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Targeting PI3K Pathway in Pancreatic Ductal Adenocarcinoma: Rationale and Progress

Siddharth Mehra1, Nilesh Deshpande1, Nagaraj Nagathihalli1,2

  • 1Division of Surgical Oncology, Department of Surgery, Miller School of Medicine, University of Miami, Miami, FL 33136, USA.

Cancers
|September 10, 2021
PubMed

Insights

Targeting the phosphatidylinositol-3-kinase (PI3K)/Akt pathway can reduce pancreatic ductal adenocarcinoma (PDAC) tumor growth. This review discusses PI3K inhibition

Area of Science:

  • Oncology
  • Molecular Biology
  • Cancer Research

Background:

  • Pancreatic ductal adenocarcinoma (PDAC) is a deadly cancer with a poor prognosis.
  • Over 90% of PDAC tumors have K-Ras mutations activating pro-tumorigenic pathways like PI3K-Akt.
  • The PI3K/Akt pathway is crucial in promoting PDAC aggressiveness.

Purpose of the Study:

  • To discuss the significance of targeting PI3K signaling in PDAC.
  • To review the biological impact of PI3K inhibition on tumor-stromal immune crosstalk.
  • To update on challenges in therapeutic targeting of PI3K in PDAC.

Main Methods:

  • Review of existing literature on PI3K/Akt pathway in PDAC.
  • Analysis of therapeutic strategies targeting PI3K and downstream effectors.
  • Discussion of preclinical findings, including studies on genetic mouse models.

Main Results:

  • Targeting the PI3K/Akt/mTOR pathway has shown potential in reducing tumor burden and improving survival.
  • PI3K inhibition can modulate the tumor-stromal immune crosstalk within the pancreatic cancer microenvironment.

Conclusions:

  • Targeting PI3K signaling is a promising strategy for PDAC treatment.
  • Understanding the modulation of the tumor microenvironment by PI3K inhibition is critical.
  • Overcoming therapeutic challenges is essential for effective PI3K-targeted therapies in PDAC.
Keywords:
PI3K/Akt pathwayRASUrolithin Aimmune microenvironmentpancreatic cancertumor-stromal crosstalk

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