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Cancer Genetics and Pharmacology: Advancing Precision Therapeutics

A special issue of Current Issues in Molecular Biology (ISSN 1467-3045). This special issue belongs to the section "Biochemistry, Molecular and Cellular Biology".

Deadline for manuscript submissions: 31 May 2026 | Viewed by 1287

Special Issue Editor


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Guest Editor
School of Life Sciences, University of Technology Sydney, Sydney, Australia
Interests: DNA methylation; transcriptome; cancer genetics

Special Issue Information

Dear Colleagues,

Cancer genetics stands at the forefront of oncology research, elucidating the molecular dynamics behind cancer development and progression. Recent breakthroughs in genomic technologies, together with a growing database on genetic anomalies, have been crucial in advancing our understanding and treatment of cancer. Despite these strides, challenges like tumor heterogeneity, therapy resistance, and application of genetic discoveries into effective clinical practices continue to pose significant hurdles.

This Research Topic aims to enhance and broaden our understanding of cancer genetics with a focus on its integration with pharmacology. It seeks to spur innovations in drug development, refine therapeutic methods, and advance the implementation of precise, genetics-driven treatment models. By tackling critical issues such as drug resistance and using genetic markers for customized treatment, it endeavors to move the field toward a more cohesive and targeted approach to cancer therapy.

To address the complexities of this field, we invite contributions that explore, but are not limited to, the following themes:

  • Genetic Mutations and Cancer: Key drivers and their role in targeted therapy.
  • Genomic Technologies: Impact of advanced tools like NGS and CRISPR-Cas9.
  • Tumor Heterogeneity: Influence on treatment strategies and disease outcomes.
  • Biomarkers and Diagnostics: Importance in early detection and therapeutic accuracy.
  • Targeted Therapies: Development and hurdles in interventions informed by genetics.
  • Immunogenomics: Genetic factors affecting immune evasion and immunotherapy.
  • Epigenetic Modifications: Potential targets and pharmaceutical interventions.
  • Pharmacogenomics and Personalized Medicine: Customizing treatments based on genetic profiles.
  • Translational Research: Bridging genetic discoveries with clinical practice.
  • Future Directions: Emerging therapies and strategic innovations in precision medicine.

Through a comprehensive evaluation, this Research Topic will deepen our understanding of cancer genetics' foundation, paving the way for revolutionary advancements in cancer treatment.

Dr. Baoming Wang
Guest Editor

Manuscript Submission Information

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Please visit the Instructions for Authors page before submitting a manuscript. The Article Processing Charge (APC) for publication in this open access journal is 2200 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 genetics
  • epigenetic modifications
  • pharmacogenomics
  • personalized medicine

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Published Papers (1 paper)

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Research

23 pages, 12076 KB  
Article
Loss of WT1 Drives Adaptive Plasticity in CCDC6-RET Selpercatinib-Resistant Papillary Thyroid Cancer
by Giuseppe Siragusa, Laura Tomasello, Mattia Biondo, Fabiola Vaglica, Carla Giordano, Giorgio Arnaldi and Giuseppe Pizzolanti
Curr. Issues Mol. Biol. 2026, 48(3), 274; https://doi.org/10.3390/cimb48030274 - 4 Mar 2026
Viewed by 896
Abstract
Background: Papillary Thyroid Cancer (PTC) harboring CCDC6-RET translocation is typically classified as a differentiated epithelial tumor. Although Selpercatinib, a RET-selective drug, was recently approved for use in advanced PTC, the emergence of drug resistance has already been observed. Tumor plasticity, including non-canonical [...] Read more.
Background: Papillary Thyroid Cancer (PTC) harboring CCDC6-RET translocation is typically classified as a differentiated epithelial tumor. Although Selpercatinib, a RET-selective drug, was recently approved for use in advanced PTC, the emergence of drug resistance has already been observed. Tumor plasticity, including non-canonical Epithelial–Mesenchymal Transition (EMT) programs, is recognized as a key mechanism underlying drug resistance. The downregulation of the transcription factor Wilms’ Tumor 1 (WT1) in cancer is associated with increased motility, invasiveness, and metastatic potential. Methods: In this study, we developed a selpercatinib-resistant PTC-derived cell line, TPC-1-SelpR. Bioinformatic analyses were conducted to study the promoter of the CCDC6-RET gene and the transcriptomic landscape of PTC from RNAseq data. Subsequent real-time PCR, Western blot, and imaging techniques, such as confocal microscopy (CM) and fluorescence microscopy (FM), were employed to study the effects of WT1 loss-of-function following RNAi silencing. Results: In TPC-1-SelpR, WT1 expression appears downregulated compared to its counterpart, TPC-1. Crucially, WT1 silencing induced a context-dependent modulation of the CCDC6-RET driver: while WT1 silencing reduced CCDC6-RET expression in TPC-1, in TPC-1-SelpR, a post-transcriptional compensation of CCDC6-RET was observed. The gene expression of several factors involved in EMT, such as Twist, Vimentin, Integrin beta-1, and Profilin, was rewired in TPC-1-SelpRWT1-knockdown. Although the Vimentin protein product decreased, CM and FM analyses confirmed a reorganization of residual protein: the subcellular redistribution was more dispersed in TPC-1-SelpRWT1-knockdown. Further upregulation of the stemness factor Sox2 over the differentiation factor Sox17 occurred. These molecular changes were associated with higher cell motility of TPC-1-SelpRWT1-knockdown. Conclusions: Collectively, these findings suggest that WT1 is a critical regulator involved in tumor plasticity, thereby supporting selpercatinib resistance. Full article
(This article belongs to the Special Issue Cancer Genetics and Pharmacology: Advancing Precision Therapeutics)
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