Related Experiment Video

Updated: Jun 21, 2026

Intracellular Phosphoflow Cytometry of Acute Myeloid Leukemia Patient-Derived Xenotransplants
07:38

Intracellular Phosphoflow Cytometry of Acute Myeloid Leukemia Patient-Derived Xenotransplants

Published on: June 6, 2025

Targeting the PI3K/AKT/mTOR signaling network in acute myelogenous leukemia

Alberto M Martelli1, Camilla Evangelisti, Francesca Chiarini

  • 1Università di Bologna, Dipartimento di Scienze Anatomiche Umane, 40126 Bologna, Italy. alberto.martelli@unibo.it

Expert Opinion on Investigational Drugs
|August 15, 2009
PubMed
Abstract

Insights

Targeting the PI3K/Akt/mammalian target of rapamycin (mTOR) pathway shows promise for treating acute myelogenous leukemia (AML). Inhibitors may offer a less toxic and more effective therapy for AML patients.

Area of Science:

  • Oncology
  • Molecular Biology
  • Pharmacology

Background:

  • The PI3K/Akt/mammalian target of rapamycin (mTOR) signaling pathway is crucial for cell growth, proliferation, and survival.
  • This pathway is frequently dysregulated in various cancers, including acute myelogenous leukemia (AML).

Purpose of the Study:

  • To review the constitutive activation of the PI3K/Akt/mTOR signaling network in AML.
  • To discuss the potential of targeting this pathway for AML therapy.

Main Methods:

  • Literature search for articles on PI3K/Akt/mTOR pathway activation in AML.
  • Identification of studies evaluating small molecule inhibitors of this cascade.

Main Results:

  • The PI3K/Akt/mTOR pathway significantly influences AML cell proliferation, survival, and drug resistance.
  • Targeting this network can suppress leukemic cell growth, including leukemic stem cells.

Conclusions:

  • Standard chemotherapy for AML has reached its toxicity limits, necessitating novel strategies.
  • Targeting the PI3K/Akt/mTOR pathway with inhibitors, alone or in combination, offers a potentially less toxic and more effective treatment for AML.
  • Clinical development of selective PI3K/Akt/mTOR inhibitors for AML is ongoing.

Related Concept Videos

PI3K/mTOR/AKT Signaling Pathway01:22

PI3K/mTOR/AKT Signaling Pathway

The mammalian target of rapamycin  (mTOR) is a serine/threonine kinase that regulates growth, proliferation, and cell survival in response to hormones, growth factors, or nutrient availability. This kinase exists in two structurally and functionally distinct forms: mTOR complex 1  (mTORC1) and mTOR complex 2  (mTORC2). The first form (mTORC1) is composed of a rapamycin-sensitive Raptor and proline-rich Akt substrate, PRAS40. In contrast,  mTORC2 consists of a rapamycin-insensitive companion...
mTOR Signaling and Cancer Progression03:03

mTOR Signaling and Cancer Progression

The mammalian target of rapamycin or mTOR protein was discovered in 1994 due to its direct interaction with rapamycin. The protein gets its name from a yeast homolog called TOR. The mTOR protein complex in mammalian cells plays a major role in balancing anabolic processes such as the synthesis of proteins, lipids, and nucleotides and catabolic processes, such as autophagy in response to environmental cues, such as availability of nutrients and growth factors.
The mTOR pathway or the...
mTOR Signaling and Cancer Progression03:03

mTOR Signaling and Cancer Progression

The mammalian target of rapamycin or mTOR protein was discovered in 1994 due to its direct interaction with rapamycin. The protein gets its name from a yeast homolog called TOR. The mTOR protein complex in mammalian cells plays a major role in balancing anabolic processes such as the synthesis of proteins, lipids, and nucleotides and catabolic processes, such as autophagy in response to environmental cues, such as availability of nutrients and growth factors.
The mTOR pathway or the...
Abnormal Proliferation02:23

Abnormal Proliferation

Under normal conditions, most adult cells remain in a non-proliferative state unless stimulated by internal or external factors to replace lost cells. Abnormal cell proliferation is a condition in which the cell's growth exceeds and is uncoordinated with normal cells. In such situations, cell division persists in the same excessive manner even after cessation of the stimuli, leading to persistent tumors. The tumor arises from the damaged cells that replicate to pass the damage to the daughter...
The JAK-STAT Signaling Pathway01:20

The JAK-STAT Signaling Pathway

Several cytokine receptors have tightly bound Janus kinase or JAK proteins attached at their cytosolic tail. Small signaling molecules such as cytokines, growth hormones, or prolactins bind to the cytokine receptors and initiate their dimerization. The dimerization brings the cytosolic JAKs together that trans-phosphorylate and activates each other. The activated JAKs now phosphorylate cytosolic tails of the cytokine receptors, which serve as binding sites for adaptor proteins such as  SH2...
Targeted Cancer Therapies02:57

Targeted Cancer Therapies

The targeted cancer therapies, also known as “molecular targeted therapies,” take advantage of the molecular and genetic differences between the cancer cells and the normal cells. It needs a thorough understanding of the cancer cells to develop drugs that can target specific molecular aspects that drive the growth, progression, and spread of cancer cells without affecting the growth and survival of other normal cells in the body.
There are several types of targeted therapies against specific...