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Pharmaceuticals
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Precision Oncology: Targeting Molecular Subtypes in Cancer Therapy
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Precision Oncology: Targeting Molecular Subtypes in Cancer Therapy

A special issue of Pharmaceuticals (ISSN 1424-8247). This special issue belongs to the section "Pharmacology".

Deadline for manuscript submissions: 29 May 2026 | Viewed by 3781

Special Issue Editors

Dr. Shuhei Suzuki

E-Mail Website
Guest Editor
1. Department of Internal Medicine (Clinical Oncology), Yamagata Prefectural Shinjo Hospital, 720-1 Kanazawa, Shinjo 996-8585, Japan
2. Yamagata Hereditary Tumor Research Center, Yamagata University, 1-4-12 Kojirakawa, Yamagata 990-8560, Japan
Interests: drug resistance; cancer stem cells; drug repositioning; cancer genomic testing; germline mutation; genetic cancer; genetic counseling
Dr. Jiro Ogura

E-Mail Website
Guest Editor
Department of Pharmacology, Yamagata University, 2-2-2 Iida-Nishi, Yamagata 990-9585, Japan
Interests: pharmaceutical sciences; pharmacokinetics; drug development; drug metabolic enzymes; drug transporters

Special Issue Information

Dear Colleagues,

Precision oncology has revolutionized cancer treatment by identifying specific molecular alterations that drive tumor growth and developing targeted therapies against these alterations. This shift from the traditional approach to personalized medicine has led to remarkable improvements in patient outcomes across multiple cancer types.

This Special Issue, entitled "Precision Oncology: Targeting Molecular Subtypes in Cancer Therapy", aims to explore current challenges and future directions in molecular subtyping for cancer treatment. We seek to highlight innovative approaches for identifying and targeting specific molecular subtypes, overcoming resistance mechanisms, and implementing precision diagnostics in clinical practice.

Recent technological advances in genomic profiling, liquid biopsies, and artificial intelligence have dramatically enhanced our ability to identify actionable molecular alterations and monitor treatment response in real time. These developments create unprecedented opportunities for refining treatment selection and developing novel therapeutic strategies for molecularly defined patient subgroups.

We invite the submission of original research articles and comprehensive reviews addressing molecular subtyping methodologies, biomarker discovery, resistance mechanisms, multi-omics integration, emerging diagnostic technologies, and innovative clinical trial designs for molecular subtypes in oncology.

Dr. Shuhei Suzuki
Dr. Jiro Ogura
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. Pharmaceuticals is an international peer-reviewed open access monthly 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

  • cancer chemotherapy
  • cancer genomic profiling test
  • next-generation sequencing
  • genetic variants
  • molecular targeted therapy
  • molecular tumor board
  • liquid biopsy

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Published Papers (3 papers)

