Topic Editors

Department of Molecular Medicine and Medical Biotechnology, Federico II Faculty of Naples, 80138 Napoli, Italy
Dr. Renata Grifantini
Head Translational Research Unit, Istituto Nazionale di Genetica Molecolare (INGM), Milano, Italy

Anti-Tumor Immune Responses 2.0

Abstract submission deadline
closed (30 June 2024)
Manuscript submission deadline
closed (31 August 2024)
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6176

Topic Information

Dear Colleagues,

It remains unclear how and when, during multi-step tumor progression via clonal selection, cancer cells are selected for their high mutational burden, as well as how the immune system is first alerted to their presence and begins its initial, often unsuccessful, attempts at eliminating them. At present, it is impossible to say which of the dozens of immunotherapy strategies under development will become the precursors of anti-cancer treatments that will prove to be vastly more effective than those developed to date and that will generate robust, durable responses for the majority of patients receiving treatment. For example, advances in molecular genetics, biochemistry, virus biology, cellular and system biology, and cellular immunology have recently converged with discoveries in drugs and antibodies to generate novel, potentially powerful ways to harness the immune response to eradicate human tumors. At this time, the action of the immune system has improved two types of attacks against infectious agents or cells targeted for destruction or neutralization. These involve humoral and cellular immunity, as some types of cells, particularly macrophages and NK cells, have an innate ability to recognize cells that should be destroyed. In this issue, we would like to discuss the frontiers in this area of research concerning cancer cell types where these phenomena have been proven to be positively active at the level of hematopoietic malignancies and, most importantly, in solid tumors with advanced immune therapies. Examples of instances where these strategies fail are of great value for better understanding how cancer cells evade this immune mechanism using the most recent genome biology technologies to determine which other genes/proteins/pathways are involved in these coordinated, interconnecting actions.

Prof. Dr. Massimo Zollo
Dr. Renata Grifantini
Topic Editors

Keywords

  • genetics
  • biochemistry
  • virology
  • system biology
  • immune evasion
  • immune cells
  • immune drugs
  • immune antibodies
  • signaling pathways
  • immune therapies
  • antitumor vaccines

Participating Journals

Journal Name Impact Factor CiteScore Launched Year First Decision (median) APC
Antibodies
antibodies
3.0 7.1 2012 23 Days CHF 1800
Cancers
cancers
4.5 8.0 2009 16.3 Days CHF 2900
Immuno
immuno
2.1 2.6 2021 28.1 Days CHF 1000
International Journal of Molecular Sciences
ijms
4.9 8.1 2000 18.1 Days CHF 2900
Vaccines
vaccines
5.2 8.9 2013 17.6 Days CHF 2700

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Published Papers (3 papers)

