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Advances in Next-Generation Sequencing for Aging and Cancer Research
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Advances in Next-Generation Sequencing for Aging and Cancer Research

A Special Issue of International Journal of Molecular Sciences (ISSN 1422-0067) belonging to the section "Molecular Informatics".

Deadline for manuscript submissions: 20 October 2026 | Viewed by 3317

Editor

Dr. Hyunsoo Kim

E-Mail Website
Guest Editor
Institute for Health Informatics, University of Minnesota, Minneapolis, MN 55455, USA
Interests: aging; inflammation; senescence; inflammaging; SASP; IGFBP7; vascular biology; endothelial dysfunction; neuroinflammation; computational biology; bioinformatics; systems biology; multi-omics; sequencing; transcriptomics; Alzheimer’s disease

Special Issue Information

Dear Colleagues,

Next-generation sequencing (NGS) technologies have revolutionized biomedical research, offering unprecedented resolution and throughput to decode the molecular mechanisms underlying aging and cancer. This Special Issue focuses on the latest advancements in NGS applications that illuminate the complex interplay between genomic, transcriptomic, and epigenomic alterations in aging tissues and cancerous cells. By enabling high-resolution profiling of somatic mutations, gene expression dynamics, and epigenetic modifications, NGS provides critical insights into cellular senescence, tumor evolution, clonal heterogeneity, and age-related disease progression. The integration of bulk and single-cell sequencing, long-read technologies, and multi-omics approaches is transforming our understanding of how aging influences cancer susceptibility and how cancer disrupts normal aging processes. We welcome contributions that explore novel NGS-based methodologies, bioinformatics pipelines, and translational applications in aging and oncology. Studies leveraging NGS to identify biomarkers, therapeutic targets, or mechanisms of resistance in age-associated cancers are particularly encouraged. This Special Issue aims to bridge the gap between aging biology and cancer genomics, fostering interdisciplinary research that advances precision medicine and healthy aging.

Dr. Hyunsoo Kim
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 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-anonymized peer-review process. A guide for authors and other relevant information for submission of manuscripts is available on the Instructions for Authors page. International Journal of Molecular Sciences is an international peer-reviewed open access semimonthly journal published by MDPI.

Please visit the Instructions for Authors page before submitting a manuscript. There is an Article Processing Charge (APC) for publication in this open access journal. For details about the APC please see here. 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

  • next-generation sequencing
  • aging
  • cancer genomics
  • cellular senescence
  • single-cell sequencing
  • epigenomics
  • transcriptomics
  • tumor evolution
  • biomarkers
  • precision medicine

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Published Papers (3 papers)

