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Cancers
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Multi-Omics Analysis in the Study of Carcinogenesis
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Multi-Omics Analysis in the Study of Carcinogenesis

A special issue of Cancers (ISSN 2072-6694). This special issue belongs to the section "Cancer Pathophysiology".

Deadline for manuscript submissions: 15 September 2025 | Viewed by 6039

Special Issue Editor

Dr. Dimiter Avtanski

E-Mail Website
Guest Editor
Friedman Diabetes Institute at Lenox Hill Hospital, Northwell Health, Lenox Hill Hospital, New York, NY, USA
Interests: obesity; cytokine; diabetes; breast cancer; steroid
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

Multi-omics analyses have been established as powerful tools in investigating carcinogenesis, offering a broad view of the molecular mechanisms underlying cancer initiation and progression. The importance of integrating data obtained from multi-omics analyses with data derived from single-omics methods has been widely acknowledged. Correlating datasets from genomics, transcriptomics, proteomics, and metabolomics with clinical practice observations has proven to be a powerful approach to distinguishing different subtypes of patients within a population, as well as in the search for novel drug targets. In addition, the use of machine and deep learning in multi-omics data analyses is promising for the future development of oncology research.

This Special Issue welcomes the submission of a broad range of research and review manuscripts investigating the implications of multi-omics analysis in oncology research. We believe that such a group of articles will benefit basic science and clinical research scientists by providing a valuable summary of knowledge from various disciplines.

Dr. Dimiter Avtanski
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 communications are invited. For planned papers, a title and short abstract (about 100 words) can be sent to the Editorial Office for announcement on this website.

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. Cancers is an international peer-reviewed open access semimonthly 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

  • carcinogenesis
  • cancer initiation and progression
  • oncology research
  • multi-omics analyses
  • genomics
  • transcriptomics, proteomics
  • metabolomics

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Published Papers (3 papers)

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Research

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20 pages, 7697 KiB  
Article
MiRNA Profiling of Areca Nut-Induced Carcinogenesis in Head and Neck Cancer
by Hung-Han Huang, Joseph T. Chang, Guo-Rung You, Yu-Fang Fu, Eric Yi-Liang Shen, Yi-Fang Huang, Chia-Rui Shen and Ann-Joy Cheng
Cancers 2024, 16(21), 3710; https://doi.org/10.3390/cancers16213710 - 3 Nov 2024
Viewed by 1503
Abstract
Background: While miRNAs are increasingly recognized for their role in tumorigenesis, their involvement in head and neck cancer (HNC) remains insufficiently explored. Additionally, the carcinogenic mechanisms of areca nut, a major habitual carcinogen in Southeast Asia, are not well understood. Methods and results: [...] Read more.
Background: While miRNAs are increasingly recognized for their role in tumorigenesis, their involvement in head and neck cancer (HNC) remains insufficiently explored. Additionally, the carcinogenic mechanisms of areca nut, a major habitual carcinogen in Southeast Asia, are not well understood. Methods and results: This study adopts a systematic approach to identify miRNA profiles associated with areca nut-induced HNC. Using miRNA microarray analysis, we identified 292 miRNAs dysregulated in areca nut-treated HNC cells, with 136 upregulated and 156 downregulated. Bioinformatic analysis of the TCGA-HNSC dataset uncovered a set of 692 miRNAs relevant to HNC development, comprising 449 overexpressed and 243 underexpressed in tumor tissues. Integrating these datasets, we defined a signature of 84 miRNAs, including 39 oncogenic miRNAs (OncomiRs) and 45 tumor-suppressive miRNAs (TsmiRs), highlighting their pivotal role in areca nut-induced carcinogenesis. MultiMiR analysis identified 740 genes cross-regulated by eight hub TsmiRs, significantly impacting key cancer-related pathways (p53, PI3K-AKT, MAPK, and Ras) and critical oncogenic processes. Moreover, we validated miR-499a-5p as a vital regulator, demonstrating its ability to mitigate areca nut-induced cancer progression by reducing cell migration, invasion, and chemoresistance. Conclusions: Thus, this miRNA signature addresses a crucial gap in understanding the molecular underpinnings of areca nut-induced carcinogenesis and offers a promising platform for clinical applications in risk assessment, diagnosis, and prognosis of areca nut-associated malignancies. Full article
(This article belongs to the Special Issue Multi-Omics Analysis in the Study of Carcinogenesis)
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Review

