Mutagenesis mechanism-based FLT3 length mutation typing and the clinical significance deserve attention
10.3760/cma.j.cn115356-20231110-00070
- VernacularTitle:基于发生机制的FLT3长度突变分型及其临床意义值得重视
- Author:
Yang ZHANG
1
;
Xiaosu ZHOU
;
Hongxing LIU
Author Information
1. 河北燕达陆道培医院检验医学科，廊坊 065201
- Keywords:
Leukemia;
FLT3 internal tandem duplication;
FLT3 length mutations;
DNTT;
Terminal deoxynucleotidyl transferase
- From:
Journal of Leukemia & Lymphoma
2024;33(6):329-333
- CountryChina
- Language:Chinese
-
Abstract:
FLT3 internal tandem duplication (ITD) mutations are common in acute myeloid leukemia and show an important significance in guiding prognostic stratification and targeted therapy. With the widespread application of high-throughput sequencing technology and the increased ability to analyze mutation sequences, it has been found that more than half of FLT3-ITD mutations are not just tandem duplications but are also accompanied by some complex situations such as the addition of non-template sequences. Recent studies have revealed the sequence characteristics, mutagenesis mechanisms and related clinical prognostic significance of FLT3 length mutations (FLT3-LM). FLT3-LM with added non-template sequences is formed by abnormally activated terminal deoxynucleotidyl transferase. These patients show different treatment responses and prognosis when treated with chemotherapy, targeted therapy, and allogeneic hematopoietic stem cell transplantation, which provides a new perspective to understand FLT3-LM mutations more accurately and provides proposals for FLT3-LM typing based on the mutagenesis mechanism. The new typing rules can better reflect the differences in biological characteristics of the disease and more accurately guide the prognostic stratification and development of individualized treatment for patients with FLT3-LM mutations.
