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Adaptive Mechanisms in Cancer Cells

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Cancer cells accumulate genetic changes at an abnormally rapid rate due to the defects in the DNA repair mechanisms. From an evolutionary perspective, such genetic instability is advantageous for cancer development. Mutant cell lines accumulate a series of beneficial mutations that contribute to their progression into cancer.
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Related Experiment Video

Updated: Nov 8, 2025

Transfer of Manipulated Tumor-associated Neutrophils into Tumor-Bearing Mice to Study their Angiogenic Potential In Vivo

Transfer of Manipulated Tumor-associated Neutrophils into Tumor-Bearing Mice to Study their Angiogenic Potential In Vivo

Published on: July 20, 2019

In cancer, all roads lead to NADPH.

Gulam Mohmad Rather¹, Alvinsyah Adhityo Pramono², Zoltan Szekely³

¹Rutgers Cancer Institute of New Jersey, Rutgers, The State University of New Jersey, New Brunswick, NJ, USA.

Pharmacology & Therapeutics

|April 24, 2021

Summary

Cancer cells need more NADPH for growth and survival. Targeting its production offers a new strategy for cancer therapy by disrupting this essential metabolic pathway.

Keywords:

Calmodulin NAD NAD kinase NADPH ROS

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Transfer of Manipulated Tumor-associated Neutrophils into Tumor-Bearing Mice to Study their Angiogenic Potential In Vivo

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Published on: May 12, 2023

Area of Science:

Biochemistry
Cancer Biology
Metabolic Pathways

Background:

Cancer cells exhibit elevated requirements for nicotinamide adenine dinucleotide phosphate (NADPH).
NADPH is crucial for nucleotide synthesis and cellular defense against reactive oxygen species (ROS).
Several mechanisms contribute to increased NADPH generation in cancer cells.

Purpose of the Study:

To elucidate the diverse pathways responsible for elevated NADPH levels in cancer.
To identify potential therapeutic targets within NADPH synthesis pathways for cancer treatment.

Main Methods:

Review of recent studies on NADPH generation mechanisms in cancer.
Analysis of the roles of specific enzymes and signaling pathways (e.g., AKT, NADK, G6PD, malic enzymes, calmodulin).
Investigation of NADPH's role in IDH1/2 mutant cancers and oncometabolite production.

Main Results:

Activated AKT phosphorylates NAD kinase (NADK), enhancing its activity.
Glucose-6-phosphate dehydrogenase and malic enzymes convert NADP to NADPH, often overexpressed in mutant p53 tumors.
Calmodulin overexpression also boosts NADK activity.
In IDH1/2 mutant cancers, NADPH is essential for generating the oncometabolite D-2-hydroxyglutarate.

Conclusions:

The heightened demand for NADPH in cancer cells presents a vulnerability.
Targeting the synthesis of NADPH is a promising therapeutic strategy for various cancers.