Exploring the Molecular Basis of Cancer: Perspectives from Genetics and Epigenetics

A special issue of Biology (ISSN 2079-7737). This special issue belongs to the section "Genetics and Genomics".

Deadline for manuscript submissions: 30 November 2026 | Viewed by 1746

Special Issue Editor


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Guest Editor
Department of Gastrointestinal Medical Oncology, The University of Texas MD Anderson Cancer Center, Houston, TX 77030, USA
Interests: cancer genetics; epigenetics; tumor heterogeneity; histone modification; next-generation sequencing (NGS); cancer transcriptomics; gene regulation; mouse model; chromatin remodeling
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Special Issue Information

Dear Colleagues,

Cancer remains a significant global health challenge, prompting extensive research into its molecular foundations to discover new therapeutic strategies. Advances in genetic and epigenetic analyses, along with integrated "omics" techniques—such as genomics, transcriptomics, proteomics, and epigenomics—are reshaping our understanding of cancer biology. The molecular basis of cancer involves complex genetic and epigenetic changes that drive tumor initiation, progression, and therapeutic resistance.

This Special Issue aims to enhance our understanding of these molecular mechanisms through innovative research in genetics, epigenetics, and integrated "omics" approaches, offering new insights into the diverse and dynamic biology of cancer. We invite submissions of original research, reviews, short communications, perspectives, and commentaries that explore the role of bioinformatics and machine learning in cancer biology. Relevant topics include, but are not limited to, tumor subtype classification, immunotherapy, T cell exhaustion, gene regulation, cancer prognosis, cancer transcriptomics, epigenomics, and predictive models for drug response.

The goal of this Special Issue is to highlight innovations that will improve precision medicine and deepen our understanding of cancer mechanisms. By showcasing recent discoveries in genetic and epigenetic mechanisms, we aim to foster insights that will lead to innovative therapies and personalized treatment approaches for cancer.

Dr. Shilpa Dhar
Guest Editor

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Keywords

  • cancer genetics
  • epigenetics
  • tumor heterogeneity
  • histone modification
  • next-generation sequencing (NGS)
  • cancer transcriptomics
  • gene regulation
  • mouse model
  • chromatin remodeling
  • CHIP-Seq
  • ATAC-seq
  • mutation
  • amplification

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Published Papers (1 paper)

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Research

23 pages, 2667 KB  
Article
Dual Effect of EZH2 Gene Editing with CRISPR/Cas9 in Lung Cancer
by Joice M. Menezes, Diego C. de Mello, Kelly C. Saito, Edna T. Kimura and Cesar S. Fuziwara
Biology 2026, 15(3), 251; https://doi.org/10.3390/biology15030251 - 29 Jan 2026
Viewed by 1116
Abstract
Lung adenocarcinoma is the most common form of lung cancer with a 5-year survival rate of 15%, largely due to asymptomatic metastasis and late diagnosis. Overexpression of Polycomb group (PcG) proteins, particularly EZH2, the catalytic component of Polycomb Repressive Complex 2 (PRC2), has [...] Read more.
Lung adenocarcinoma is the most common form of lung cancer with a 5-year survival rate of 15%, largely due to asymptomatic metastasis and late diagnosis. Overexpression of Polycomb group (PcG) proteins, particularly EZH2, the catalytic component of Polycomb Repressive Complex 2 (PRC2), has been associated with the pathogenesis of lung cancer, frequently showing correlation with cancer progression and poor prognosis. In this study, EZH2 levels were modulated by CRISPR/Cas9 gene editing and PRC2 activity was inhibited with EZH2 inhibitor EPZ6438 or EED inhibitor MAK683. EZH2 gene editing reduced cell proliferation, migration, invasion, and colony formation and reduced NFκ-B signaling activation, indicating an antitumoral effect in vitro. Moreover, EZH2 inhibition also increased the expression of differentiation-related genes, such as GATA5, FOXA2, and lung surfactants, indicating a pro-differentiation effect. However, EZH2-edited cells injected into an immunocompromised mouse model generated larger tumors compared to unedited cells. This was accompanied by increased expression of other PcG genes, including EZH1, CBX2, RING1, EED, and SUZ12, suggesting a compensatory interaction between PRC2 and PRC1 complexes. These findings provide significant clinical relevance, both in elucidating the mechanisms of novel molecular targets and in guiding treatment strategies for lung cancer when using epigenetic inhibitors. Full article
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