Search for Articles:
Title / Keyword
Author / Affiliation / Email
Journal
Article Type
 
 
Advanced Search
 
Section
Special Issue
Volume
Issue
Number
Page
 
10.5
5.2
Journals
Cells
Special Issues
Advances in Molecular Research on Cancer Drug Targets and Drug...
share announcement

Advances in Molecular Research on Cancer Drug Targets and Drug Resistance

A special issue of Cells (ISSN 2073-4409).

Deadline for manuscript submissions: 20 August 2026 | Viewed by 2467

Special Issue Editors

Dr. Yuhao Xie

E-Mail Website
Guest Editor
Department of Pharmaceutical Sciences, College of Pharmacy and Health Sciences, St. John’s University, Queens, NY, USA
Interests: pharmacology; ABC transporters; multidrug resistance (MDR); oncology; cancer therapy; anticancer drug; clinical case; cell biology; internal & external medicine
Prof. Dr. Concettina La Motta

E-Mail Website
Guest Editor
Department of Pharmacy, University of Pisa, 56126 Pisa, Italy
Interests: drug design; drug development; enzyme inhibitors; cancer; inflammation
Special Issues, Collections and Topics in MDPI journals
Dr. Rakesh Kumar Srivastava

E-Mail Website
Guest Editor
LSU Health Sciences Center—New Orleans, New Orleans, LA, USA
Interests: cancer therapy; presision medicine/personalized therapy; prevention; diabetes; nutrition; stem cell; biomarker development; nano-technology; immunology; drug discovery and development; microRNA; angiogenesis; autophagy; tumor microenvironment and metastasis; health disparity; COVID-19 therapeutics
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

Cancer remains a formidable global health challenge, necessitating continuous innovation in therapeutic strategies. Significant advancements in treatment have emerged from a deeper molecular understanding of cancer biology, leading to the identification of specific drug targets and the development of targeted therapies. However, despite these successes, the challenge of drug resistance frequently limits treatment efficacy and contributes to disease recurrence. This underscores the critical need for ongoing molecular research to not only discover novel targets but also to overcome the complex mechanisms by which cancer cells evade therapeutic agents.

Therefore, this Special Issue aims to compile cutting-edge original research and comprehensive review articles that advance our understanding of the molecular basis of cancer drug targets and the mechanisms of drug resistance. Our objective is to gather a comprehensive collection of at least 10 articles, with the potential for the Special Issue to be printed in book form if this number is achieved.

In this Special Issue, research areas may include the discovery and validation of novel molecular targets, elucidation of molecular mechanisms of intrinsic and acquired drug resistance, the role of tumor heterogeneity and the tumor microenvironment in resistance, strategies to overcome resistance, development of biomarkers for predicting response and resistance, and studies on new anti-cancer agents and resistance modulators.

We look forward to receiving your contributions.

Dr. Yuhao Xie
Prof. Dr. Concettina La Motta
Dr. Rakesh Kumar Srivastava
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 short 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. 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
  • drug targets
  • drug resistance
  • molecular mechanisms
  • targeted therapy
  • tumor microenvironment
  • personalized medicine
  • biomarkers

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 (3 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

21 pages, 2837 KB  
Article
Comparative Proteomic Profiling of Responses to Standard Systemic Treatment Regimens in Pancreatic Cancer
by Amirsalar Mansouri, Olivia Hart, Sina Aslanabadi, Conner Hartupee, Dicle Yalcin, Garima Sinha, Chiswili Yves Chabu, Aleksandra Cios, Zetao Cheng, Sudhakar Ammanamanchi, Jovanny Zabaleta, John H. Stewart IV, John T. West, Mitesh J. Borad, Bolni Marius Nagalo, Jiri Adamec and Omeed Moaven
Cells 2026, 15(6), 531; https://doi.org/10.3390/cells15060531 - 17 Mar 2026
Viewed by 491
Abstract
Pancreatic ductal adenocarcinoma (PDAC) is an aggressive malignancy with a 5-year survival rate of 13.3%. First-line treatment relies on two chemotherapy regimens, FOLFIRINOX (FOLFNX) or gemcitabine plus nab-paclitaxel (GEMPAC). However, direct clinical comparisons between these regimens have yielded inconsistent results across survival and [...] Read more.
Pancreatic ductal adenocarcinoma (PDAC) is an aggressive malignancy with a 5-year survival rate of 13.3%. First-line treatment relies on two chemotherapy regimens, FOLFIRINOX (FOLFNX) or gemcitabine plus nab-paclitaxel (GEMPAC). However, direct clinical comparisons between these regimens have yielded inconsistent results across survival and toxicity endpoints, and the molecular basis of heterogeneous treatment responses remains poorly defined. To investigate regimen-specific tumor-cell-intrinsic mechanisms, we performed quantitative proteomic profiling of a primary PDAC-derived MIA PaCa-2 cell line following treatment with FOLFNX or GEMPAC. Differentially expressed proteins were analyzed using Gene Ontology, KEGG, and Ingenuity Pathway Analysis to define pathway-level alterations, and findings were contextualized using TCGA transcriptomic data. Proteomic analyses revealed that FOLFNX and GEMPAC engage in distinct cytotoxic programs. FOLFNX predominantly suppressed ribosome biogenesis and mitochondrial translation, consistent with sustained metabolic and biosynthetic stress, whereas GEMPAC preferentially disrupted mitotic cytokinesis and phosphatidylinositol phosphate biosynthesis, consistent with mitotic failure. Integration with TCGA data showed that FOLFNX-altered proteins aligned with favorable prognostic expression signatures, whereas GEMPAC-associated proteins were enriched among adverse profiles, reflecting engagement of distinct tumor-intrinsic programs. Together, these findings provide mechanistic insight into differential chemotherapy responses and establish a foundation for proteomics-based biomarkers to guide personalized chemotherapy selection in PDAC. Full article
(This article belongs to the Special Issue Advances in Molecular Research on Cancer Drug Targets and Drug Resistance)
►▼ Show Figures

