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Cancers
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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: closed (31 March 2026) | Viewed by 2746

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 250 words) can be sent to the Editorial Office for assessment.

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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 (2 papers)

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Research

13 pages, 2692 KB  
Article
The Role of Tumor Immune Microenvironment and Clinical Factors in Head and Neck Cancer Prognosis Among African American Men and Women
by Shaynie Segal, Jianhong An, Matan Berkovsky, Geena Jung, Ashley Stone, Vicky Yau, Juan Lin, Richard V. Smith and Shanye Yin
Cancers 2026, 18(3), 481; https://doi.org/10.3390/cancers18030481 - 31 Jan 2026
Cited by 1 | Viewed by 778
Abstract
Background: Head and Neck Squamous Cell Carcinoma (HNSCC) causes half a million deaths each year; therefore, it is essential to understand the factors that affect patient prognosis. Many studies fail to investigate the biological drivers behind survival disparities, especially sex-specific differences within [...] Read more.
Background: Head and Neck Squamous Cell Carcinoma (HNSCC) causes half a million deaths each year; therefore, it is essential to understand the factors that affect patient prognosis. Many studies fail to investigate the biological drivers behind survival disparities, especially sex-specific differences within racial groups. This study serves as a foundational project to begin elucidating biological differences in the tumor microenvironment between male and female African American HNSCC patients. Methods: A total of 111 patients who were diagnosed with HNSCC and identify as African American were grouped by sex. Analyses of socioeconomic status, co-morbidities, tumor characteristics, and treatment were conducted. Spatial transcriptomic analysis was performed on four randomly selected primary HNSCC tumor tissues. Results: No sex-based differences were observed in socioeconomic measures, treatments, tumor stage, follow-up, recurrence, or cause of death (all p > 0.15), though females had higher median income than males (p = 0.035). Comorbidity profiles were also largely comparable between males and females. Evaluating tumor microenvironments, we found that male tumors were dominated by malignant cells and fibroblasts, with limited adaptive immune infiltration. By contrast, female tumors displayed markedly higher proportions of immune cells, including T cells and B cells. Male tumors harbored sparse T cells, largely skewed toward exhausted phenotypes while female tumors displayed abundant T cell infiltration consistent with immunologically active tumor microenvironment. Conclusions: Clinical and demographic factors showed minimal sex-based differences among African American HNSCC patients, spatial transcriptomic profiling revealed strikingly distinct immune microenvironments by sex. These findings suggest that biological, rather than simply clinical, differences may drive survival disparities. This project serves as a novel and foundational study promoting the use of spatial transcriptomics to evaluate possible survival disparities within HNSCC populations to alleviate survival disparities. Full article
(This article belongs to the Special Issue Genetic Alterations and the Tumor Microenvironment)
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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 1587
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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