Search for Articles:
Title / Keyword
Author / Affiliation / Email
Journal
Article Type
 
 
Advanced Search
 
Section
Special Issue
Volume
Issue
Number
Page
 
9.9
5.1
Journals
Cells
Special Issues
Signaling Pathways and Mechanisms in Cancer Therapy Resistance
share announcement

Signaling Pathways and Mechanisms in Cancer Therapy Resistance

A special issue of Cells (ISSN 2073-4409). This special issue belongs to the section "Cellular Pathology".

Deadline for manuscript submissions: 31 December 2025 | Viewed by 4177

Special Issue Editor

Dr. Natarajan Aravindan

E-Mail Website
Guest Editor
Department of Physiological Sciences, College of Veterinary Medicine, Oklahoma State University, Stillwater, OK 74078, USA
Interests: cancer biology; radiation oncology/biology; developmental therapeutics; space radiation; oxidative stress; neuroblastoma; pancreatic cancer; therapy resistance; tumor evolution; cancer stem cells; targeted therapy
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

Acquired therapy resistance in cancer cells substantially confines the clinical effectiveness of targeted anticancer therapies. The evolution of therapy resistance is coordinated by the ongoing acquisition of genetic, epigenetic, molecular, and microenvironmental modifications. These unique or synchronized modifications lead to the activation of diverse yet functional signaling pathways that dictate the development of resistance to treatments. Moreover, the cellular signaling of therapy resistance in interdisciplinary collaborations with nanomedicine, immunology, experimental therapeutics, cancer stem cell biology, and energy metabolism covers an essential element in translational drug development research. The growing interest in this field of cancer therapy resistance, uniquely composed of complex molecular circuits in cancer cell types, has resulted in the emergence of innovative research areas that cover molecular targeting and explore the impact of lineage selection and/or transformation, differentiation, survival advantage, and dissemination to combat therapy resistance.

In this Special Issue, we aim to collate original research and review articles that address the current landscape of cellular signaling and mechanisms in cancer therapy resistance, including genetic and epigenetic modifications in therapy resistance, signaling pathways controlling resistance, pathways directed for targeted experimental therapies, and research addressing cancer cell therapy resistance.

Dr. Natarajan Aravindan
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 short 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. Cells 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 2700 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

  • cancer therapy
  • therapy resistance
  • molecular mechanisms
  • cell signaling pathways
  • genetic and epigenetic modifications
  • combination therapies

Benefits of Publishing in a Special Issue

  • Ease of navigation: Grouping papers by topic helps scholars navigate broad scope journals more efficiently.
  • Greater discoverability: Special Issues support the reach and impact of scientific research. Articles in Special Issues are more discoverable and cited more frequently.
  • Expansion of research network: Special Issues facilitate connections among authors, fostering scientific collaborations.
  • External promotion: Articles in Special Issues are often promoted through the journal's social media, increasing their visibility.
  • Reprint: MDPI Books provides the opportunity to republish successful Special Issues in book format, both online and in print.

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

Published Papers (2 papers)

Download All Papers
Order results
Result details
Show export options expand_more Show export options expand_less
Select all
Export citation of selected articles as:

