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Exploring the Tumor Microenvironment: Innovations and Challenges in Enhancing Immunotherapy Efficacy
Editor: Rada Amin Ali and Terry Lichtor

Submission Deadline: 1 June 2025 (Status: Open)


Special Issue Editor(s)


Dr. Rada Amin Ali      Email   |   Website
University of Nebraska–Lincoln, Lincoln, NE, USA
Interests: tumor microenvironment; immunotherapy; immune system; precision medicine



Dr. Terry Lichtor      Email   |   Website
Department of Neurosurgery, Rush University Medical Center, Chicago, IL, USA
Interests: brain tumors; immunotherapy; gene therapy; Alzheimer’s disease; MRI imaging; neuro-oncology


Special Issue Information

Dear Colleagues,

The tumor microenvironment (TME) plays a crucial role in shaping the efficacy of immunotherapy treatments for cancer. This dynamic and complex ecosystem, which includes tumor cells, cancer stem cells, immune cells, stromal components, and extracellular matrix, can significantly influence tumor progression and response to therapy. Recent research highlights both the opportunities and challenges associated with targeting the TME to improve immunotherapy outcomes. Understanding the interplay between the TME and immune response is essential for advancing personalized immunotherapy.

We invite authors to contribute to our upcoming topics, focusing on the intricate interplay between the TME and therapeutic strategies aimed at enhancing immune responses against cancer. Topics of interest include, but are not limited to:

• The role of the TME in shaping immune responses and influencing immunotherapy efficacy

• Molecular mechanism of the tumor ecosystem

• Innovations in targeting any component of TME to enhance treatment responses

• Advances in novel therapeutic approaches and technologies for TME modulation

• Biomarkers and profiling techniques for assessing TME characteristics and predicting therapeutic outcomes

Dr. Rada Amin Ali and Dr. Terry Lichtor
Guest Editors


Keywords

tumor microenvironment; immunotherapy; immune system; precision medicine


Manuscript Submission Information

Manuscripts should be submitted via our online editorial system at https://www.discovmed.com/Journalx_dm/authorLogOn.action by registering and logging in to this website. Once you are registered, click here to start your submission. Manuscripts can be submitted now or up until the deadline. All papers will go through peer-review process. Accepted papers will be published in the journal (as soon as accepted) and meanwhile listed together on the special issue website.

Submitted manuscripts should not have been published previously, nor be under consideration for publication elsewhere (except conference proceedings papers). All manuscripts will be thoroughly refereed through a double-blind peer-review process. Please visit the Instruction for Authors page before submitting a manuscript. Submitted manuscripts should be well formatted in good English.

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  • Article
    Sara Sadat Aghamiri, Rada Amin
    Discovery Medicine. 2025, 37(192): 166-181. https://doi.org/10.24976/Discov.Med.202537192.14

    Background: Glioblastoma multiforme (GBM) is one of the deadliest and most heterogeneous forms of brain cancer, characterized by its resistance to conventional therapies. Within GBM, a subpopulation of slow-cycling cells, often linked to quiescence and stemness, plays a crucial role in treatment resistance and tumor recurrence. This study aimed to identify novel biomarkers associated with these slow-cycling GBM cells.

    Methods: We utilized The Cancer Genome Atlas (TCGA)-GBM dataset and presented the reproducible bioinformatics analysis for our results.

    Results: Our analysis highlighted Membrane-Associated Protein 17 (MAP17) as strongly associated with the slow-cycling phenotype. We found that the protein cargo MAP17 expression is related to mesenchymal signatures and stem cell-related pathways. Also, MAP17 was linked to a distinct metabolic profile, characterized by significant enrichment in pathways related to folate, zinc, and fatty acids. Moreover, the immune cell distribution analysis revealed that MAP17 correlates with key molecular immune processes, including interferon-gamma (IFN-γ) signaling and antigen presentation, as well as immunosuppressive cells like myeloid-derived suppressor cells (MDSCs) and macrophages. MAP17-high tumors also showed elevated expression of several immune checkpoint inhibitors, indicating an immunosuppressive microenvironment.

    Conclusion: These findings provide insight into the role of MAP17 in quiescence, stemness, and immune evasion, positioning it as a promising therapeutic target.