Journal of Medical Oncology and Therapeutics

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Editorial - Journal of Medical Oncology and Therapeutics (2025) Volume 10, Issue 2

Oncogenes vs. Tumor Suppressor Genes: A Delicate Balance in Cancer Development

Thomas Pretzell *

Department of Medical Physics, University College London, UK

*Corresponding Author:
Thomas Pretzell
Department of Medical Physics, University College London, UK
E-mail: thomas.pretzell@ic.ac.uk

Received: 1-Mar-2025, Manuscript No. JMOT-25-162120; Editor assigned: 4-Mar-2025, PreQC No. JMOT-25-162120 (PQ) Reviewed:17-Mar-2025, QC No. JMOT-25-162120Revised:24-Mar-2025, Manuscript No. JMOT-25-162120; Published:31-Mar-2025, DOI: 10.35841/jmot- 10.2.255

Citation: Pretzell T. Oncogenes vs. Tumor suppressor genes: A delicate balance in cancer development. J Med Oncl Ther. 2025;10(2):255

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Introduction

Cancer is a complex disease that arises from genetic and epigenetic alterations that disrupt normal cellular functions. Among the key players in cancer development are oncogenes and tumor suppressor genes, which have opposing roles in cell growth and proliferation. While oncogenes promote uncontrolled cell division, tumor suppressor genes act as safeguards to prevent malignancy. The intricate balance between these two types of genes is crucial in maintaining normal cellular homeostasis, and when disrupted, it can lead to tumorigenesis [1].

Oncogenes are mutated or overexpressed versions of normal genes known as proto-oncogenes, which regulate cell growth and differentiation. When activated through genetic mutations, amplifications, or chromosomal rearrangements, oncogenes drive excessive proliferation and survival of cells, contributing to tumor formation. Some well-known oncogenes include RAS, MYC, and HER2, all of which have been implicated in various types of cancer [2].

Oncogenes can become abnormally active through several mechanisms. Point mutations can lead to a gain-of-function change, as seen in RAS mutations that lock the protein in an active state, promoting continuous signaling for cell growth. Gene amplifications, such as the overexpression of HER2 in breast cancer, result in excessive signaling for proliferation. Additionally, chromosomal translocations, like the formation of the BCR-ABL fusion gene in chronic myeloid leukemia (CML), create hyperactive proteins that drive cancer progression [3].

In contrast to oncogenes, tumor suppressor genes serve as the body's defense mechanisms against uncontrolled cell division. These genes regulate processes such as DNA repair, apoptosis, and cell cycle control. TP53, RB1, and BRCA1/2 are well-known tumor suppressor genes that play crucial roles in preventing tumor formation. When these genes are inactivated or lost due to mutations, cells lose their ability to suppress abnormal growth, leading to cancer development [4].

Tumor suppressor genes typically require two-hit inactivation to lose their function, as described by Knudson’s two-hit hypothesis. This means both copies of the gene must be mutated or deleted to fully impair its function. A classic example is TP53, often called the “guardian of the genome,” which regulates DNA repair and apoptosis. Inactivating mutations in TP53 are found in over 50% of human cancers, allowing cancer cells to evade apoptosis and accumulate additional mutations [5].

The interplay between oncogenes and tumor suppressor genes determines whether a cell follows normal regulatory mechanisms or undergoes malignant transformation. In a healthy cell, tumor suppressors keep oncogenes in check, preventing excessive growth. However, when oncogenes become hyperactive and tumor suppressors are lost, a perfect storm for cancer development arises. This imbalance leads to uncontrolled proliferation, genomic instability, and resistance to cell death, hallmarks of cancer [6].

Understanding the roles of oncogenes and tumor suppressor genes has led to the development of targeted cancer therapies. Tyrosine kinase inhibitors (TKIs), such as imatinib (Gleevec), specifically target oncogenic proteins like BCR-ABL, successfully treating CML. Similarly, monoclonal antibodies like trastuzumab (Herceptin) target HER2-positive breast cancer cells. However, restoring tumor suppressor function is more challenging, as most mutations in these genes result in loss of function rather than gain-of-function alterations [7].

Despite advances in targeted therapies, challenges remain in effectively treating cancers driven by oncogenes and tumor suppressor gene loss. Many oncogene-driven cancers develop drug resistance through secondary mutations, rendering targeted therapies ineffective over time. Additionally, reactivating tumor suppressor genes in a clinical setting remains difficult, as most traditional drugs are unable to restore their function. Gene therapy and small-molecule activators of tumor suppressors are emerging as potential solutions [8].

Ongoing research aims to develop innovative strategies to counteract oncogene activation and restore tumor suppressor function. CRISPR gene editing and RNA-based therapies are being explored to correct genetic defects at the molecular level [9].

Personalized medicine approaches, using genomic profiling, allow clinicians to tailor treatments based on the specific oncogenic mutations and tumor suppressor gene alterations present in a patient’s cancer [10].

Conclusion

The balance between oncogenes and tumor suppressor genes is fundamental to cellular homeostasis, and its disruption is a defining characteristic of cancer. While oncogenes drive malignant transformation through unchecked cell proliferation, tumor suppressor genes act as brakes that prevent cancer from developing. Understanding these mechanisms has paved the way for targeted therapies, but significant challenges remain in overcoming drug resistance and restoring tumor suppressor function. Future research holds promise for more effective, personalized cancer treatments that address the delicate balance between these critical genes.

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