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Updated: Aug 19, 2026

Methods for Evaluating the Role of c-Fos and Dusp1 in Oncogene Dependence
Published on: January 7, 2019
c-Myc as a therapeutic target in cancer
1Section of Hematology/Oncology, Children's Hospital of Pittsburgh, Rangos Research Center, Room 2100, 3460 Fifth Avenue, Pittsburgh, PA 15213, USA. edward_prochownik@poplar.chp.edu
Abstract:
c-Myc is frequently deregulated in human cancers. The c-Myc oncoprotein is a transcription factor, with many of its target genes encoding proteins that initiate and maintain the transformed state. c-Myc is also part of a dynamic network whose members interact selectively with one another and with various transcriptional coregulators and histone-modifying enzymes. This knowledge highlights several points that might be amenable to attack. This review summarizes progress in controlling the extent of c-Myc transcription, translation, interaction with other myc network members, DNA binding and transcriptional activation. Inhibition of c-Myc can be achieved with many of these approaches; however, clinical efficacy will likely require intervention at several levels, perhaps in combination with traditional chemotherapeutic drugs or agents that target other oncoproteins.
Insights
The c-Myc oncoprotein drives cancer by regulating genes essential for cell growth. Targeting c-Myc
Area of Science:
- Oncology
- Molecular Biology
- Cancer Genetics
Background:
- The c-Myc oncoprotein is a transcription factor frequently deregulated in human cancers.
- c-Myc target genes are crucial for initiating and maintaining the transformed state in cancer cells.
- c-Myc functions within a complex network involving protein interactions and transcriptional regulation.
Purpose of the Study:
- To review current strategies for controlling c-Myc activity in cancer.
- To highlight potential therapeutic targets within the c-Myc network.
- To discuss the potential for combination therapies involving c-Myc inhibition.
Main Methods:
- Review of scientific literature on c-Myc biology and therapeutic targeting.
- Summary of approaches targeting c-Myc transcription, translation, protein interactions, DNA binding, and transcriptional activation.
- Analysis of clinical efficacy and combination strategies.
Main Results:
- Multiple strategies exist to inhibit c-Myc at various levels of its function.
- The c-Myc network offers several points for therapeutic intervention.
- Combination therapies may be necessary for effective clinical outcomes.
Conclusions:
- Targeting c-Myc presents a promising avenue for cancer therapy.
- Intervention at multiple levels of c-Myc regulation is likely required for clinical success.
- Combining c-Myc inhibition with traditional chemotherapy or other targeted agents may enhance efficacy.
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