunotolerance and subsequent tumor cell escape from immune surveillance. In this dynamic process, immune effector cells are silenced and become progressively anergic, thus contributing to explaining the mechanisms of drug resistance in unresponsive and relapsed MM patients. Besides traditional treatments, several new strategies seek to re-establish the immunological balance in the BMME, especially in already-treated MM patients, by targeting key components of the immunoediting process. Immune checkpoints, such as CXCR4, T cell immunoreceptor with immunoglobulin and ITIM domains (TIGIT), PD-1, and CTLA-4, have been identified as common immunotolerance steps for immunotherapy. B-cell maturation antigen (BCMA), expressed on MMPCs, is a target for CAR-T cell therapy, antibody-(Ab) drug conjugates (ADCs), and bispecific mAbs. Approved anti-CD38 (daratumumab, isatuximab), anti-VLA4 (natalizumab), and anti-SLAMF7 (elotuzumab) mAbs interfere with immunoediting pathways. New experimental drugs currently being evaluated (CD137 blockers, MSC-derived microvesicle blockers, CSF-1/CSF-1R system blockers, and Th17/IL-17/IL-17R blockers) or already approved (denosumab and bisphosphonates) may help slow down immune escape and disease progression. Thus, the identification of deregulated mechanisms may identify novel immunotherapeutic approaches to improve MM patients’ outcomes. Full article

(This article belongs to the Special Issue Immune Microenvironment in Solid and Hematological Malignancies)

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Other

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Open AccessBrief Report

A Proliferation-Inducing Ligand and B-Cell Activating Factor Are Upregulated in Patients with Essential Thrombocythemia

and

J. Clin. Med. 2022, 11(16), 4663; https://doi.org/10.3390/jcm11164663 - 09 Aug 2022

Cited by 1 | Viewed by 817

Abstract

A proliferation-inducing ligand (APRIL) and B-cell activating factor (BAFF) are cytokines belonging to the tumor necrosis factor family which play an essential role in B-cell maturation, differentiation, and survival. Recent evidence indicates their importance in hematological disorders; however, their function in essential thrombocytosis (ET) pathogenesis remains elusive. Therefore, we aimed to analyze the role of APRIL and BAFF in megakaryocytopoiesis in ET patients. We observed elevated levels of APRIL and BAFF in the plasma of ET patients compared with healthy controls, while no differences were found among patients with different JAK2(V617F) statuses. In addition, APRIL levels were positively associated with the number of platelets and WBC count. In the bone marrow, APRIL but not BAFF levels were higher in ET patients with the JAK2(V617F) mutation; however, JAK2(V617F)-negative patients showed slightly reduced levels of BAFF. In ET patients, we showed that the differentiation of CD34+ progenitor cells towards megakaryocytes induces the expression of both APRIL and BAFF. More importantly, APRIL neutralization significantly reduced platelet production. In conclusion, our data provide evidence that blocking APRIL signaling, which acts as an autocrine growth factor for terminal megakaryocytopoiesis, inhibits platelet production in ET patients, regardless of the status of JAK2(V617F) mutation. Full article

(This article belongs to the Special Issue Immune Microenvironment in Solid and Hematological Malignancies)

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Special Issue "Immune Microenvironment in Solid and Hematological Malignancies"

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