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Development and Maintenance of a Preclinical Patient Derived Tumor Xenograft Model for the Investigation of Novel Anti-Cancer Therapies
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PI3K/Akt/mTOR Signaling Pathway as a Target for Colorectal Cancer Treatment
Premila D Leiphrakpam1,2, Chandrakanth Are1,2
1Graduate Medical Education, College of Medicine, University of Nebraska Medical Center, Omaha, NE 68198, USA.
International Journal of Molecular Sciences
|March 28, 2024
Summary
Targeted therapies have advanced colorectal cancer (CRC) treatment, but resistance necessitates understanding molecular pathways like PI3K/Akt/mTOR. This review explores PI3K/Akt/mTOR
Area of Science:
- Oncology
- Molecular Biology
- Cancer Therapeutics
Background:
- Pathway-specific targeted therapy has transformed colorectal cancer (CRC) treatment.
- Tumor heterogeneity in CRC often leads to treatment resistance.
- The phosphatidylinositol 3-kinase/protein kinase B/mammalian target of the rapamycin (PI3K/Akt/mTOR) pathway is frequently altered in CRC.
Purpose of the Study:
- To review the role of the PI3K/Akt/mTOR signaling pathway in CRC.
- To discuss current PI3K/Akt/mTOR-targeted agents for CRC treatment.
- To highlight limitations and future directions in targeting this pathway for CRC.
Main Methods:
- Literature review of studies on PI3K/Akt/mTOR signaling in CRC.
- Analysis of clinical trial data for PI3K/Akt/mTOR inhibitors in CRC.
- Synthesis of information on CRC molecular mechanisms and targeted therapies.
Main Results:
- Aberrant PI3K/Akt/mTOR activation drives CRC initiation, progression, and metastasis.
- This pathway is critical for the development of drug resistance in CRC.
- Several PI3K/Akt/mTOR-targeted agents are in clinical trials for CRC.
Conclusions:
- Understanding PI3K/Akt/mTOR signaling is crucial for overcoming CRC treatment resistance.
- Targeting the PI3K/Akt/mTOR pathway offers potential for novel CRC therapies.
- Further research is needed to optimize PI3K/Akt/mTOR-targeted agents and combination strategies for CRC.
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