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Cancers
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Unique Perspectives in Cancer Signaling (2nd Edition)
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Unique Perspectives in Cancer Signaling (2nd Edition)

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

Deadline for manuscript submissions: closed (18 April 2026) | Viewed by 2676

Special Issue Editor

Prof. Dr. Peiwen Fei

E-Mail Website
Guest Editor
1. Cancer Biology Program, University of Hawaii Cancer Center, Honolulu, HI 96813, USA
2. Graduate Program of Molecular Biosciences and Bioengineering, University of Hawaii, Honolulu, HI 96813, USA
Interests: cancer signaling; cancer etiology; Fanconi anemia (FA) signaling; cancer treatment; genetic model; cancer genetics and biology
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

This Special Issue is the second edition of “Unique Perspectives in Cancer Signaling”.

We are pleased to introduce a Special Issue on cancer signaling with a focus on unique, interdisciplinary perspectives for investigating key pathways that drive cancer initiation and progression. These perspectives can entail novel technological–computational implementations, translational–clinical-level applications, or even epidemiological enhancements of basic science understandings. Across these diverse inquiries, this edition on “cancer signaling” aims to define nuanced contexts surrounding oncogenic signaling for the development of therapeutic and preventive strategies against various cancers. Reviews are expected to focus on specific disease types or signaling pathways through a multidisciplinary lens. Original research articles with a focus along these scopes will also be considered.

Prof. Dr. Peiwen Fei
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

  • oncogenesis
  • cancer signaling
  • technology
  • translational
  • clinical
  • epidemiology

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Published Papers (2 papers)

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Research

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21 pages, 5249 KB  
Article
Mechanistic Insights into Proglumide’s Role in Immune Cell Efficacy and Response to Immune Checkpoint Inhibitor Therapy in Hepatocellular Carcinoma
by Priyanka S. Doneparthi, Hong Cao, Wenqiang Chen, Wenyu Dou, Hong-Bin Fang and Jill. P. Smith
Cancers 2025, 17(18), 2998; https://doi.org/10.3390/cancers17182998 - 14 Sep 2025
Cited by 1 | Viewed by 1277
Abstract
Background: New strategies are needed to improve the response to immune checkpoint inhibitors for the treatment of hepatocellular carcinoma. Methods: Mice bearing HCC tumors were treated with PBS (control), a PD-1 antibody (PD-1Ab), proglumide, or the combination of proglumide and the PD-1Ab. The [...] Read more.
Background: New strategies are needed to improve the response to immune checkpoint inhibitors for the treatment of hepatocellular carcinoma. Methods: Mice bearing HCC tumors were treated with PBS (control), a PD-1 antibody (PD-1Ab), proglumide, or the combination of proglumide and the PD-1Ab. The tumor microenvironment (TME) was evaluated histologically for fibrosis and by immunohistochemistry for immune cells. To investigate the mechanisms involved in T-cell efficiency, mouse spleen cells were isolated and examined for T-cell exhaustion markers and cytokine release. The mouse microbiome was analyzed using whole-genome sequencing before therapy and at the end of the study. Results: The combination of proglumide with a PD-1Ab decreased tumoral fibrosis better than monotherapy, and altered the immune cell signature in the TME by decreasing M2-polarized macrophages and increasing the influx of CD8+ T-cells. Proglumide monotherapy or in combination with the PD-1Ab decreased T-cell exhaustion markers and improved cytokine release. The combination therapy resulted in changes to the microbiome, including increased beneficial bacteria and genera known to enhance the efficacy of ICIs. Conclusions: Co-administration of proglumide with ICIs resulted in remodeling of the TME, changing a “cold” tumor to a “hot” immune-responsive tumor, activating T-cells, and altering the host microbiome to a population of bacteria that are beneficial. Full article
(This article belongs to the Special Issue Unique Perspectives in Cancer Signaling (2nd Edition))
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Review

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21 pages, 1208 KB  
Review
Understanding Cancer Health Disparities
by Jun Zhang, Wei Du, Youping Deng, Herbert Yu and Peiwen Fei
Cancers 2026, 18(3), 476; https://doi.org/10.3390/cancers18030476 - 31 Jan 2026
Viewed by 984
Abstract
Cancer health disparities represent profound inequalities in incidence, outcomes, and survivorship across populations. While traditionally examined through distinct lenses of either molecular biology or social epidemiology, these disparities arise from the complex interplay of genetic susceptibility, epigenetic dysregulation, and social determinants of health [...] Read more.
Cancer health disparities represent profound inequalities in incidence, outcomes, and survivorship across populations. While traditionally examined through distinct lenses of either molecular biology or social epidemiology, these disparities arise from the complex interplay of genetic susceptibility, epigenetic dysregulation, and social determinants of health (SDoH). This review proposes that DNA damage and genomic instability serve as a critical mechanistic bridge, integrating exposures from the societal level to cellular dysfunction. We synthesize evidence demonstrating how SDoH—such as systemic inequities, environmental exposures, and chronic stress—converge with genetic and epigenetic factors to disproportionately increase DNA damage burden, impair repair mechanisms, and accelerate tumorigenesis in marginalized communities. Using the elevated gastrointestinal cancer rates among Native Hawaiians and Pacific Islanders (NH/PI) as a case study, we illustrate how historical, environmental, and socioeconomic factors interact with biological pathways to drive disparities. The review highlights key advances in DNA damage research—from somatic mutation theory to the modern understanding of chronic genomic stress—and explores how innovations in single-cell genomics, biomarker discovery, and computational modeling can unravel disparity etiologies. We argue that a translational framework linking social exposure data to molecular biomarkers of DNA damage is essential for moving beyond descriptive disparities to mechanistic understanding. Ultimately, addressing cancer equity requires interdisciplinary strategies that bridge molecular oncology, public health, and community-engaged research, targeting the root causes where social inequities become biologically embedded as genomic instability. Full article
(This article belongs to the Special Issue Unique Perspectives in Cancer Signaling (2nd Edition))
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