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09:29
Development and Maintenance of a Preclinical Patient Derived Tumor Xenograft Model for the Investigation of Novel Anti-Cancer Therapies
Published on: September 30, 2016
Novel targets in solid tumors: MEK inhibitors
Wells A Messersmith1, Manuel Hidalgo, Michael Carducci
1Sidney Kimmel Cancer Center, Johns Hopkins University, Baltimore, MD 21231, USA. wmesser1@jhmi.edu
Clinical Advances in Hematology & Oncology : H&O
|December 5, 2006
Summary
Newer MAPK/ERK kinase (MEK) inhibitors show promise in targeted cancer therapy, with partial responses observed in melanoma and pancreatic cancer. Genetic selection, particularly for B-raf mutations, may guide future individualized treatment strategies.
Area of Science:
- Oncology
- Pharmacology
- Molecular Biology
Background:
- Mitogen-activated protein kinase (MAPK)/extracellular signal-regulated kinase (ERK) kinase (MEK) inhibitors represent a novel class of targeted cancer therapies.
- Initial clinical trials with MEK inhibitors yielded disappointing results, prompting the development of newer agents with improved pharmacokinetic and pharmacodynamic profiles.
Purpose of the Study:
- To evaluate the efficacy and safety of novel MEK inhibitors in various cancer types.
- To explore the potential for genetic-based patient selection in MEK inhibitor therapy.
Main Methods:
- Clinical trials involving newer MEK inhibitor agents.
- Assessment of treatment responses, including partial responses and stable disease.
- Monitoring of common toxicities associated with MEK inhibitors.
Main Results:
- Partial responses observed in patients with advanced melanoma and pancreatic cancer.
- Prolonged stable disease noted across several tumor types.
- Common adverse events included rash, diarrhea, edema, and visual disturbances.
Conclusions:
- Novel MEK inhibitors demonstrate therapeutic potential in specific advanced cancers.
- The sensitivity of B-raf mutated cell lines suggests a role for genetic markers in patient selection.
- Further clinical validation is required to confirm the efficacy of individualized MEK inhibitor therapy based on genetic profiles.
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