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Related Experiment Video

Updated: Jun 4, 2026

Identification of Mediators of T-cell Receptor Signaling via the Screening of Chemical Inhibitor Libraries

Identification of Mediators of T-cell Receptor Signaling via the Screening of Chemical Inhibitor Libraries

Published on: January 22, 2019

[PI3K inhibitor].

Seiji Yano¹, Shinji Takeuchi, Tadaaki Yamada

¹Division of Medical Oncology Cancer Research Institute, Kanazawa University, Japan.

Gan to Kagaku Ryoho. Cancer & Chemotherapy

|March 4, 2011

Summary

The PI3K-Akt pathway is crucial in cancer development and is activated by several mechanisms. Targeting this pathway with PI3K inhibitors is a promising therapeutic strategy currently under clinical investigation.

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Last Updated: Jun 4, 2026

Identification of Mediators of T-cell Receptor Signaling via the Screening of Chemical Inhibitor Libraries

Identification of Mediators of T-cell Receptor Signaling via the Screening of Chemical Inhibitor Libraries

Published on: January 22, 2019

Area of Science:

Oncology
Molecular Biology
Signal Transduction

Background:

The Phosphoinositide 3-kinase/Akt (PI3K-Akt) pathway is a key signaling cascade downstream of growth factor receptors.
Aberrant activation of the PI3K-Akt pathway is implicated in numerous cancers through mechanisms like receptor activation, PTEN loss, and PI3K mutations.

Purpose of the Study:

To highlight the significance of the PI3K-Akt pathway as a therapeutic target in oncology.
To review the development and clinical evaluation of PI3K inhibitors.

Main Methods:

Literature review of PI3K-Akt pathway activation in cancer.
Overview of current PI3K inhibitor development and clinical trials.

Main Results:

The PI3K-Akt pathway is frequently dysregulated in various cancer types.
Multiple PI3K inhibitors have entered clinical trials, indicating therapeutic potential.

Conclusions:

The PI3K-Akt pathway represents a critical target for cancer therapy.
Ongoing clinical trials are evaluating the efficacy and safety of PI3K inhibitors for cancer treatment.