Graphical abstract

23 pages, 5213 KB  
Article
Identification and Experimental Validation of Triosephosphate Isomerase 1 as a Functional Biomarker of SHetA2 Sensitivity in Ovarian Cancer
by Laura F. Mortan, Zitha Redempta Isingizwe and Doris Mangiaracina Benbrook
Cells 2026, 15(3), 267; https://doi.org/10.3390/cells15030267 - 30 Jan 2026
Viewed by 634
Abstract
Background: Our objective was to identify and validate proteins that predict which patients with ovarian cancer will respond to SHetA2, an investigational drug in a phase 1 trial for patients with advanced or recurrent solid tumors (clinicaltrials.gov: NCT04928508). Methods: Cells were cultured from [...] Read more.
Background: Our objective was to identify and validate proteins that predict which patients with ovarian cancer will respond to SHetA2, an investigational drug in a phase 1 trial for patients with advanced or recurrent solid tumors (clinicaltrials.gov: NCT04928508). Methods: Cells were cultured from ascites from nine consented patients under an institutional review board-approved protocol. SHetA2 or olaparib sensitivities were determined using metabolic viability assays in ascites-derived cultures or ovarian cancer cell lines. Expression of four SHetA2 target proteins and sixteen proteins previously identified in an ovarian cancer mouse model were measured using microcapillary electrophoresis. Triosephosphate isomerase 1 (TPI1) was modulated by siRNA or lentivirus vector-mediated overexpression. Metabolites were measured using mass spectrometry. Results: TPI1 was elevated in SHetA2-sensitive compared to SHetA2-resistant ascites-derived cultures (two-way ANOVA q-value = 0.0003). The majority of (5/9) cultures were olaparib-resistant and SHetA2-sensitive. TPI1 was higher in olaparib-resistant cultures (two-way ANOVA q-value = 0.0003). Reduction in or overexpression of TPI1 reduced or increased SHetA2 potency, respectively, in two ovarian cancer cell lines (t-tests; p < 0.05). SHetA2 reduced the metabolites in glycolysis downstream of TPI1, the tricarboxylic acid cycle and oxidative pentose phosphate pathway. Conclusions: TPI1 is a candidate functional biomarker of SHetA2 sensitivity in ovarian cancer. Full article
(This article belongs to the Special Issue Advances in Molecular Research on Cancer Drug Targets and Drug Resistance)
►▼ Show Figures

Graphical abstract

Review

Jump to: Research

25 pages, 2352 KB  
Review
Factors Influencing Immunotherapy Response in Neuroblastoma: From Tumor Microenvironment to Combination Strategies
by Xiaoran Du, Rui Dong and Kuiran Dong
Cells 2026, 15(5), 441; https://doi.org/10.3390/cells15050441 - 28 Feb 2026
Viewed by 655
Abstract
Neuroblastoma is the most common extracranial solid tumor in children, and the prognosis for high-risk patients remains dismal. Immunotherapies, represented by anti-GD2 monoclonal antibodies and chimeric antigen receptor T cells (CAR-T), have significantly improved the survival of high-risk neuroblastoma patients and become part [...] Read more.
Neuroblastoma is the most common extracranial solid tumor in children, and the prognosis for high-risk patients remains dismal. Immunotherapies, represented by anti-GD2 monoclonal antibodies and chimeric antigen receptor T cells (CAR-T), have significantly improved the survival of high-risk neuroblastoma patients and become part of standard therapy. However, their efficacy exhibits significant inter-individual heterogeneity, with some patients showing primary resistance or secondary relapse. This review aims to analyze the multi-faceted factors influencing the response to immunotherapy in neuroblastoma, including: (1) the inherent immunosuppressive properties of the tumor microenvironment, such as infiltration of myeloid-derived suppressor cells and tumor-associated macrophages, as well as checkpoint molecules and metabolic barriers; (2) tumor cell-intrinsic characteristics, such as low tumor mutational burden, MYCN amplification-associated downregulation of MHC-I, and heterogeneity of GD2 antigen expression; (3) host factors, such as systemic immune status and Fc receptor polymorphisms; and (4) treatment-related factors, such as combination strategies and the development of novel immunotherapeutic products. A deep understanding of these interrelated factors is crucial for developing predictive biomarkers, designing novel combination strategies and next-generation immunotherapies, and ultimately achieving precise immunotherapy for neuroblastoma. Full article
(This article belongs to the Special Issue Advances in Molecular Research on Cancer Drug Targets and Drug Resistance)
►▼ Show Figures

Graphical abstract

Show export options expand_more Show export options expand_less
Select all
Export citation of selected articles as:
 
Displaying articles 1-3
Back to TopTop