# Biological characteristics and prognosis of acute myeloid leukemia in elderly patients

**Authors:** Zhe Chen, Lina Ding, Jieni Yu, Jing Jin, Zhijian Zhang, Jiaping Fu, Pan Hong, Leihua Fu

PMC · DOI: 10.3389/fgene.2025.1524177 · Frontiers in Genetics · 2025-04-04

## TL;DR

This study explores how genetic mutations and chromosomal changes affect the prognosis of elderly patients with acute myeloid leukemia.

## Contribution

The study identifies specific gene mutations and chromosomal abnormalities that are predictive of poor outcomes in elderly AML patients.

## Key findings

- Elderly AML patients with FLT3, ASXL1, or TP53 mutations had lower complete remission rates.
- TP53 mutations and 17p abnormalities were strongly associated with shorter overall survival.
- Favorable prognosis genes typically seen in younger AML patients do not apply to elderly patients.

## Abstract

Our study aimed to investigate the effects of chromosomal aberrations and genetic mutations of elderly individuals diagnosed with AML and determine its prognostic significance.

We retrospectively collected data over nearly 7 years from our hospital, encompassing 90 cases of elderly AML patients. Baseline information of patients was gathered and followed up, and statistical analysis was conducted using SPSS 25.0.

Among the 90 elderly non-M3 AML patients, 56 (62.2%) exhibited multiple gene mutations, with 9 (10%) patients displaying five or more gene mutations. The incidence of NPM1 mutation was significantly higher in patients with normal karyotypes compared to those with abnormal karyotypes (P = 0.001). Patients with FLT3, ASXL1, or TP53 mutations displayed lower rates of CR compared to wild-type counterparts. Kaplan-Meier analysis revealed that TET2 mutation (P = 0.0474), FLT3-ITD mutation (P = 0.0364), TP53 mutation (P = 0.0031), and 17p abnormality (P = 0.00285) were predictive of shorter OS. TP53 mutations (P = 0.0440), 17p abnormalities (P = 0.0272), 7q abnormalities (P = 0.0174), and complex karyotypes (P = 0.0447) were associated with shorter RFS.

Our findings suggest that elderly AML patients exhibit distinctive genetic profiles, and favorable prognosis genes do not seem to apply to elderly AML patients.

## Linked entities

- **Genes:** NPM1 (nucleophosmin 1) [NCBI Gene 4869], FLT3 (fms related receptor tyrosine kinase 3) [NCBI Gene 2322], ASXL1 (ASXL transcriptional regulator 1) [NCBI Gene 171023], TP53 (tumor protein p53) [NCBI Gene 7157], TET2 (tet methylcytosine dioxygenase 2) [NCBI Gene 54790]
- **Diseases:** acute myeloid leukemia (MONDO:0015667), AML (MONDO:0018874)

## Full-text entities

- **Genes:** FLT3 (fms related receptor tyrosine kinase 3) [NCBI Gene 2322] {aka CD135, FLK-2, FLK2, STK1}, NPM1 (nucleophosmin 1) [NCBI Gene 4869] {aka B23, NPM}, TP53 (tumor protein p53) [NCBI Gene 7157] {aka BCC7, BMFS5, LFS1, P53, TRP53}, TET2 (tet methylcytosine dioxygenase 2) [NCBI Gene 54790] {aka IMD75, KIAA1546, MDS}, ASXL1 (ASXL transcriptional regulator 1) [NCBI Gene 171023] {aka BOPS, MDS}
- **Diseases:** AML (MESH:D015470), 17p abnormalities (MESH:C538045), 7q abnormalities (MESH:C537821)
- **Species:** Homo sapiens (human, species) [taxon 9606]

## Full text

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## Figures

3 figures with captions in the complete paper: https://tomesphere.com/paper/PMC12006902/full.md

## References

20 references — full list in the complete paper: https://tomesphere.com/paper/PMC12006902/full.md

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Source: https://tomesphere.com/paper/PMC12006902