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Research

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14 pages, 5011 KB  
Article
Fusion-Negative NTRK Overexpression Exhibit Biological Relevance in Colorectal Cancer: Implications for Prediction of Responses to Kinase Inhibitors
by Abdulaziz Alfahed
Pharmaceuticals 2025, 18(10), 1562; https://doi.org/10.3390/ph18101562 - 16 Oct 2025
Viewed by 601
Abstract
Background/Objectives: The aims of this study are to define the roles of the neurotrophic tyrosine receptor kinase genes NTRK1, NTRK2 and NTRK3 (NTRK1/2/3) in CRC and to determine the clinicopathological, molecular, cancer signalling and potential predictive significances of NTRK1/2/3 [...] Read more.
Background/Objectives: The aims of this study are to define the roles of the neurotrophic tyrosine receptor kinase genes NTRK1, NTRK2 and NTRK3 (NTRK1/2/3) in CRC and to determine the clinicopathological, molecular, cancer signalling and potential predictive significances of NTRK1/2/3 expression in CRC, irrespective of NTRK gene fusion. Methods: Standard statistical tests in SPSS were utilised to interrogate the associations and correlations between NTRK1/2/3 expression and clinicopathological, molecular and genomic features in two CRC cohorts. NTRK1/2/3 expression deregulation was also investigated using correlation and regression analyses. Furthermore, gene set enrichment analysis (GSEA) and pathway/drug ontology enrichment analysis (POEA/DOEA) were utilised to interrogate the enrichment of cancer signalling pathways, as well as NTRK and other tyrosine kinase inhibitor response in the CRC cohorts. Results: Whilst NTRK1 expression was higher in the CRC subset with microsatellite instability, NTRK2/3 expression was preferentially overexpressed in the microsatellite stable subsets. Moreover, there was differential NTRK1/2/3 expression with respect to clinicopathological and molecular/genomic indices. In addition, this study demonstrated that NTRK1/2/3 expression was deregulated by a combination of copy number alterations (NTRK2), aberrant methylation (NTRK1/2/3) and potentially and cryptic gene fusion (NTRK3). Furthermore, GSEA and POEA demonstrated that NTRK1/2/3-high CRC subsets exhibited enrichment of and cross-talks among the NTRK signalling pathways, as well as of known cancer signalling pathways. The GSEA and DOEA showed that NTRK signalling was enriched for kinase inhibitors responses, representing evidence that NTRK1/2/3 expression may serve as biomarkers for multiple kinase inhibitors, including entrectinib—the tissue-agnostic kinase inhibitor for cancers with NTRK gene fusions. Conclusions: The results demonstrated that fusion-negative NTRK signalling may be active in CRC and may contribute to the molecular pathogenesis and biology of the disease. The results also demonstrated that the NTRK1/2/3 expression may be predictive multiple kinase inhibitors. Full article
(This article belongs to the Special Issue Precision Oncology: Targeting Molecular Subtypes in Cancer Therapy)
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17 pages, 6308 KB  
Article
PARP Inhibition in Colorectal Cancer—A Comparison of Potential Predictive Biomarkers for Therapy
by Abdulaziz Alfahed
Pharmaceuticals 2025, 18(6), 905; https://doi.org/10.3390/ph18060905 - 17 Jun 2025
Cited by 1 | Viewed by 1270
Abstract
Background/Objectives: PARP inhibitors (PARPis) currently play frontline roles in the management of prostate, pancreatic, ovarian and breast cancers, but their roles in colorectal cancer (CRC) management have yet to be clarified. Importantly, the specific predictive biomarkers for PARPis in CRC are still [...] Read more.
Background/Objectives: PARP inhibitors (PARPis) currently play frontline roles in the management of prostate, pancreatic, ovarian and breast cancers, but their roles in colorectal cancer (CRC) management have yet to be clarified. Importantly, the specific predictive biomarkers for PARPis in CRC are still matters of investigations. The aim of this study is to identify the potential predictive biomarkers of PARP inhibition in CRC. Methods: Gene set enrichment analyses (GSEAs) and drug ontology enrichment analyses (DOEAs) of PARPi response gene sets were applied as the surrogates of PARPi response to two CRC cohorts in order to compare the predictive capacities of TP53 mutation status, MSI status, as well as PARP1 and PARP2 expression for PARP inhibition to those of a homologous repair deficiency surrogate, and large-scale state transition (LST). Differential enrichment score (ES) and ontology enrichment (OE) analyses were used to interrogate the differential correlation of the predictive biomarkers with PARPi response, relative to LST. Results: The results demonstrated that LST-low, rather than LST-high, CRC subsets exhibited an enrichment of the PARPi response, in contrast to what has been established for other cancers. Furthermore, CRC subsets with wild-type TP53, positive MSI, as well as high PARP1 and PARP2 expression exhibited an enrichment of the PARPi response gene sets. Moreover, there was no differential enrichment of the PARPi response between LST and each of the MSI statuses, PARP1 expression and PARP2 expression. Furthermore, the preliminary differential enrichment observed between the LST-based and TP53 mutation status-based PARPi responses could not be validated with further testing. Conclusions: MSI status, TP53 mutation status as well as PARP1 and PARP2 expression may be substitutes for low LST as predictive biomarkers of PARPi response in CRC. Full article
(This article belongs to the Special Issue Precision Oncology: Targeting Molecular Subtypes in Cancer Therapy)
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Review

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30 pages, 2940 KB  
Review
The Role of Non-Coding Regions in Breast Cancer: From Gene Regulation to Therapeutic Implications
by Hussein Sabit, Sara Sobhy, Shaimaa Abdel-Ghany, Al-Hassan Soliman Wadan, Olubukola Ayodele, Yasser Albrahim, Hirendra N. Banerjee, Ahmed Elhashash and Borros Arneth
Pharmaceuticals 2025, 18(9), 1370; https://doi.org/10.3390/ph18091370 - 12 Sep 2025
Cited by 1 | Viewed by 1481
Abstract
Breast cancer (BC) remains one of the most prevalent cancers worldwide and a significant cause of cancer-related mortality among women. Despite significant advancements in understanding the genetic foundations of BC, numerous research initiatives have historically focused on protein-coding genes, which constitute merely about [...] Read more.
Breast cancer (BC) remains one of the most prevalent cancers worldwide and a significant cause of cancer-related mortality among women. Despite significant advancements in understanding the genetic foundations of BC, numerous research initiatives have historically focused on protein-coding genes, which constitute merely about 2% of the human genome. This focus has produced significant insights into oncogenes such as HER2, TP53, and BRCA1, along with tumor suppressor genes. Nonetheless, it has led to the non-coding portions of the genome garnering relatively less focus. Recent studies illuminate the crucial significance of non-coding DNA in cancer biology, highlighting its regulatory roles and influence on tumor formation, metastasis, and treatment resistance. This review examines the importance of non-coding DNA in BC. It provides an in-depth analysis of essential non-coding regions, their functions in gene regulation and chromatin structure, and their implications for various BC subtypes. Examining these facets, we seek to reveal the potential of non-coding DNA as a viable source of novel diagnostic markers and treatment approaches. Full article
(This article belongs to the Special Issue Precision Oncology: Targeting Molecular Subtypes in Cancer Therapy)
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