Editorial - Journal of Medical Oncology and Therapeutics (2025) Volume 10, Issue 2
Targeting Oncogenes in Precision Oncology: Advances and Challenges
Peter Rieke *
Department of Pharmacology, Utrecht University, Netherland
- *Corresponding Author:
- Peter Rieke
Department of Pharmacology, Utrecht University, Netherland
E-mail: peter.rieke@nki.nl
Received: 1-Mar-2025, Manuscript No. JMOT-25-162125; Editor assigned: 4-Mar-2025, PreQC No. JMOT-25-162125 (PQ) Reviewed:17-Mar-2025, QC No. JMOT-25-162125Revised:24-Mar-2025, Manuscript No. JMOT-25-162125; Published:31-Mar-2025, DOI: 10.35841/jmot- 10.2.259
Citation: Rieke P. Targeting oncogenes in precision oncology: Advances and challenges. J Med Oncl Ther. 2025;10(2):259
Introduction
Cancer is a complex disease driven by genetic and molecular alterations, among which oncogenes play a critical role in tumor development and progression. Oncogenes are mutated or overexpressed genes that promote uncontrolled cell growth, leading to cancer formation. The emergence of precision oncology—an approach that tailors treatments based on a patient’s unique genetic profile—has revolutionized cancer therapy by directly targeting oncogenic drivers. Despite significant progress, several challenges remain in effectively targeting oncogenes for therapeutic purposes [1].
Oncogenes originate from normal cellular genes called proto-oncogenes, which regulate essential cellular processes like growth, differentiation, and apoptosis. Mutations, amplifications, or translocations can convert proto-oncogenes into oncogenes, causing them to drive continuous cellular proliferation. Some of the most well-known oncogenes include KRAS, BRAF, MYC, HER2, and EGFR, which are frequently implicated in various cancers, such as lung, breast, and colorectal cancers [2].
Recent advancements in molecular biology and genomic sequencing have led to the development of therapies specifically designed to inhibit oncogene-driven cancers. Targeted therapies, such as tyrosine kinase inhibitors (TKIs), monoclonal antibodies, and small-molecule inhibitors, have shown promising results in treating cancers with oncogenic mutations. For example, EGFR inhibitors (e.g., erlotinib, gefitinib) are effective in non-small cell lung cancer (NSCLC) patients with EGFR mutations, while BRAF inhibitors (e.g., vemurafenib, dabrafenib) are used for melanoma patients with BRAF V600E mutations [3].
The integration of next-generation sequencing (NGS) into clinical practice has transformed precision oncology by enabling comprehensive genetic profiling of tumors. NGS allows for the identification of actionable oncogenic mutations, guiding clinicians in selecting the most effective targeted therapies. Additionally, liquid biopsies, which detect circulating tumor DNA (ctDNA), provide a minimally invasive method to monitor oncogene-driven cancer progression and treatment response in real time [4].
Despite the progress in oncogene-targeted therapies, several challenges hinder their long-term success. One of the primary obstacles is drug resistance, which can occur through secondary mutations, activation of alternative pathways, or tumor heterogeneity. For instance, KRAS-mutant cancers have historically been difficult to target, though recent breakthroughs, such as KRAS G12C inhibitors (e.g., sotorasib and adagrasib), have shown promise. However, resistance to these inhibitors can still develop, necessitating combination therapies or novel drug designs [5].
To address resistance mechanisms, researchers are exploring combination therapies that target multiple pathways simultaneously. For example, combining EGFR inhibitors with MET or MEK inhibitors can help prevent resistance in EGFR-mutant lung cancer. Similarly, immune checkpoint inhibitors, such as PD-1/PD-L1 inhibitors, are being investigated in combination with targeted therapies to enhance anti-tumor responses [6].
The success of precision oncology relies on the identification of reliable biomarkers that predict treatment response. Companion diagnostics, which are tests used to determine the presence of targetable oncogenic alterations, play a crucial role in ensuring that patients receive the most effective therapies. However, variability in biomarker expression and tumor heterogeneity can complicate treatment decisions [7].
Advances in drug development are leading to the emergence of next-generation inhibitors, PROTAC (proteolysis-targeting chimera) degraders, and RNA-based therapies aimed at directly targeting oncogenic proteins. Additionally, the use of CRISPR-Cas9 gene editing holds potential for precisely modifying oncogene-driven pathways, though ethical and safety concerns must be addressed before clinical applications can be fully realized [8].
Recent studies suggest that certain oncogene-driven cancers, once considered less responsive to immunotherapy, may benefit from immune-based treatments when used in combination with targeted therapies. For example, combining BRAF inhibitors with immune checkpoint inhibitors has improved outcomes in melanoma patients. Understanding the interaction between oncogenes and the immune system could lead to novel treatment strategies [9].
As research progresses, the future of oncogene targeting in precision oncology will likely involve a multi-pronged approach—integrating genomics, artificial intelligence (AI)-driven drug discovery, and combination therapies to enhance treatment effectiveness. Clinical trials are also essential in evaluating the efficacy and safety of novel oncogene-targeted therapies before they become widely available [10].
Conclusion
Targeting oncogenes in precision oncology has transformed cancer treatment, offering hope to patients with oncogene-driven tumors. While significant progress has been made in developing targeted therapies, challenges such as drug resistance and tumor heterogeneity remain. Future advancements in genetic profiling, combination therapies, and innovative drug design will further refine oncogene-targeted treatments, ultimately improving outcomes for cancer patients. Precision oncology continues to evolve, bringing us closer to more effective and personalized cancer therapies.
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