Molecular Drivers of Oncogenesis and Tumor Evolution: Mechanisms and Cellular Pathways
A special issue of Cells (ISSN 2073-4409).
Deadline for manuscript submissions: 31 July 2026 | Viewed by 15
Special Issue Editors
2. Doctoral School, Iuliu Hațieganu University of Medicine and Pharmacy, 400337 Cluj-Napoca, Romania
3. The Academy of Medical Sciences, 030167 Bucharest, Romania
Interests: microRNAs; biomarkers; apoptosis; cancer profiling; immunology
Special Issues, Collections and Topics in MDPI journals
Interests: non-coding RNAs; cancer biology; tumor immunology; transcriptomics
Special Issue Information
Dear Colleagues,
Cancer initiation, progression and therapeutic response result are driven by complex and dynamic molecular processes that extend beyond the acquisition of driver mutations. Many tumors evolve through intricate mechanisms, that include interactions between genetic and epigenetic changes, metabolic reprogramming, immunologic pressure, and the tumor microenvironment, leading to intratumoral heterogeneity and marked adaptive potential. All these molecular drivers modulate oncogenic programs, impact clonal evolution, and determine the metastatic behavior, and therapeutic resistance in various cancer types.
Tumor evolution is an intricate process, that is controlled by selective pressures of tissue-specific environments, immune surveillance mechanisms, and by therapeutic interventions. A number of factors, such as genomic instability, epigenetic plasticity, and signaling pathway rewiring allow malignant cells to adapt to these selective pressures, ultimately leading to treatment failure and cancer progression.
The present Special Issue aims to gather original research papers, as well as review articles that discuss molecular drivers of oncogenesis and tumor evolution in various cancer types. We invite contributions that are focused on oncogenic signaling pathways, tumor suppressors and oncogenes, clonal evolution, tumor microenvironment interactions, tumor-immune system interactions, metastasis, angiogenesis, metabolic reprogramming, intratumoral heterogeneity, mechanisms of therapeutic resistance, and translational studies that undertake the discovery of biomarkers. We encourage researchers to submit studies that connect molecular findings with real-world applications, such as the discovery of biomarkers, precision oncology, and longitudinal disease monitoring.
Prof. Dr. Ioana Berindan-Neagoe
Dr. Alexandru Tirpe
Guest Editors
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-blind peer-review process. A guide for authors and other relevant information for submission of manuscripts is available on the Instructions for Authors page. Cells 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 2700 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
- oncogenesis
- cancer progression
- cancer biology
- tumor immunology
- tumor microenvironment
- metastasis
- angiogenesis
- metabolic reprogramming
- therapy resistance
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