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Cancers
Special Issues
Molecular Pathways in Cancers (2nd Edition)
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Molecular Pathways in Cancers (2nd Edition)

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

Deadline for manuscript submissions: 30 November 2025 | Viewed by 2565

Special Issue Editors

Dr. Ion Cristóbal

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Guest Editor
Translational Oncology Division, Oncohealth Institute, IIS-Fundación Jiménez Díaz-UAM, 28040 Madrid, Spain
Interests: oncology; hematology; patient outcome; prognostic markers; healthcare quality; innovation; molecular processes
Special Issues, Collections and Topics in MDPI journals
Dr. Marta Rodríguez Moreno

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Guest Editor
1. Pathology Department, IIS-Fundación Jiménez Díaz-UAM, E-28040 Madrid, Spain
2. Center for the Biomedical Research Network in Oncology (CIBERONC), E-28040 Madrid, Spain
Interests: lymphoproliferative neoplasias; lymphoma; NOTCH signaling pathway; liquid biopsy; cancer bioinformatics
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

Despite the continuous advances in anticancer therapies, the survival rates in most tumor types remain very poor, especially in those patients with advanced stages of the disease. There is a direct relationship between our level of understanding of each cancer’s molecular pathogenesis and our capacity to develop novel and effective therapeutic strategies.

For this Special Issue, we welcome contributions that improve our knowledge of the molecular alterations that deregulate key signaling pathways and govern tumor progression in highly prevalent human cancers. We would like to focus this Special Issue on studies that combine basic and translational research and provide significant findings with a clear clinical and therapeutic impact.

Dr. Ion Cristóbal
Dr. Marta Rodríguez Moreno
Guest Editors

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

  • highly prevalent cancers
  • tumor microenvironment
  • oncogenesis
  • progression
  • novel targeted therapy
  • prognosis

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

Published Papers (2 papers)

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Research

13 pages, 2846 KB  
Article
Insight into the Wnt Pathway in Sporadic Small Bowel Adenocarcinoma
by Takayoshi Nishimoto, Atsushi Tatsuguchi, Takeshi Yamada, Sho Kuriyama, Aitoshi Hoshimoto, Jun Omori, Naohiko Akimoto, Katya Gudis, Keigo Mitsui, Shu Tanaka, Shunji Fujimori, Tsutomu Hatori, Akira Shimizu and Masanori Atsukawa
Cancers 2025, 17(18), 2965; https://doi.org/10.3390/cancers17182965 - 10 Sep 2025
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Abstract
Background/Objectives: The Wnt signaling pathway is pivotal in the adenoma–carcinoma sequence; however, its role in small bowel adenocarcinoma (SBA) remains insufficiently characterized. We analyzed the clinicopathological significance of Wnt pathway-related gene mutations and the expression of downstream or associated proteins in SBA. Methods: [...] Read more.
Background/Objectives: The Wnt signaling pathway is pivotal in the adenoma–carcinoma sequence; however, its role in small bowel adenocarcinoma (SBA) remains insufficiently characterized. We analyzed the clinicopathological significance of Wnt pathway-related gene mutations and the expression of downstream or associated proteins in SBA. Methods: Immunohistochemical staining for β-catenin, cyclin D1, c-Myc, E-cadherin, and Wnt5a was performed in 75 primary SBA surgical specimens. Targeted next-generation sequencing was conducted in 48 of these cases. Results: The genomic alterations in the Wnt pathway were identified as APC (14.6%) and CTNNB1 (8.3%), with no overlap between the two mutations. Aberrant (reduced membranous and/or nuclear) expression of β-catenin was observed in 37% of cases. Cyclin D1 and c-Myc were expressed in 60% and 41% of cases, respectively. Aberrant expression of β-catenin and/or Wnt5a was present in 60% of cases and was correlated with cyclin D1 and c-Myc expression. Mutations in APC and CTNNB1 were found in intestinal- and gastrointestinal-type SBAs, but were absent in gastric-type SBA. In intestinal-type SBA, the mutation frequency of APC and CTNNB1 was 39%, closely aligning with the 45% aberrant expression of β-catenin. Aberrant expression of β-catenin and/or Wnt5a, a ligand of the noncanonical Wnt pathway, was detected in 60% of cases and showed a correlation with both cyclin D1 and c-Myc expression. Conclusions: These findings suggest that both canonical and noncanonical Wnt pathway-related proteins are involved in SBA carcinogenesis and progression. Notably, the canonical Wnt pathway appears to play a predominant role in intestinal-type SBA. Full article
(This article belongs to the Special Issue Molecular Pathways in Cancers (2nd Edition))
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17 pages, 1795 KB  
Article
Transcriptome Analysis of Canine Histiocytic Sarcoma Tumors and Cell Lines Reveals Multiple Targets for Therapy
by Alexander I. Engleberg, Ya-Ting Yang, Peter Z. Schall, Marilia Takada, Tuddow Thaiwong-Nebelung, Jacquelyn M. Evans, Elaine A. Ostrander and Vilma Yuzbasiyan-Gurkan
Cancers 2025, 17(6), 954; https://doi.org/10.3390/cancers17060954 - 12 Mar 2025
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Abstract
Background: Histiocytic sarcoma (HS) is a highly aggressive malignancy characterized by the excessive proliferation of histiocytes in dogs and humans. A subset of dog breeds, including the Bernese Mountain Dog (BMD), show a remarkably high prevalence of HS. Previous work by us [...] Read more.
Background: Histiocytic sarcoma (HS) is a highly aggressive malignancy characterized by the excessive proliferation of histiocytes in dogs and humans. A subset of dog breeds, including the Bernese Mountain Dog (BMD), show a remarkably high prevalence of HS. Previous work by us and others has identified somatic driver mutations of HS in the PTPN11 and KRAS genes that activate the MAPK pathway in about 60% of canine HS. However, no somatic driver mutations have been identified in the remaining 40%. Objectives: Our goals are to study HS in BMDs to gain insight into the molecular pathogenesis of the disease, and identify rational approaches to therapy. Methods: Here, we report our whole transcriptome analysis of 18 well-characterized BMD HS tumor tissues, as well as three HS cell lines. Results: Our analysis reveals the significant upregulation of molecular pathways involving the FOXM1, AURKB, PLK1, and E2F genes, in HS as well as hemophagocytic HS, providing new information regarding pathways that may be targeted with inhibitors. In addition, we document the expression of multiple checkpoint genes, suggesting the option of treatment with small-molecule inhibitors together with checkpoint inhibitors. Further, we show that the transcriptomes of three canine HS cell lines mirror those of canine patient tumors, further highlighting their potential use in drug discovery and efficacy studies. Finally, we demonstrate, for the first time, that aurora kinase inhibitors are effective in curtailing the growth of HS cells in vitro and show synergism with MAPK inhibition. Conclusions: This study provides the most detailed analysis of the canine HS transcriptome to date, highlighting key pathways in its pathogenesis and suggesting new avenues for both single and combination treatment strategies, which may be pertinent to the treatment of human HS. Full article
(This article belongs to the Special Issue Molecular Pathways in Cancers (2nd Edition))
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