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Intracellular Phosphoflow Cytometry of Acute Myeloid Leukemia Patient-Derived Xenotransplants

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NRF2: KEAPing Tumors Protected.

Ray Pillai^1,2,3, Makiko Hayashi¹, Anastasia-Maria Zavitsanou¹

¹Department of Pathology, Perlmutter Cancer Center, New York University School of Medicine, New York, New York.

Cancer Discovery

|February 1, 2022

Summary

The Kelch-like ECH-associated protein 1 (KEAP1)/nuclear factor erythroid 2-related factor 2 (NRF2) pathway, normally protective, drives cancer growth and treatment resistance when activated. Understanding its dysregulation is key to developing new cancer therapies.

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Area of Science:

Oncology
Molecular Biology
Cancer Research

Background:

The KEAP1/NRF2 pathway is crucial for cellular defense against toxins and oxidative stress.
Aberrant activation of this pathway in cancer confers a survival advantage to tumor cells.
NRF2 activation promotes tumor initiation, progression, and resistance to therapy.

Purpose of the Study:

To review the role of KEAP1/NRF2 pathway dysregulation in cancer.
To elucidate mechanisms by which NRF2 activation promotes tumorigenesis.
To discuss therapeutic strategies targeting the NRF2 pathway in cancer.

Main Methods:

Literature review of genetic, epigenetic, and posttranslational alterations activating the KEAP1/NRF2 pathway.
Analysis of NRF2's role in cancer metabolism, stress response, and immune evasion.
Examination of clinical data on NRF2 pathway alterations and treatment resistance.

Main Results:

KEAP1/NRF2 pathway alterations are prevalent in various solid tumors.
Activated NRF2 rewires tumor metabolism, enhances proliferation, and suppresses stress.
NRF2 pathway activation is linked to resistance against diverse cancer therapies.

Conclusions:

Dysregulation of the KEAP1/NRF2 pathway is a significant driver of cancer hallmarks.
Targeting the NRF2 pathway presents a promising therapeutic avenue for overcoming treatment resistance.