Molecular Integrative Genomics in Cancer

A special issue of Current Oncology (ISSN 1718-7729).

Deadline for manuscript submissions: 15 July 2026 | Viewed by 449

Special Issue Editor


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Guest Editor
Institute for Population and Precision Health, University of Chicago, Chicago, IL 60637, USA
Interests: integrative molecular genomics in cancer epidemiology; oncogene-sis and its use in disease classification; therapeutic response and prognosis of different human cancers
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Special Issue Information

Dear Colleagues,

In the era of precision medicine, molecular genomics play an important role in current oncology practice. The cancer genome itself may be used as a reliable biomarker. Molecular genomics not only help in understanding the pathogenesis of cancer; they also help in diagnosis, molecular classification, target selection for newer drugs, and selection of existing targeted therapy. More recently, the application of liquid biopsy opens a field of almost non-invasive ways for clinical follow-up and decision-making. Different molecular genomics applications range from tumor DNA and/or RNA sequencing and epigenetic testing to the analysis of circulating cell-free DNA and exosomes. One form of genomic alteration may correlate with others, and also some are associated with proteomic changes seen in cancer. Recent studies have also revealed interactions between genomic markers (e.g., mutation and gene expression) and also between genomic markers and environmental exposure or interaction with gender. Therefore, the integration of different genomic markers, clinical and histological features, environmental exposure, etc., can provide more helpful information for a clear understanding of pathogenesis, clinically meaningful classification, or subgrouping of patients for better precision medicine.

In this Special Issue of Current Oncology, we are inviting papers focused on any integration of molecular genomics or multi-omics data with clinical or environmental factors in relation to cancer development, progression, treatment, and anti-cancer chemotherapy resistance.  

We welcome original research articles and reviews. Research areas may include (but are not limited to) the following:

  1. DNA sequencing, mutation, genome stability;
  2. RNA, microRNA sequencing, gene pathway;
  3. Methylation, histone modification;
  4. Liquid biopsy.

I look forward to receiving your contributions.

Dr. Muhammad Kibriya
Guest Editor

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Keywords

  • somatic mutation
  • cytogenetic abnormality
  • amplification
  • deletion
  • gene fusion
  • MSI, methylation
  • liquid biopsy
  • cell-free DNA
  • gene–environment interaction
  • targeted therapy
  • precision medicine

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Published Papers (1 paper)

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Research

22 pages, 1768 KB  
Article
Mutation and Microsatellite Instability (MSI) Affect the Differential Gene Expression of Folic Acid and 5-Flourouracil Metabolism-Related Genes in Colorectal Carcinoma
by Muhammad Rafiqul Islam, Farzana Jasmine, Daniil Vasiljevs, Maruf Raza, Armando Almazan, Habibul Ahsan and Muhammad G. Kibriya
Curr. Oncol. 2025, 32(12), 661; https://doi.org/10.3390/curroncol32120661 - 26 Nov 2025
Abstract
In colorectal carcinoma (CRC), 5-fluorouracil (5-FU) remains the cornerstone of adjuvant systemic therapy, with folic acid (FA) serving as an essential adjunct. Expression of genes related to the metabolism and action of 5-FU and FA can be influenced by patient- and tumor-specific biological [...] Read more.
In colorectal carcinoma (CRC), 5-fluorouracil (5-FU) remains the cornerstone of adjuvant systemic therapy, with folic acid (FA) serving as an essential adjunct. Expression of genes related to the metabolism and action of 5-FU and FA can be influenced by patient- and tumor-specific biological factors. In this study, we explore differential gene expression profiles of 180 genes representing 14 different gene sets associated with different 5-FU and FA metabolism processes, at both gene and pathway levels across clinical and molecular subgroups. In 71 patients with CRC, paired tumors and normal colonic tissues were analyzed. In CRC tissue, several gene sets (including Cell Cycle Checkpoint, Oxidative Stress Response, and Signaling Pathway, etc.) were upregulated, while three gene sets (Apoptotic, Tumor Suppressor, and Endoplasmic Reticulum Stress) were downregulated. Kirsten rat sarcoma virus (KRAS), tumor protein p53 (TP53), and microsatellite instability (MSI) status impacted gene expression across molecular subgroups. At the individual gene level, among cell cycle genes, the BUB3 mitotic checkpoint protein (BUB3) was upregulated in MSI tumors compared to MSS, whereas SMAD family member 4 (SMAD4) was downregulated in MSS tumors compared to MSI. DNA fragmentation factor alpha (DFFA) was downregulated in MSI and upregulated in MSS. Notably, thymidylate synthetase (TYMS) was more upregulated in MSI tumors (1.65-fold; 95% CI: 1.27–2.13) compared to MSS (1.19-fold; 95% CI: 1.02–1.39). Dysregulation of these genes across these factors will broaden our understanding of 5-FU-based treatment in CRC. Furthermore, targeting dysregulated pathways could form the basis for improved precision therapies tailored to CRC subtypes. Full article
(This article belongs to the Special Issue Molecular Integrative Genomics in Cancer)
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