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33 pages, 3790 KiB  
Review
Exploring the Genetic Orchestra of Cancer: The Interplay Between Oncogenes and Tumor-Suppressor Genes
by Sajal Raj Singh, Rakesh Bhaskar, Shampa Ghosh, Bhuvaneshwar Yarlagadda, Krishna Kumar Singh, Prashant Verma, Sonali Sengupta, Mitko Mladenov, Nikola Hadzi-Petrushev, Radoslav Stojchevski, Jitendra Kumar Sinha and Dimiter Avtanski
Cancers 2025, 17(7), 1082; https://doi.org/10.3390/cancers17071082 - 24 Mar 2025
Viewed by 1875
Abstract
Cancer is complex because of the critical imbalance in genetic regulation as characterized by both the overexpression of oncogenes (OGs), mainly through mutations, amplifications, and translocations, and the inactivation of tumor-suppressor genes (TSGs), which entail the preservation of genomic integrity by inducing apoptosis [...] Read more.
Cancer is complex because of the critical imbalance in genetic regulation as characterized by both the overexpression of oncogenes (OGs), mainly through mutations, amplifications, and translocations, and the inactivation of tumor-suppressor genes (TSGs), which entail the preservation of genomic integrity by inducing apoptosis to counter the malignant growth. Reviewing the intricate molecular interplay between OGs and TSGs draws attention to their cell cycle, apoptosis, and cancer metabolism regulation. In the present review, we discuss seminal discoveries, such as Knudson’s two-hit hypothesis, which framed the field’s understanding of cancer genetics, leading to the next breakthroughs with next-generation sequencing and epigenetic profiling, revealing novel insights into OG and TSG dysregulation with opportunities for targeted therapy. The key pathways, such as MAPK/ERK, PI3K/AKT/mTOR, and Wnt/β-catenin, are presented in the context of tumor progression. Importantly, we further highlighted the advances in therapeutic strategies, including inhibitors of KRAS and MYC and restoration of TSG function, despite which mechanisms of resistance and tumor heterogeneity pose daunting challenges. A high-level understanding of interactions between OG-TSGs forms the basis for effective, personalized cancer treatment—something to strive for in better clinical outcomes. This synthesis should integrate foundational biology with translation and, in this case, contribute to the ongoing effort against cancer. Full article
(This article belongs to the Special Issue Multi-Omics Analysis in the Study of Carcinogenesis)
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47 pages, 3289 KiB  
Review
Translational Advances in Oncogene and Tumor-Suppressor Gene Research
by Radoslav Stojchevski, Edward Agus Sutanto, Rinni Sutanto, Nikola Hadzi-Petrushev, Mitko Mladenov, Sajal Raj Singh, Jitendra Kumar Sinha, Shampa Ghosh, Bhuvaneshwar Yarlagadda, Krishna Kumar Singh, Prashant Verma, Sonali Sengupta, Rakesh Bhaskar and Dimiter Avtanski
Cancers 2025, 17(6), 1008; https://doi.org/10.3390/cancers17061008 - 17 Mar 2025
Viewed by 2067
Abstract
Cancer, characterized by the uncontrolled proliferation of cells, is one of the leading causes of death globally, with approximately one in five people developing the disease in their lifetime. While many driver genes were identified decades ago, and most cancers can be classified [...] Read more.
Cancer, characterized by the uncontrolled proliferation of cells, is one of the leading causes of death globally, with approximately one in five people developing the disease in their lifetime. While many driver genes were identified decades ago, and most cancers can be classified based on morphology and progression, there is still a significant gap in knowledge about genetic aberrations and nuclear DNA damage. The study of two critical groups of genes—tumor suppressors, which inhibit proliferation and promote apoptosis, and oncogenes, which regulate proliferation and survival—can help to understand the genomic causes behind tumorigenesis, leading to more personalized approaches to diagnosis and treatment. Aberration of tumor suppressors, which undergo two-hit and loss-of-function mutations, and oncogenes, activated forms of proto-oncogenes that experience one-hit and gain-of-function mutations, are responsible for the dysregulation of key signaling pathways that regulate cell division, such as p53, Rb, Ras/Raf/ERK/MAPK, PI3K/AKT, and Wnt/β-catenin. Modern breakthroughs in genomics research, like next-generation sequencing, have provided efficient strategies for mapping unique genomic changes that contribute to tumor heterogeneity. Novel therapeutic approaches have enabled personalized medicine, helping address genetic variability in tumor suppressors and oncogenes. This comprehensive review examines the molecular mechanisms behind tumor-suppressor genes and oncogenes, the key signaling pathways they regulate, epigenetic modifications, tumor heterogeneity, and the drug resistance mechanisms that drive carcinogenesis. Moreover, the review explores the clinical application of sequencing techniques, multiomics, diagnostic procedures, pharmacogenomics, and personalized treatment and prevention options, discussing future directions for emerging technologies. Full article
(This article belongs to the Special Issue Multi-Omics Analysis in the Study of Carcinogenesis)
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