cancers-logo

Journal Browser

Journal Browser

The Tumor Microenvironment and Molecular Aberrations Convey Immune Evasion (Third Edition)

A special issue of Cancers (ISSN 2072-6694). This special issue belongs to the section "Cancer Immunology and Immunotherapy".

Deadline for manuscript submissions: 30 September 2026 | Viewed by 490

Special Issue Editor


E-Mail Website
Guest Editor
Department of Medical & Molecular Sciences, College of Health Sciences, University of Delaware, Newark, DE 19716, USA
Interests: DNA methylation; cancer invasion and metastasis in breast and pancreatic cancers; carcinoma-associated fibroblasts; epithelial–mesenchymal transition; AKT signaling pathway; tumor microenvironment and immune evasion
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

This Special Issue is the third edition of "The Tumor Microenvironment and Molecular Aberrations Convey Immune Evasion", following the success of the first edition (https://www.mdpi.com/journal/cancers/special_issues/TMMIE) and the second edition, “Volume II” (https://www.mdpi.com/journal/cancers/special_issues/4BPEBEU010).

It is widely recognized that the complex interplay between immunity and cancer determines whether cancer cells survive or are destroyed. The balance between tumoricidal and tumor-promoting activity depends on the strength of the antitumor immune response. In general, immune evasion mechanisms employed by cancers include downregulation of antigen presentations or recognition, depletion of immune effector cells, blockade immune cell maturation, accumulation of immunosuppressive cells, production of inhibitory cytokines, chemokines, or ligands/receptors, establishment of a hypoxic tumor microenvironment, activation of cancer-promoting metabolic pathways, and upregulation of immune checkpoint modulators.

Restoring or stimulating tumoricidal effects—together surgical resection, chemotherapy, radiotherapy, hormone-based therapies, kinase inhibitors, DNA repair disruptors, small=molecule inhibitors, signal transduction pathway modifiers, epigenome reprogramming, and cytokine-based treatments—may enable promising therapeutic regimens to eradicate aggressive cancers. This Special Issue welcomes papers that elucidate mechanisms of immune escape or propose strategies for enhancing immune surveillance, particularly in combination with non-immune interventions to eradicate human cancers.

Dr. Huey-Jen Lin
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 communications are invited. For planned papers, a title and short abstract (about 250 words) can be sent to the Editorial Office for assessment.

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. Cancers 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 2900 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

  • CD8+ tumor-infiltrating lymphocytes
  • cytotoxic T lymphocytes -associated protein 4
  • dendritic cells
  • immune evasion
  • hypoxia-inducible factors
  • myeloid-derived suppressor cells
  • natural killer
  • programmed death receptor and ligand
  • regulatory T cells
  • tumor-associated macrophages
  • tumor microenvironment

Benefits of Publishing in a Special Issue

  • Ease of navigation: Grouping papers by topic helps scholars navigate broad scope journals more efficiently.
  • Greater discoverability: Special Issues support the reach and impact of scientific research. Articles in Special Issues are more discoverable and cited more frequently.
  • Expansion of research network: Special Issues facilitate connections among authors, fostering scientific collaborations.
  • External promotion: Articles in Special Issues are often promoted through the journal's social media, increasing their visibility.
  • Reprint: MDPI Books provides the opportunity to republish successful Special Issues in book format, both online and in print.

Further information on MDPI's Special Issue policies can be found here.

Related Special Issues

Published Papers (1 paper)

Order results
Result details
Select all
Export citation of selected articles as:

Review

23 pages, 1140 KB  
Review
Breast Cancer Milieu Maneuvers Cancer-Associated Macrophages to Synergize Neoplastic Repertoires
by Huey-Jen Lin, Yingguang Liu, Brooke Langevin and Jiayuh Lin
Cancers 2026, 18(10), 1596; https://doi.org/10.3390/cancers18101596 - 14 May 2026
Viewed by 246
Abstract
Breast cancer is one of the most devastating malignancies in women worldwide. A growing body of evidence has linked neoplastic growth, invasion, metastasis, immune escape, and therapeutic resistance to infiltrating tumor-associated macrophages. In a breast cancer mass, macrophages are largely polarized to two [...] Read more.
Breast cancer is one of the most devastating malignancies in women worldwide. A growing body of evidence has linked neoplastic growth, invasion, metastasis, immune escape, and therapeutic resistance to infiltrating tumor-associated macrophages. In a breast cancer mass, macrophages are largely polarized to two main subtypes, M1 and M2, albeit with continuum intermediates, based on their immunological behaviors, gene signatures, and functional roles. While the former portrays proinflammatory and anti-cancer effects, the latter elicits the opposite impacts. M2 macrophages have gained rising attention as they are largely involved in fostering an immune-suppressive, cancer-promoting landscape and are imperative for malignant features across breast cancer subtypes. Through a positive feedback paracrine loop, M2 macrophages can be enriched by a plethora of dysregulated oncogenic signaling mediators, exemplified by CSF1/CSF1R, STAT3, IL-6, YAP, PI3K, PDK1, and AKT. These modulators could be released from or activated by surrounding malignant cells, fibroblasts, secreted extracellular vesicles, cell fragments generated after chemotherapies, hypoxia, dysregulated immune checkpoint pathways or oncometabolites. This review aims to discern the molecular cues fortifying M2 subpopulations. Moreover, recent advances in single-cell sequencing, spatial, and computational approaches have refined the understanding of TAM heterogeneity, while clinical translation remains limited by low therapeutic specificity, compensatory signaling, and differences between murine and human macrophage biology. Future therapeutic regimens should include strategies aimed at correcting aberrations that favor M2 polarization and are justified with divergences between humans and mice. Full article
Show Figures

Figure 1

Back to TopTop