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Cancers
Special Issues
Genetic Alterations and the Tumor Microenvironment
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Genetic Alterations and the Tumor Microenvironment

A special issue of Cancers (ISSN 2072-6694). This special issue belongs to the section "Tumor Microenvironment".

Deadline for manuscript submissions: 31 March 2026 | Viewed by 513

Special Issue Editor

Dr. Shanye Yin

E-Mail Website
Guest Editor
Department of Pathology, Albert Einstein College of Medicine, Bronx, NY, USA
Interests: tumor microenvironment; cancer immunology; immune checkpoint blockade; single-cell spatial analysis
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

The evolution of cancer is governed not only by the accumulation of genetic mutations but also by the selective pressures exerted by its local ecosystem—the tumor microenvironment (TME). This complex and dynamic niche, composed of immune cells, stromal elements, vasculature, and extracellular matrices, both constrains and enables the emergence of malignant phenotypes. Somatic mutations reshape the interactions between cancer cells and their microenvironment, driving immune evasion, therapeutic resistance, and metastatic dissemination. Conversely, microenvironmental signals influence the evolutionary path of tumor genomes and sculpt clonal selection under immune and therapeutic pressures. This Special Issue seeks to highlight the emerging insights into the reciprocal relationship between genetic alterations and the TME, with an emphasis on their role in tumor progression and treatment responses. We welcome contributions spanning molecular mechanisms, cellular dynamics, and translational advances, including studies on mutational landscapes, immune modulation, spatial and single-cell analyses, and strategies to therapeutically target the tumor–microenvironment axis.

Dr. Shanye Yin
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 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. 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

  • tumor microenvironment
  • cancer immunology
  • immune checkpoint blockade
  • somatic mutations
  • T cell signaling
  • immune evasion
  • macrophage polarization
  • cancer immunotherapy resistance
  • single-cell transcriptomics
  • spatial analysis

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Published Papers (1 paper)

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Research

22 pages, 6033 KB  
Article
Survivin Is a Central Mediator of Cell Proliferation in HPV-Negative Head and Neck Squamous Cell Carcinoma
by Jing Zhu, Jianhong An, Erqiang Hu, Gregory Rosenblatt, Gabriela Berner, Aadita Roy, Nicole Kawachi, Nitisha Shrivastava, Vikas Mehta, Jeffrey E. Segall, Michael B. Prystowsky and Thomas J. Ow
Cancers 2025, 17(17), 2864; https://doi.org/10.3390/cancers17172864 - 31 Aug 2025
Viewed by 368
Abstract
Background/Objectives: HNSCC is a highly aggressive malignancy marked by the dysregulation of the cell cycle. In HPV− HNSCC, mutations in the CDKN2A gene frequently result in the loss of the p16 protein, a key inhibitor of the cyclin D1/CDK4/6 complex. This loss [...] Read more.
Background/Objectives: HNSCC is a highly aggressive malignancy marked by the dysregulation of the cell cycle. In HPV− HNSCC, mutations in the CDKN2A gene frequently result in the loss of the p16 protein, a key inhibitor of the cyclin D1/CDK4/6 complex. This loss results in unchecked G1/S phase progression. The CDK4/6 inhibitor palbociclib has shown therapeutic potential in HPV− HNSCC by inducing G1 phase arrest and reducing cell viability. In this study, we investigated the molecular mechanisms by which palbociclib affects cell viability in HPV− HNSCC. Methods: Four HPV− HNSCC cell lines were treated with palbociclib, and RNA sequencing was performed to assess changes in gene expression. Cell viability was measured using the MTT assay. To further investigate protein localization, interactions, and function, we used immunofluorescence staining, co-immunoprecipitation, small molecule inhibitors, and siRNA-mediated knockdown. Results: We demonstrate that palbociclib downregulates survivin, a protein that plays dual roles in mitosis and apoptosis, thereby inhibiting cell proliferation. We also found that survivin is overexpressed in HPV− HNSCC. Inhibiting survivin dimerization using the compound LQZ-7i significantly reduces cell viability and promotes its export from the nucleus to the cytoplasm. Additionally, we identified USP1, a deubiquitinase, as both a downstream target of CDK4/6 and a key regulator of survivin stability. Inhibiting USP1 activity or silencing its expression significantly reduces survivin levels. Conclusions: Our findings highlight survivin as a critical mediator of cell proliferation in HPV− HNSCC and suggest that targeting the CDK4/6-USP1-survivin axis may offer a promising therapeutic strategy. Full article
(This article belongs to the Special Issue Genetic Alterations and the Tumor Microenvironment)
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