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Research

26 pages, 1030 KB  
Article
Low-Pass Nanopore Sequencing of Plasma cfDNA Reveals Fragmentomic, Epigenomic, and Age-Associated Signatures Under Ultra-Low-Coverage Conditions
by Andrey Eremin, Alexander Sergeev, Tsimur Hasanau and Maria Zvereva
Int. J. Mol. Sci. 2026, 27(13), 5739; https://doi.org/10.3390/ijms27135739 - 25 Jun 2026
Viewed by 598
Abstract
Circulating cell-free DNA (cfDNA) enables minimally invasive assessment of chromatin organization and DNA modifications. Whether such information can be reliably recovered under conditions of limited plasma input (below 1 mL) and ultra-low sequencing depth remains unclear. We performed low-pass whole-genome Oxford Nanopore sequencing [...] Read more.
Circulating cell-free DNA (cfDNA) enables minimally invasive assessment of chromatin organization and DNA modifications. Whether such information can be reliably recovered under conditions of limited plasma input (below 1 mL) and ultra-low sequencing depth remains unclear. We performed low-pass whole-genome Oxford Nanopore sequencing (down to 0.01× coverage) of plasma cfDNA from young and elderly donors and jointly analyzed fragment length distributions and base modifications (5mC, 5hmC, 6mA). In parallel, we analyzed an enzymatically fragmented model DNA system to assess whether controlled in vitro fragmentation can reproduce cfDNA-like nucleosomal profiles and associated modification patterns. Despite shallow coverage, cfDNA samples displayed reproducible mono-, di-, tri-, and tetra-nucleosomal peaks, indicating that major fragmentomic features can be retained under ultra-low-coverage conditions. Modification-aware basecalling enabled exploratory quantification of global modification fractions across nucleosomal size classes and nomination of candidate group-specific modification loci. Overall, these results support the feasibility of low-pass nanopore sequencing as an exploratory framework for simultaneous cfDNA fragmentomic and epigenomic profiling in low-input studies. Full article
(This article belongs to the Special Issue Advances in Next-Generation Sequencing for Aging and Cancer Research)
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20 pages, 3804 KB  
Article
Therapeutic Stress-Induced Remodeling of Transposable Elements and TE-Gene Chimeras in KYSE150 Esophageal Squamous Cell Carcinoma Cells
by Muhammad Majid, Muhammad Moeen, Nouman Amjad, Hashim Khan, Zhaojian Sun, Linping Wu and Zhiyuan Li
Int. J. Mol. Sci. 2026, 27(8), 3471; https://doi.org/10.3390/ijms27083471 - 13 Apr 2026
Viewed by 1084
Abstract
Transposable elements (TEs) are major contributors to genome plasticity and can reshape gene regulation through stress-responsive activation and the formation of TE-gene chimeric transcripts. Although therapeutic stress is known to perturb transcriptional networks in cancer cells, its impact on canonical TE transcription and [...] Read more.
Transposable elements (TEs) are major contributors to genome plasticity and can reshape gene regulation through stress-responsive activation and the formation of TE-gene chimeric transcripts. Although therapeutic stress is known to perturb transcriptional networks in cancer cells, its impact on canonical TE transcription and TE-gene chimera formation in esophageal squamous cell carcinoma (ESCC) remains poorly defined. To address this, we performed a comprehensive transcriptome-wide analysis of TE expression and TE-gene chimeric transcripts in KYSE150 ESCC cells following combined 125I radiation and carfilzomib treatment. The TE analysis showed 148 dysregulated TEs, characterized by ERV1 LTR element enrichment and distinct treatment-control sample separation, indicating structured remodeling of the TE transcriptome. We identified 301 significant TE-gene chimeric events, indicating category-specific remodeling with an increase in TE-initiated and TE-exonic chimeras and a decrease in TE-terminal events. The TE families that underwent the most transcriptional changes were not those that drove chimeric events, indicating that global TE activation does not passively cause chimera remodeling. The gene repression was strongly associated with chimeric transcripts, and gene expression changes were negatively correlated with chimerism frequency. SPANXN1, IL1RL1, and RSAD2, strongly downregulated genes, produced novel TE-derived isoforms and were high-potential functional candidates. Epigenetic context analysis showed considerable overlap between exonized chimeras and candidate cis-regulatory elements, suggesting a potential association with regulatory genomic contexts. Pathway enrichment analysis showed synchronized transcriptomic reprogramming and cell cycle and DNA repair pathway activation and autophagy inhibition. In esophageal cancer cells, concurrent genotoxic and proteotoxic stress causes complex TE remodeling, linking traditional TE transcriptional alterations to structured TE-gene chimera development and stress-related transcriptome reprogramming. Full article
(This article belongs to the Special Issue Advances in Next-Generation Sequencing for Aging and Cancer Research)
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15 pages, 1163 KB  
Article
Ensemble of Time-Evolving SASP Gene Sets Identifies IGFBP7 and CDKN1A as a Potential Marker Pair for Senescent Fibroblast Subpopulations Across Tissues
by Hyunsoo Kim, Erich Kummerfeld, Laura J. Niedernhofer, Constantin Aliferis, Paul D. Robbins and Jinhua Wang
Int. J. Mol. Sci. 2026, 27(7), 3012; https://doi.org/10.3390/ijms27073012 - 26 Mar 2026
Viewed by 1182
Abstract
The senescence-associated secretory phenotype (SASP) is a hallmark of senescent cells and plays a critical role in the development and progression of various age-related diseases, including cancer, cardiovascular disorders, and neurodegenerative diseases. In this study, we characterize SASP heterogeneity using single-cell RNA sequencing [...] Read more.
The senescence-associated secretory phenotype (SASP) is a hallmark of senescent cells and plays a critical role in the development and progression of various age-related diseases, including cancer, cardiovascular disorders, and neurodegenerative diseases. In this study, we characterize SASP heterogeneity using single-cell RNA sequencing (scRNA-seq) data, focusing on the transcriptional signatures associated with elevated expression of individual SASP genes in mature senescent cells, as well as time-dependent variation in SASP expression across the early and mature senescent states in the WI-38 human lung fibroblast cell line. We generated multiple gene sets, each representing the transcriptional landscape linked to high expression of a specific SASP gene, and integrated them into an ensemble that reflects the temporal dynamics of SASP gene expression. Applying SASP scores derived from this ensemble of gene sets (SASP scores/EGS) to publicly available scRNA-seq datasets from human lung, skin, and eye tissues enabled the identification of senescent fibroblasts and revealed IGFBP7 as a consistently upregulated marker in p21+ or p16+ fibroblasts across diverse human tissues. Our framework supports improved detection of both early and mature fibroblast replicative senescent cells, offering valuable insights into aging and age-related disease research. Full article
(This article belongs to the Special Issue Advances in Next-Generation Sequencing for Aging and Cancer Research)
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