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Genomic Research in Carcinogenesis, Cancer Progression and Recurrence
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Genomic Research in Carcinogenesis, Cancer Progression and Recurrence

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

Deadline for manuscript submissions: 20 November 2025 | Viewed by 229

Special Issue Editor

Dr. Magdalena Orzechowska

E-Mail Website
Guest Editor
Department of Molecular Carcinogenesis, Medical University of Lodz, 90-752 Lodz, Poland
Interests: molecular carcinogenesis; molecular mechanisms of cancer recurrence; systems biology; bioinformatics
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

Current research highlights the importance of genomics in predicting tumor progression, identifying driver mutations, and informing personalized therapies in many types of cancer. This Special Issue will cover genomic alterations, driver mutations, tumor evolution metrics, and the integration of genomics with clinicopathological and artificial intelligence-aided approaches to predict and understand cancer outcomes, progression, and recurrence. Contributions will include a broad range of topics, such as:

  • Genomic alterations in carcinogenesis: mechanisms of genetic and epigenetic changes leading to cancer initiation and driving carcinogenesis.
  • Genomic drivers of cancer progression: identification and characterization of genomic mutations and variations that drive tumor growth and metastasis.
  • Genomic markers for cancer recurrence: development and validation of genomic biomarkers for predicting cancer recurrence.
  • Precision medicine and genomic targeting: applications of genomic data in personalized cancer therapies and targeted treatments.
  • Bioinformatics and computational approaches: advanced computational methods for analyzing genomic data in cancer research.

Dr. Magdalena Orzechowska
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 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. 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

  • genomic profiling
  • carcinogenesis
  • metastasis
  • recurrence
  • precision medicine
  • tumor evolution metrics
  • sequencing
  • tumor markers

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Published Papers (1 paper)

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27 pages, 5430 KiB  
Article
Gene Monitoring in Obesity-Induced Metabolic Dysfunction in Rats: Preclinical Data on Breast Neoplasia Initiation
by Francisco Claro, Jr., Joseane Morari, Camila de Angelis, Emerielle Cristine Vanzela, Wandir Antonio Schiozer, Lício Velloso and Luis Otavio Zanatta Sarian
Int. J. Mol. Sci. 2025, 26(15), 7296; https://doi.org/10.3390/ijms26157296 - 28 Jul 2025
Abstract
Obesity and metabolic dysfunction are established risk factors for luminal breast cancer, yet current preclinical models inadequately recapitulate the complex metabolic and immune interactions driving tumorigenesis. To develop and characterize an immunocompetent rat model of luminal breast cancer induced by chronic exposure to [...] Read more.
Obesity and metabolic dysfunction are established risk factors for luminal breast cancer, yet current preclinical models inadequately recapitulate the complex metabolic and immune interactions driving tumorigenesis. To develop and characterize an immunocompetent rat model of luminal breast cancer induced by chronic exposure to a cafeteria diet mimicking Western obesogenic nutrition. Female rats were fed a cafeteria diet or standard chow from weaning. Metabolic parameters, plasma biomarkers (including leptin, insulin, IGF-1, adiponectin, and estrone), mammary gland histology, tumor incidence, and gene expression profiles were longitudinally evaluated. Gene expression was assessed by PCR arrays and qPCR. A subgroup underwent dietary reversal to assess the reversibility of molecular alterations. Cafeteria diet induced significant obesity (mean weight 426.76 g vs. 263.09 g controls, p < 0.001) and increased leptin levels without altering insulin, IGF-1, or inflammatory markers. Histological analysis showed increased ductal ectasia and benign lesions, with earlier fibroadenoma and luminal carcinoma development in diet-fed rats. Tumors exhibited luminal phenotype, low Ki67, and elevated PAI-1 expression. Gene expression alterations were time point specific and revealed early downregulation of ID1 and COX2, followed by upregulation of MMP2, THBS1, TWIST1, and PAI-1. Short-term dietary reversal normalized several gene expression changes. Overall tumor incidence was modest (~12%), reflecting early tumor-promoting microenvironmental changes rather than aggressive carcinogenesis. This immunocompetent cafeteria diet rat model recapitulates key metabolic, histological, and molecular features of obesity-associated luminal breast cancer and offers a valuable platform for studying early tumorigenic mechanisms and prevention strategies without carcinogen-induced confounders. Full article
(This article belongs to the Special Issue Genomic Research in Carcinogenesis, Cancer Progression and Recurrence)
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