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New Advances in Cancer Genomics

A special issue of International Journal of Molecular Sciences (ISSN 1422-0067). This special issue belongs to the section "Molecular Biology".

Deadline for manuscript submissions: 20 December 2025 | Viewed by 1631

Special Issue Editor


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Guest Editor
Department of Clinical Oncology, Graduate School of Medical and Dental Sciences, Institute of Science Tokyo, 1-5-45 Yushima, Bunkyo-Ku, Tokyo 113-8510, Japan
Interests: medical oncology; cancer genomic medicine; targeted therapy

Special Issue Information

Dear Colleagues,

This Special Issue will focus on recent advances in cancer genomics, covering a wide range of topics such as genomic and structural variations, biomarker discovery, and novel methodologies for understanding cancer biology. With the rapid development of emerging technologies, we also welcome studies that explore computational approaches, artificial intelligence, and their potential to enhance the interpretation of complex genomic data. These technologies hold promise for improving patient outcomes and accelerating precision oncology.

Contributions addressing the integration of genomics into clinical practice, highlighting translational research, or proposing innovative solutions to current challenges in cancer genomics are particularly encouraged. Furthermore, we are interested in research targeting "undruggable" oncogenes, such as KRAS, focusing on drug discovery and development strategies that overcome previous limitations. Studies exploring novel therapeutic approaches and molecular mechanisms to address these challenging targets are highly welcomed.

This Special Issue aims to provide a platform for cutting-edge and multidisciplinary research that pushes the boundaries of cancer genomics and fosters collaboration across different scientific domains.

Topics of interest include, but are not limited to:

  • Genomic and structural variations in cancer
  • Biomarker discovery for precision oncology
  • The integration of multi-omics data with AI for personalized cancer care
  • AI-driven diagnostics and treatment planning in oncology
  • Drug discovery for undruggable targets, including KRAS

Dr. Yoshihito Kano
Guest Editor

Manuscript Submission Information

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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. 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

  • cancer genomics
  • biomarker discovery
  • precision oncology
  • KRAS and undruggable targets
  • artificial intelligence in oncology
  • multi-omics data integration
  • drug discovery

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Published Papers (3 papers)

