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Licensee MDPI, Basel, Switzerland. This article is an open access article distributed under the terms and conditions of the Creative Commons Attribution (CC BY) license.  \nDepartment of Life Sciences, School of Life and Health Sciences, University of Nicosia, Nicosia 2417, Cyprus; [papaneophytou.c@unic.ac.cy](papaneophytou.c@unic.ac.cy); Tel.: +357-22841941  \nAbstract  \nDrug resistance represents one of the most critical challenges in modern medicine, undermining the efficacy of therapies across both bacterial infections and cancer. Although these conditions arise in fundamentally distinct biological systems, they are governed by shared evolutionary pressures that drive the emergence and selection of resistant populations. This narrative review provides an integrative, cross-disciplinary perspective on drug resistance, focusing on bacteria and cancer and emphasizing the shared evolutionary and molecular mechanisms underlying treatment failure in both domains. Key resistance strategies include efflux-mediated drug export, target modification, enzymatic drug inactivation, metabolic reprogramming, epigenetic and transcriptional plasticity, and protection conferred by specialized microenvironments. These processes are further reinforced by phenotypic heterogeneity, including bacterial persister cells and cancer stem-like cells, which contribute to recurrence and multidrug resistance. Collectively, these parallels define drug resistance as a convergent evolutionary phenomenon driven by adaptability under selective pressure. Recognizing these shared mechanisms reveals important translational opportunities for therapeutic intervention. Strategies such as combination therapy, drug repurposing, nanotechnology-enabled delivery systems, and host-directed approaches offer promising avenues to prevent, delay, or overcome resistance. By integrating insights from microbiology and oncology, this review proposes a unified framework for resistance biology and highlights the potential of cross-disciplinary strategies to improve treatment durability and clinical outcomes.  \nKeywords: drug resistance; antimicrobial resistance; cancer drug resistance; efflux pumps; metabolic reprogramming; persister cells; combination therapy; drug repurposing  \n1. Introduction  \nDrug resistance refers to the reduced effectiveness of a treatment against a disease or condition [1] . It most commonly arises in microorganisms and cancer cells, which can survive treatments that were previously effective, posing a major threat to global health [2] . Driven mainly by evolutionary pressure for survival, the emergence of resistance is one of the biggest challenges in modern medicine. It weakens the effectiveness of current therapies, limits treatment choices, and is prevalent in both infectious diseases and cancer [3] . Essentially, any biological system capable of evolving and producing phenotypic variation can develop resistance under selective pressure, whether this variation pre-exists within a population or appears newly after exposure to a therapeutic agent [4] . At the molecular and population levels, the same core evolutionary principles, including clonal selection, fitness landscape remodeling, epistatic interactions, and phenotypic plasticity, operate  \nacross microbial and neoplastic systems, suggesting that resistance is best understood as a general property of adapting cell populations rather than a phenomenon unique to any single disease context [5] .  \nTherapeutic resistance has long been a persistent challenge that continues to develop. Each new treatment applies selective pressure, quickly favoring resistant subpopulations. This recurring pattern, while a serious clinical concern","cbCaieHbI90nEVws","https://ap.wps.com/l/cbCaieHbI90nEVws","pdf",2278397,49,"English","# Introduction\n## Shared evolutionary principles across bacteria and cancer\n## Mechanisms and clinical relevance of resistance\n# Treatment failure and translational opportunities\n## Combination therapy, drug repurposing, and delivery strategies","[{\"question\":\"What is the core idea behind drug resistance in both bacteria and cancer?\",\"answer\":\"Drug resistance emerges under selective evolutionary pressures and reflects adaptable cell populations rather than being unique to a single disease type. Similar evolutionary principles operate across microbial and neoplastic systems.\"},{\"question\":\"Which resistance strategies are highlighted in the review?\",\"answer\":\"Key strategies include efflux-mediated drug export, target modification, enzymatic drug inactivation, metabolic reprogramming, epigenetic and transcriptional plasticity, and protection from specialized microenvironments. Phenotypic heterogeneity such as persister cells and cancer stem-like cells is also emphasized.\"},{\"question\":\"How can translational approaches help prevent or overcome resistance?\",\"answer\":\"The review points to combination therapy, drug repurposing, nanotechnology-enabled delivery systems, and host-directed approaches. These strategies aim to prevent, delay, or overcome resistance by leveraging shared mechanisms across microbiology and oncology.\"}]","Two Worlds, One Battle - How Bacteria and Malignancies Converge on Drug Resistance | PDF",1790088523,123]