Mechanisms of cancer drug resistance.

By Michael M. Gottesman. Annual Review of Medicine, 2002

2,652 citations recorded by the source corpus.

Subfields: Molecular Biology, Oncology, Pharmacology

View Paper: https://www.semanticscholar.org/paper/930c22f5a698df8c4ea4f9573e5ec2aae3a6d195

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In Molecular Biology

1. K. Borden
2. H. Zahreddine
3. J. Shim
4. Bowen Du
5. Liangfang Zhang
6. C. J. Hu
7. Matthew D. Hall
8. Tian Xia

In Oncology

1. K. Borden
2. H. Zahreddine
3. J. Shim
4. Bowen Du
5. Matthew D. Hall
6. Liangfang Zhang
7. C. J. Hu
8. Huan Meng

In Pharmacology

1. J. Shim
2. Liangfang Zhang
3. C. J. Hu
4. Bowen Du
5. K. Borden
6. H. Zahreddine
7. Zongxi Li
8. Huan Meng

Citations in the corpus

• Mechanisms and insights into drug resistance in cancer (2013, background): “Among the 48 known ABC transporters in humans, elevation of three members, P-gp (MDR1 gene product), Multidrug resistance-associated protein 1 (MRP1) and mitoxantrone resistance protein [MXR; also known as breast cancer resistance protein (BCRP) or placenta ABC protein (ABCP)], have been correlated ”
• Targeting MAPK Signaling in Cancer: Mechanisms of Drug Resistance and Sensitivity (2020, background): “Classically, drug resistance was considered to be caused by mutations in the target protein that interfere with drug binding, elimination of the drug from the target cell by transporters, or enhanced degradation [16].”
• Prediction of synergistic anti-cancer drug combinations based on drug target network and drug induced gene expression profiles (2017, background): “Drug resistance and side effect have been considered as the main reasons for the failure of cancer chemotherapy [2,3].”
• Nanoparticle-based combination therapy toward overcoming drug resistance in cancer. (2012, background): “Among the many cellular mutations that diminish the effectiveness of anticancer drugs, the over-expression of multidrug transporters and the altered apoptosis are the two underlying mechanisms through which cancer cells acquire resistance to multiple structurally and mechanistically different drugs ”
• Engineered Design of Mesoporous Silica Nanoparticles to Deliver Doxorubicin and Pgp siRNA to Overcome Drug Resistance in a Cancer Cell Line (2010, positive): “In this regard, it has been demonstrated that the increase in intracellular drug concentration as a result of the suppression of drug efflux pumps leads to almost proportional activation of antiapoptotic cellular defense.(7,9) As one example, a cationic liposome carrier system was developed to deliv”
• Nanoparticle therapeutics: an emerging treatment modality for cancer (2008, background): “Targeting efflux-pump-mediated resistance? A major clinical obstacle that limits the efficacy of cancer therapeutics is the resistance of cancer cells to a multitude of chemotherapeutic and biological agents, known as multidrug resistance (MDR”
• Role of hypoxia in cancer therapy by regulating the tumor microenvironment (2019, background): “In addition, hypoxia results in a decrease in pH and creates an acidic TME.”
• Cisplatin Resistance: A Cellular Self-Defense Mechanism Resulting from Multiple Epigenetic and Genetic Changes (2012, background): “…cassette transporter known for years as P-glycoprotein or MDR1, functions as a pump to efflux a variety of structurally unrelated anticancer drugs, leading to cellular resistance to re- lated substrates but not to cisplatin (Gottesman et al., 2002; Gottesman, 2002; Gillet and Gottesman, 2010).”
• Mechanisms of Taxol resistance related to microtubules (2003, background): “It is thought that the high expression of P-glycoprotein in the gastrointestinal tract mediates Taxol resistance.”
• Tumour-initiating cells: challenges and opportunities for anticancer drug discovery (2009, background): “Many tumour-initiating cells are thought to be resistant to chemotherapeutics such as paclitaxel and doxorubicin, for various reasons including their quiescent or slowly proliferating natur”
• Nanocarriers for drug delivery applications (2018, background): “However, cancer cells attain a defense mechanism by the efflux pump overexpression, self-repairing capacity, altered targets or by increased metabolism of the drug (Gottesman 2002; Bradshaw and Arceci 1998).”
• Targeting Epithelial–Mesenchymal Transition (EMT) to Overcome Drug Resistance in Cancer (2016, background): “Drug resistance (or chemoresistance) can be divided into two groups: intrinsic (or de novo) drug resistance and acquired drug resistance [2,3].”