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Genetic variations accumulating within populations over generations give rise to biological evolution. Evolutionary changes can result in the formation of novel varieties and entire new species. These changes are responsible for the diverse forms of life inhabiting the planet. The evidence for evolution suggests that all living organisms descended from common ancestors.

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Related Experiment Video

Updated: Jan 25, 2026

Flow Cytometry to Estimate Leukemia Stem Cells in Primary Acute Myeloid Leukemia and in Patient-derived-xenografts, at Diagnosis and Follow Up

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Clonal evolution patterns in acute myeloid leukemia with NPM1 mutation.

Sibylle Cocciardi¹, Anna Dolnik¹, Silke Kapp-Schwoerer¹

¹Department of Internal Medicine III, University Hospital of Ulm, Ulm, 89081, Germany.

Nature Communications

|May 4, 2019

Summary

This summary is machine-generated.

Genetic analysis of acute myeloid leukemia (AML) reveals that while most relapses stem from persistent clones, some NPM1-mutated AML cases involve NPM1 loss, suggesting new or treatment-associated AML origins.

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Area of Science:

Hematology
Cancer Genetics
Molecular Oncology

Background:

Mutations in the nucleophosmin 1 (NPM1) gene are key drivers in acute myeloid leukemia (AML) pathogenesis.
Understanding genetic evolution from diagnosis to relapse is crucial for AML treatment strategies.

Purpose of the Study:

To investigate the genetic landscape of NPM1-mutated (NPM1^mut) AML at diagnosis and relapse.
To characterize the distinct genetic profiles of NPM1^mut loss cases at relapse.

Main Methods:

Analysis of mutation status for five recurrently mutated oncogenes in 129 paired NPM1^mut AML samples.
Whole exome sequencing (WES) and RNA-Seq performed on NPM1^mut loss samples at relapse.

Main Results:

A significant genetic shift was observed between diagnosis and relapse in NPM1^mut AML, including 11 cases with NPM1^mut loss.
NPM1^mut loss patients at relapse exhibited unique mutational patterns with minimal overlap with diagnosis samples, affecting different signaling pathways.
Patients with persistent NPM1^mut showed high mutation overlap between diagnosis and relapse.

Conclusions:

Relapse in NPM1^mut AML typically arises from persistent leukemic clones.
NPM1^mut loss at relapse suggests alternative etiologies, including de novo or treatment-associated AML (tAML).