# Endoplasmic Reticulum Stress in Acute Myeloid Leukemia: Pathogenesis, Prognostic Implications, and Therapeutic Strategies

## TL;DR

This paper reviews how endoplasmic reticulum stress contributes to the development and treatment resistance of acute myeloid leukemia.

## Contribution

The paper synthesizes current understanding of ER stress mechanisms and their therapeutic implications in AML.

## Key findings

- ER stress and UPR activation are key in AML pathogenesis.
- AML cells use UPR to avoid cell death and resist therapy.
- ER stress has prognostic and therapeutic relevance in AML.

## Abstract

Acute myeloid leukemia (AML) is a heterogeneous hematological malignancy that poses a significant therapeutic challenge due to its high recurrence rate and demanding treatment regimens. Increasing evidence suggests that endoplasmic reticulum (ER) stress and downstream activation of the unfolded protein response (UPR) pathway play a key role in the pathogenesis of AML. ER stress is triggered by the accumulation of misfolded or unfolded proteins within the ER. This causes activation of the UPR to restore cellular homeostasis. However, the UPR can shift from promoting survival to inducing apoptosis under prolonged or excessive stress conditions. AML cells can manipulate the UPR pathway to evade apoptosis, promoting tumor progression and resistance against various therapeutic strategies. This review provides the current knowledge on ER stress in AML and its prognostic and therapeutic implications.