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Updated: Jan 27, 2026

Nanomechanics of Drug-target Interactions and Antibacterial Resistance Detection
Published on: October 25, 2013
Polytherapy and Targeted Cancer Drug Resistance
Nilanjana Chatterjee1, Trever G Bivona1
1Department of Medicine, University of California, San Francisco, 600 16(th) Street, Box 2140, Genentech Hall, San Francisco, CA 94158, USA; Department of Cellular and Molecular Pharmacology, University of California, San Francisco, 600 16(th) Street, Box 2140, Genentech Hall, San Francisco, CA 94158, USA; Helen Diller Family Comprehensive Cancer Center, University of California, San Francisco, 600 16(th) Street, Box 2140, Genentech Hall, San Francisco, CA 94158, USA.
Abstract:
A current challenge in cancer treatment is drug resistance. Even the most effective therapies often fail to produce a complete and durable tumor response and ultimately give rise to therapy resistance and tumor relapse. However, how resistance arises in cancer remains incompletely understood. While drug resistance in cancer is thought to be driven by irreversible genetic mutations, emerging evidence also implicates reversible proteomic and epigenetic mechanisms in the development of drug resistance. Tumor microenvironment-mediated mechanisms and tumor heterogeneity can significantly contribute to cancer treatment resistance. Here, we discuss the diverse and dynamic strategies that cancers use to evade drug response, the promise of upfront combination and intermittent therapies and therapy switching in forestalling resistance, and epigenetic reprogramming to combat resistance.
Insights
Cancer drug resistance is a major challenge, driven by genetic and reversible mechanisms. Understanding these diverse strategies is key to developing new therapies to overcome treatment failure and tumor relapse.
Area of Science:
- Oncology
- Cancer Biology
- Pharmacology
Background:
- Cancer treatment often faces challenges with drug resistance, leading to incomplete responses and tumor relapse.
- While genetic mutations are known drivers, reversible proteomic and epigenetic factors also contribute to resistance.
- Tumor microenvironment and heterogeneity significantly impact treatment efficacy and resistance development.
Purpose of the Study:
- To discuss the diverse strategies cancers employ to evade drug response.
- To explore the potential of combination, intermittent, and switching therapies in preventing resistance.
- To highlight the role of epigenetic reprogramming in combating cancer drug resistance.
Main Methods:
- Literature review and synthesis of current research on cancer drug resistance mechanisms.
- Discussion of therapeutic strategies aimed at overcoming or preventing drug resistance.
- Analysis of the interplay between tumor biology, microenvironment, and treatment response.
Main Results:
- Cancer employs multifaceted strategies, including genetic and reversible mechanisms, to resist therapy.
- Combination, intermittent, and switching therapies show promise in delaying or overcoming resistance.
- Epigenetic reprogramming offers a potential avenue for combating established drug resistance.
Conclusions:
- Addressing cancer drug resistance requires a comprehensive understanding of its diverse underlying mechanisms.
- Innovative therapeutic approaches, including combination strategies and epigenetic modulation, are crucial for improving patient outcomes.
- Further research into tumor heterogeneity and microenvironment interactions is essential for developing effective, durable cancer treatments.
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