Research

Jump to: Review

24 pages, 7771 KiB  
Article
Mirvetuximab Soravtansine Induces Potent Cytotoxicity and Bystander Effect in Cisplatin-Resistant Germ Cell Tumor Cells
by Lucia Kucerova, Adriana Fekiacova, Natalia Udvorkova, Pavlina Malcharkova, Viktoria Blahova, Silvia Jochova, Katarina Kalavska, Zuzana Cierna and Michal Mego
Cells 2025, 14(4), 287; https://doi.org/10.3390/cells14040287 - 15 Feb 2025
Viewed by 1099
Abstract
Patients with treatment-refractory/relapsing germ cell tumors (GCTs) have a dismal prognosis due to a lack of any effective therapy. Moreover, the efficacy of newly approved targeted therapies remains unexplored for cisplatin-resistant GCTs. Previously, it was demonstrated that folate receptor α (FRα) is overexpressed [...] Read more.
Patients with treatment-refractory/relapsing germ cell tumors (GCTs) have a dismal prognosis due to a lack of any effective therapy. Moreover, the efficacy of newly approved targeted therapies remains unexplored for cisplatin-resistant GCTs. Previously, it was demonstrated that folate receptor α (FRα) is overexpressed in many tumor types and efficiently targeted by the antibody–drug conjugate (ADC) mirvetuximab soravtansine (MIRV) in cisplatin-resistant cancers. We hypothesized that FRα represents an attractive target for treating treatment-refractory GCTs. We determined the expression of the FOLR1 gene in a broad range of GCT cell lines and tumor xenografts. We tested the antitumor efficacy of MIRV on cisplatin-resistant GCT cells in vitro and explored the ability of MIRV treatment to induce a bystander effect in the direct coculture of FRα-high and FRα-low cells. We found that the FOLR1 gene has significantly higher expression in testicular GCTs (TGCTs) than in normal testicular tissue. FOLR1 is highly expressed in the TCam2, JEG3, JAR, and NOY1 cell lines and their respective cisplatin-resistant variants. MIRV treatment induced apoptosis and a potent antiproliferative effect in cisplatin-resistant GCT cells in adherent and 3D spheroid cultures in vitro. A significant decrease in FRα-low 2102EP_R_NL cells was observed in the presence of FRα-high NOY1_R_SK in the presence of 12.5 nM MIRV, showing a potent bystander effect in the direct coculture. Immunohistochemical analysis confirmed significantly higher Folr1 protein expression in patients with TGCTs postchemotherapy than in chemo-naïve patients, as well as in patients with an unfavorable prognosis. In this study, we present data suggesting that the FOLR1 gene is highly expressed in (T)GCT cells in vitro and in vivo, and anti-FRα-targeting therapies should be investigated as a treatment modality in a subset of patients with TGCTs. Moreover, MIRV induced significant antitumor and bystander effects, thus showing its potential in further preclinical exploration and drug repurposing for a salvage treatment regime in refractory (T)GCT disease. Full article
(This article belongs to the Special Issue Signaling Pathways and Mechanisms in Cancer Therapy Resistance)
►▼ Show Figures

Figure 1

Review

Jump to: Research

15 pages, 1093 KiB  
Review
Targeting the Hippo Pathway in Cutaneous Melanoma
by Urszula Kazimierczak, Anna Przybyla, Marianna Smielowska, Tomasz Kolenda and Andrzej Mackiewicz
Cells 2024, 13(12), 1062; https://doi.org/10.3390/cells13121062 - 19 Jun 2024
Cited by 2 | Viewed by 1669
Abstract
Melanoma is the most aggressive form of skin cancer. In the advanced stage of development, it is resistant to currently available therapeutic modalities. Increased invasiveness and metastatic potential depend on several proteins involved in various signal transduction pathways. Hippo signaling plays a vital [...] Read more.
Melanoma is the most aggressive form of skin cancer. In the advanced stage of development, it is resistant to currently available therapeutic modalities. Increased invasiveness and metastatic potential depend on several proteins involved in various signal transduction pathways. Hippo signaling plays a vital role in malignant transformation. Dysfunctions of the Hippo pathway initiate the expression of tumor growth factors and are associated with tumor growth and metastasis formation. This review summarizes the recent achievements in studying the role of the Hippo pathway in melanoma pathogenesis and points to the potential specific targets for anti-melanoma therapy. Full article
(This article belongs to the Special Issue Signaling Pathways and Mechanisms in Cancer Therapy Resistance)
►▼ Show Figures

Figure 1

Show export options expand_more Show export options expand_less
Select all
Export citation of selected articles as:
 
Displaying articles 1-2
Back to TopTop