Virology Research Journal

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Editorial - Virology Research Journal (2025) Volume 9, Issue 3

Cancerâ??s Counterattack: Drug Resistance in Oncology Treatments

Wan Jing *

Department of Virology & Microbiology, University of Hong Kong, Hong Kong

*Corresponding Author:
Wan Jing
Department of Virology & Microbiology,
University of Hong Kong, Hong Kong
E-mail: wan@yale.edu

Received: 04-Sep-2024, Manuscript No. AAVRJ-25-171352; Editor assigned: 05-Sep-2024, PreQC No. AAVRJ-25-171352(PQ); Reviewed: 19-Sep-2024, QC No. AAVRJ-25-171352; Revised: 23-Sep-2024, Manuscript No. AAVRJ-25-171352(R); Published: 30-Sep-2024, DOI:10.35841/AAVRJ-9.3.203

Citation: Jing W. Cancer’s counterattack: Drug resistance in oncology treatments. Virol Res J. 2025;9(3):203

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Introduction

Cancer remains one of the leading causes of death worldwide, despite significant advances in diagnostics and therapeutics. Chemotherapy, targeted therapy, immunotherapy, and hormonal treatments have transformed cancer care, offering hope and remission to millions. Yet, a formidable challenge persists—drug resistance. Cancer cells, through a variety of adaptive mechanisms, often develop resistance to treatment, rendering once-effective therapies futile. This phenomenon, known as acquired or intrinsic drug resistance, is a major barrier to long-term remission and cure. Understanding the molecular underpinnings of resistance is essential to designing next-generation therapies and improving patient outcomes [1].

Drug resistance in oncology arises from complex, multifactorial processes. These include: Cancer cells mutate rapidly, altering drug targets and rendering therapies ineffective. For example, mutations in the BCR-ABL gene can confer resistance to imatinib in chronic myeloid leukemia (CML) patients. Overexpression of ATP-binding cassette (ABC) transporters like P-glycoprotein actively expels drugs from cancer cells, reducing intracellular drug concentrations. Cancer cells may upregulate enzymes that degrade drugs or downregulate those that activate prodrugs, affecting therapeutic efficacy. EMT promotes invasiveness and resistance, particularly in solid tumors like breast and lung cancer [2].

Hypoxia, stromal cells, and immune components can shield cancer cells from drugs or promote survival signaling. These subpopulations possess self-renewal capabilities and are inherently resistant to conventional therapies. Chemotherapy targets rapidly dividing cells, but its non-specific nature often leads to toxicity and resistance. Tumors may develop resistance through enhanced DNA repair, drug efflux, or metabolic reprogramming. For instance, platinum-based drugs like cisplatin face resistance due to increased glutathione levels and DNA repair enzyme activity [3].

Multidrug resistance (MDR) is a particularly challenging phenomenon where cancer cells become resistant to multiple structurally unrelated drugs. This is often mediated by efflux pumps and changes in apoptotic pathways. Targeted therapies aim to inhibit specific molecular pathways critical to cancer growth. However, resistance frequently develops through secondary mutations or pathway reactivation. In non-small cell lung cancer (NSCLC), EGFR inhibitors like erlotinib are initially effective, but resistance often emerges via T790M mutations or MET amplification. Similarly, in melanoma, BRAF inhibitors face resistance due to activation of alternative pathways like MEK or PI3K. Combination therapies targeting multiple nodes in the signaling cascade are being explored to overcome this resistance [4].

Immunotherapy, particularly immune checkpoint inhibitors (ICIs), has revolutionized cancer treatment. Yet, not all patients respond, and resistance can develop. Mechanisms include: Tumors may downregulate MHC molecules, evading immune detection. Tumors may express other inhibitory molecules like TIM-3 or LAG-3. Regulatory T cells, myeloid-derived suppressor cells, and cytokines like TGF-β can dampen immune responses. Understanding these mechanisms is crucial for designing combination immunotherapies and predictive biomarkers. Using multiple drugs with different mechanisms can prevent or delay resistance. For example, combining BRAF and MEK inhibitors in melanoma has shown improved outcomes. Advances in single-cell sequencing, liquid biopsies, and artificial intelligence are transforming resistance research. These tools enable real-time monitoring of tumor evolution and early detection of resistance. CRISPR-based screens are identifying novel resistance genes, while organoid models allow for functional testing of therapies in patient-derived tissues. Moreover, the integration of multi-omics data—genomics, transcriptomics, proteomics—is providing a holistic view of resistance mechanisms and therapeutic vulnerabilities [5].

Conclusion

Drug resistance in oncology is a dynamic and formidable challenge, often turning initial therapeutic success into relapse and progression. Cancer’s ability to adapt and counterattack demands equally adaptive and innovative strategies from researchers and clinicians. By unraveling the molecular intricacies of resistance and leveraging emerging technologies, we can design smarter, more durable treatments. The fight against cancer is not just about killing cells—it’s about outsmarting them.

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