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Research

18 pages, 1337 KiB  
Article
Dysregulated Alternative Splicing in Breast Cancer Subtypes of RIF1 and Other Transcripts
by Emma Parker, Laura Akintche, Alexandra Pyatnitskaya, Shin-ichiro Hiraga and Anne D. Donaldson
Int. J. Mol. Sci. 2025, 26(15), 7308; https://doi.org/10.3390/ijms26157308 - 29 Jul 2025
Viewed by 330
Abstract
Genome instability is a hallmark of cancer, often driven by mutations and altered expression of genome maintenance factors involved in DNA replication and repair. Rap1 Interacting Factor 1 (RIF1) plays a crucial role in genome stability and is implicated in cancer pathogenesis. Cells [...] Read more.
Genome instability is a hallmark of cancer, often driven by mutations and altered expression of genome maintenance factors involved in DNA replication and repair. Rap1 Interacting Factor 1 (RIF1) plays a crucial role in genome stability and is implicated in cancer pathogenesis. Cells express two RIF1 splice variants, RIF1-Long and RIF1-Short, which differ in their ability to protect cells from DNA replication stress. Here, we investigate differential expression and splicing of RIF1 in cancer cell lines following replication stress and in patients using matched normal and tumour data from The Cancer Genome Atlas (TCGA). Overall RIF1 expression is altered in several cancer types, with increased transcript levels in colon and lung cancers. RIF1 also exhibits distinct splicing patterns, particularly in specific breast cancer subtypes. In Luminal A (LumA), Luminal B (LumB), and HER2-enriched breast cancers (HER2E), RIF1 Exon 31 tends to be excluded, favouring RIF1-Short expression and correlating with poorer clinical outcomes. These breast cancer subtypes also tend to exclude other short exons, suggesting length-dependent splicing dysregulation. Basal breast cancer also shows exon exclusion, but unlike other subtypes, it shows no short-exon bias. Surprisingly, however, in basal breast cancer, RIF1 Exon 31 is not consistently excluded, which may impact prognosis since RIF1-Long protects against replication stress. Full article
(This article belongs to the Special Issue New Advances in Cancer Genomics)
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25 pages, 3180 KiB  
Article
CCR4-NOT Transcription Complex Subunit 7 (CNOT7) Protein and Leukocyte-Associated Immunoglobulin-like Receptor-1 in Breast Cancer Progression: Clinical Mechanistic Insights and In Silico Therapeutic Potential
by Mona M. Elanany, Dina Mostafa, Ahmad A. Hady, Mona Y. Y. Abd Allah, Nermin S. Ahmed, Nehal H. Elghazawy, Wolfgang Sippl, Tadashi Yamamoto and Nadia M. Hamdy
Int. J. Mol. Sci. 2025, 26(15), 7141; https://doi.org/10.3390/ijms26157141 - 24 Jul 2025
Viewed by 449
Abstract
Metastatic breast cancer (BC) spread underscores the need for novel prognostic biomarkers. This study investigated CCR4-NOT Transcription Complex Subunit 7 (CNOT7) and leukocyte-associated immunoglobulin-like receptor-1 (LAIR-1) in BC progression and natural killer (NK) cell resistance. In the current study, 90 female BC patients [...] Read more.
Metastatic breast cancer (BC) spread underscores the need for novel prognostic biomarkers. This study investigated CCR4-NOT Transcription Complex Subunit 7 (CNOT7) and leukocyte-associated immunoglobulin-like receptor-1 (LAIR-1) in BC progression and natural killer (NK) cell resistance. In the current study, 90 female BC patients (46 non-metastatic, 44 metastatic) were analyzed. CNOT7 and LAIR-1 protein levels were measured in serum via ELISA and CNOT7 expression in tissue by immunohistochemistry (IHC). In silico tools explored related pathways. Computational analyses, including in silico bioinformatics and molecular docking, explored gene functions, interactions, and ligand binding to CNOT7 and LAIR-1. CNOT7 serum levels were significantly elevated in metastatic patients (mean 4.710) versus non-metastatic patients (mean 3.229, p < 0.0001). Conversely, LAIR-1 serum levels were significantly lower in metastatic (mean 56.779) versus non-metastatic patients (mean 67.544, p < 0.0001). High CNOT7 was found in 50% (45/90) of cases, correlating with higher tumor grade, hormone receptor negativity, and increased lymph node involvement. Elevated CNOT7 and lower LAIR-1 levels were associated with worse overall survival. Pathway analysis linked CNOT7 to the PI3K/AKT/mTOR pathway. Computational findings elucidated CNOT7′s cellular roles, gene/protein interaction networks for LAIR-1/CNOT7, and distinct ligand binding profiles. High CNOT7 levels are associated with advanced BC stages and poor clinical outcomes, which suggests its utility as a prognostic biomarker. The inverse relationship between CNOT7 and LAIR-1 provides mechanistic insights into BC progression and immune evasion, further supported by in silico investigations. Full article
(This article belongs to the Special Issue New Advances in Cancer Genomics)
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26 pages, 6652 KiB  
Article
Platelet-Rich Plasma (PRP) Mitigates Silver Nanoparticle (AgNP)-Induced Pulmonary Fibrosis via iNOS/CD68/CASP3/TWIST1 Regulation: An Experimental Study and Bioinformatics Analysis
by Shaimaa R. Abdelmohsen, Ranya M. Abdelgalil, Asmaa M. Elmaghraby, Amira M. Negm, Reham Hammad, Eleni K. Efthimiadou, Sara Seriah, Hekmat M. El Magdoub, Hemat Elariny, Islam Farrag, Nahla El Shenawy, Doaa Abdelrahaman, Hussain Almalki, Ahmed A. Askar, Marwa M. El-Mosely, Fatma El Zahraa Abd El Hakam and Nadia M. Hamdy
Int. J. Mol. Sci. 2025, 26(14), 6782; https://doi.org/10.3390/ijms26146782 - 15 Jul 2025
Viewed by 486
Abstract
Platelet-rich plasma (PRP) has become an increasingly valuable biologic approach for personalized regenerative medicine because of its potent anti-inflammatory/healing effects. It is thought to be an excellent source of growth factors that can promote tissue healing and lessen fibrosis. Although this treatment has [...] Read more.
Platelet-rich plasma (PRP) has become an increasingly valuable biologic approach for personalized regenerative medicine because of its potent anti-inflammatory/healing effects. It is thought to be an excellent source of growth factors that can promote tissue healing and lessen fibrosis. Although this treatment has demonstrated effectiveness in numerous disease areas, its impact on pulmonary fibrosis (PF) caused by silver nanoparticles (AgNPs) via its antiapoptotic effects remains to be explored. AgNPs were synthesized biologically by Bacillus megaterium ATCC 55000. AgNP characterization was carried out via UV–Vis spectroscopy, X-ray diffraction (XRD), dynamic light scattering (DLS), transmission electron microscopy (TEM), and scanning electron microscopy (SEM) imaging to reveal monodispersed spheres with a mean diameter of 45.17 nm. A total of 48 male Wistar rats divided into six groups, with 8 rats per group, were used in the current study on the basis of sample size and power. The groups used were the PRP donor, control, AgNP, AgNP + PRP, AgNP + dexamethasone (Dexa) rat groups, and a recovery group. Body weights, hydroxyproline (HP) levels, and CASP3 and TWIST1 gene expression levels were assessed. H&E and Sirius Red staining were performed. Immunohistochemical studies for inducible nitric oxide synthase (iNOS) and cluster of differentiation 68 (CD68) with histomorphometry were conducted. A significant reduction in body weight (BWt) was noted in the AgNP group compared with the AgNP + PRP group (p < 0.001). HP, CASP3, and TWIST1 expression levels were significantly increased by AgNPs but decreased upon PRP (p < 0.001) treatment. Compared with those in the control group, the adverse effects of AgNPs included PF, lung alveolar collapse, thickening of the interalveolar septa, widespread lymphocytic infiltration, increased alveolar macrophage CD68 expression, and iNOS positivity in the cells lining the alveoli. This work revealed that PRP treatment markedly improved the histopathological and immunohistochemical findings observed in the AgNP group in a manner comparable to that of the Dexa. In conclusion, these results demonstrated the therapeutic potential of PRP in a PF rat model induced via AgNPs. This study revealed that PRP treatment significantly improved the histopathological and immunohistochemical alterations observed in the AgNP-induced group, with effects comparable to those of the Dexa. In conclusion, these findings highlight the therapeutic potential of PRP in a rat model of AgNP-induced PF. Full article
(This article belongs to the Special Issue New Advances in Cancer Genomics)
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