Targeting AKT/PKB to improve treatment outcomes for solid tumors

Area of Science:

• Oncology
• Molecular Biology
• Cancer Research

Background:

• The phosphoinositide 3-kinase (PI3K)/AKT pathway is vital for cellular functions, including proliferation and survival.
• Hyperactivation of the PI3K/AKT pathway, often due to genetic mutations or overexpression, is common in human cancers.
• Activated AKT plays a role in DNA repair and attenuates apoptosis, contributing to treatment resistance.

Purpose of the Study:

• To review how activated AKT mediates resistance to various cancer treatment modalities.
• To discuss the impact of AKT on tumor cell response to receptor tyrosine kinase (RTK) targeted therapies.
• To summarize clinical trials investigating AKT inhibitors in combination therapies.

Main Methods:

• Literature review of current understanding on AKT's role in cancer therapy resistance.
• Analysis of studies examining AKT's influence on response to RTK-targeted treatments.
• Compilation of data from clinical trials involving AKT inhibitors.

Main Results:

• Activated AKT confers resistance to radiotherapy, chemotherapy, and RTK-targeted therapies.
• AKT signaling influences the efficacy of RTK-targeted cancer treatments.
• Clinical trials are exploring the combination of AKT inhibitors with standard and targeted therapies.

Conclusions:

• AKT is a significant factor in cancer treatment resistance.
• Targeting AKT may enhance the effectiveness of conventional and molecular therapies.
• Further research and clinical trials are needed to fully elucidate AKT's role and optimize therapeutic strategies.