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12 pages, 636 KiB  
Article
Predictive Factors for Early Immune Recovery in NHL Patients after Autologous Transplantation: A Multicenter Prospective Study
by Anu Partanen, Antti Turunen, Outi Kuittinen, Hanne Kuitunen, Pentti Mäntymaa, Ville Varmavuo and Esa Jantunen
Cancers 2024, 16(14), 2550; https://doi.org/10.3390/cancers16142550 - 16 Jul 2024
Cited by 1 | Viewed by 685
Abstract
Early lymphocyte recovery as manifested by an absolute lymphocyte count at d+15 (ALC-15) ≥ 0.5 × 109/L after autologous hematopoietic stem cell transplantation (AHCT) has been associated with a better outcome. This prospective multicenter study aimed to clarify factors associated with [...] Read more.
Early lymphocyte recovery as manifested by an absolute lymphocyte count at d+15 (ALC-15) ≥ 0.5 × 109/L after autologous hematopoietic stem cell transplantation (AHCT) has been associated with a better outcome. This prospective multicenter study aimed to clarify factors associated with ALC-15 ≥ 0.5 × 109/L after AHCT among 178 patients with non-Hodgkin lymphoma. The mobilization capacity, as manifested by peak blood CD34+ cell numbers > 45 × 106/L correlated with higher ALC-15 levels (p = 0.020). In addition, the amount of CD3+CD4+ T cells > 31.8 × 106/kg in the infused graft predicted ALC-15 ≥ 0.5 × 109/L (p < 0.001). Also, the number of infused graft CD3+CD8+ T cells > 28.8 × 106/kg (p = 0.017) and NK cells > 4.4 × 106/kg was linked with higher ALC-15 (p < 0.001). The two-year progression-free survival after AHCT was significantly better in patients with ALC-15 ≥ 0.5 × 109/L (74 vs. 57%, p = 0.027). The five-year OS in patients with higher ALC-15 was 78% vs. 60% in those with lower ALC-15 (p = 0.136). To conclude, the mobilization capacity of CD34+ cells and detailed measures of graft cellular content mark prognostic tools that predict ALC-15 ≥ 0.5 × 109/L, which is associated with a better outcome in NHL patients after AHCT. Full article
(This article belongs to the Topic Anti-Tumor Immune Responses 2.0)
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16 pages, 3136 KiB  
Article
Anti-CD99 Antibody Therapy Triggers Macrophage-Dependent Ewing Cell Death In Vitro and Myeloid Cell Recruitment In Vivo
by Allison F. O’Neill, Evelyn M. Nguyen, Evelyn D. Maldonado, Matthew R. Chang, Jiusong Sun, Quan Zhu and Wayne A. Marasco
Antibodies 2024, 13(1), 24; https://doi.org/10.3390/antib13010024 - 18 Mar 2024
Viewed by 2426
Abstract
Background: Ewing sarcoma is a rare tumor of the bone or soft tissues characterized by diffuse membranous staining for CD99. As this tumor remains incurable in the metastatic, relapsed, and refractory settings, we explored the downstream immune implications of targeting CD99. Methods: We [...] Read more.
Background: Ewing sarcoma is a rare tumor of the bone or soft tissues characterized by diffuse membranous staining for CD99. As this tumor remains incurable in the metastatic, relapsed, and refractory settings, we explored the downstream immune implications of targeting CD99. Methods: We discovered a human anti-CD99 antibody (NOA2) by phagemid panning and investigated NOA2 immune cell-mediated cytotoxicity in vitro and in vivo focusing on the myeloid cell compartment, given that M2 macrophages are present in human tumors and associated with a poor prognosis. Results: NOA2 is capable of inducing immune effector cell-mediated Ewing death in vitro via engagement of macrophages. Mice with metastatic Ewing tumors, treated with NOA2, experience tumor growth arrest and an associated increase in intratumoral macrophages. Further, incubation of macrophages and Ewing cells with NOA2, in conjunction with anti-PILRα antibody blockade in vitro, results in the reactivation of previously dormant macrophages possibly due to interrupted binding of Ewing CD99 to macrophage PILRα. Conclusions: These studies are the first to demonstrate the role of human immune effector cells in anti-CD99-mediated Ewing tumor death. We propose that the engagement of CD99 by NOA2 results in the recruitment of intratumoral macrophages. In addition, interruption of the CD99:PILRα checkpoint axis may be a relevant therapeutic approach to activate tumor-associated macrophages. Full article
(This article belongs to the Topic Anti-Tumor Immune Responses 2.0)
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20 pages, 2300 KiB  
Review
The Role of Tumor Metabolic Reprogramming in Tumor Immunity
by Xianhong Zhang, Weiguo Song, Yue Gao, Yu Zhang, Yuqi Zhao, Shuailin Hao and Ting Ni
Int. J. Mol. Sci. 2023, 24(24), 17422; https://doi.org/10.3390/ijms242417422 - 13 Dec 2023
Cited by 3 | Viewed by 1758
Abstract
The occurrence and development of tumors require the metabolic reprogramming of cancer cells, namely the alteration of flux in an autonomous manner via various metabolic pathways to meet increased bioenergetic and biosynthetic demands. Tumor cells consume large quantities of nutrients and produce related [...] Read more.
The occurrence and development of tumors require the metabolic reprogramming of cancer cells, namely the alteration of flux in an autonomous manner via various metabolic pathways to meet increased bioenergetic and biosynthetic demands. Tumor cells consume large quantities of nutrients and produce related metabolites via their metabolism; this leads to the remodeling of the tumor microenvironment (TME) to better support tumor growth. During TME remodeling, the immune cell metabolism and antitumor immune activity are affected. This further leads to the escape of tumor cells from immune surveillance and therefore to abnormal proliferation. This review summarizes the regulatory functions associated with the abnormal biosynthesis and activity of metabolic signaling molecules during the process of tumor metabolic reprogramming. In addition, we provide a comprehensive description of the competition between immune cells and tumor cells for nutrients in the TME, as well as the metabolites required for tumor metabolism, the metabolic signaling pathways involved, and the functionality of the immune cells. Finally, we summarize current research targeted at the development of tumor immunotherapy. We aim to provide new concepts for future investigations of the mechanisms underlying the metabolic reprogramming of tumors and explore the association of these mechanisms with tumor immunity. Full article
(This article belongs to the Topic Anti-Tumor Immune Responses 2.0)
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