Cargando…
A Review of FLT3 Kinase Inhibitors in AML
Acute myeloid leukemia (AML) is a highly aggressive illness distinguished by the accumulation of abnormal hematopoietic precursors in both the bone marrow and peripheral blood. The prevalence of FLT3 gene mutations is high and escalates the probability of relapse and mortality. The survival rates fo...
Autores principales: | , , , , , , , , |
---|---|
Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
MDPI
2023
|
Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10607239/ https://www.ncbi.nlm.nih.gov/pubmed/37892567 http://dx.doi.org/10.3390/jcm12206429 |
_version_ | 1785127498897424384 |
---|---|
author | Negotei, Cristina Colita, Andrei Mitu, Iuliana Lupu, Anca Roxana Lapadat, Mihai-Emilian Popovici, Constanta Elena Crainicu, Madalina Stanca, Oana Berbec, Nicoleta Mariana |
author_facet | Negotei, Cristina Colita, Andrei Mitu, Iuliana Lupu, Anca Roxana Lapadat, Mihai-Emilian Popovici, Constanta Elena Crainicu, Madalina Stanca, Oana Berbec, Nicoleta Mariana |
author_sort | Negotei, Cristina |
collection | PubMed |
description | Acute myeloid leukemia (AML) is a highly aggressive illness distinguished by the accumulation of abnormal hematopoietic precursors in both the bone marrow and peripheral blood. The prevalence of FLT3 gene mutations is high and escalates the probability of relapse and mortality. The survival rates for AML patients, particularly those over 65, are low. FLT3 mutation screening at diagnosis is mandatory, and FLT3 inhibitors are crucial in treating AML patients with mutations. There are two categories of FLT3 mutations: FLT3-ITD located in the juxtamembrane domain and FLT3-TKD in the tyrosine kinase domain. FLT3-ITD is the most common type, affecting nearly a quarter of patients, whereas FLT3-TKD only affects 6–8% of patients. FLT3 inhibitors are now crucial in treating AML patients with FLT3 mutations. When dealing with FLT3-mutated AML, the recommended course of treatment typically involves chemotherapy and midostaurin, followed by allogeneic hematopoietic cell transplantation (HCT) to maximize the likelihood of success. Maintenance therapy can lower the risk of relapse, and gilteritinib is a better option than salvage chemotherapy for relapsed or refractory cases. Clinical trials for new or combined therapies are the most effective approach. This review discusses treatment options for patients with FLT3-mutated AML, including induction chemotherapy and options for relapsed or refractory disease. Additional treatment options may become available as more studies are conducted based on the patient’s condition and susceptibility. |
format | Online Article Text |
id | pubmed-10607239 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2023 |
publisher | MDPI |
record_format | MEDLINE/PubMed |
spelling | pubmed-106072392023-10-28 A Review of FLT3 Kinase Inhibitors in AML Negotei, Cristina Colita, Andrei Mitu, Iuliana Lupu, Anca Roxana Lapadat, Mihai-Emilian Popovici, Constanta Elena Crainicu, Madalina Stanca, Oana Berbec, Nicoleta Mariana J Clin Med Review Acute myeloid leukemia (AML) is a highly aggressive illness distinguished by the accumulation of abnormal hematopoietic precursors in both the bone marrow and peripheral blood. The prevalence of FLT3 gene mutations is high and escalates the probability of relapse and mortality. The survival rates for AML patients, particularly those over 65, are low. FLT3 mutation screening at diagnosis is mandatory, and FLT3 inhibitors are crucial in treating AML patients with mutations. There are two categories of FLT3 mutations: FLT3-ITD located in the juxtamembrane domain and FLT3-TKD in the tyrosine kinase domain. FLT3-ITD is the most common type, affecting nearly a quarter of patients, whereas FLT3-TKD only affects 6–8% of patients. FLT3 inhibitors are now crucial in treating AML patients with FLT3 mutations. When dealing with FLT3-mutated AML, the recommended course of treatment typically involves chemotherapy and midostaurin, followed by allogeneic hematopoietic cell transplantation (HCT) to maximize the likelihood of success. Maintenance therapy can lower the risk of relapse, and gilteritinib is a better option than salvage chemotherapy for relapsed or refractory cases. Clinical trials for new or combined therapies are the most effective approach. This review discusses treatment options for patients with FLT3-mutated AML, including induction chemotherapy and options for relapsed or refractory disease. Additional treatment options may become available as more studies are conducted based on the patient’s condition and susceptibility. MDPI 2023-10-10 /pmc/articles/PMC10607239/ /pubmed/37892567 http://dx.doi.org/10.3390/jcm12206429 Text en © 2023 by the authors. https://creativecommons.org/licenses/by/4.0/Licensee MDPI, Basel, Switzerland. This article is an open access article distributed under the terms and conditions of the Creative Commons Attribution (CC BY) license (https://creativecommons.org/licenses/by/4.0/). |
spellingShingle | Review Negotei, Cristina Colita, Andrei Mitu, Iuliana Lupu, Anca Roxana Lapadat, Mihai-Emilian Popovici, Constanta Elena Crainicu, Madalina Stanca, Oana Berbec, Nicoleta Mariana A Review of FLT3 Kinase Inhibitors in AML |
title | A Review of FLT3 Kinase Inhibitors in AML |
title_full | A Review of FLT3 Kinase Inhibitors in AML |
title_fullStr | A Review of FLT3 Kinase Inhibitors in AML |
title_full_unstemmed | A Review of FLT3 Kinase Inhibitors in AML |
title_short | A Review of FLT3 Kinase Inhibitors in AML |
title_sort | review of flt3 kinase inhibitors in aml |
topic | Review |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10607239/ https://www.ncbi.nlm.nih.gov/pubmed/37892567 http://dx.doi.org/10.3390/jcm12206429 |
work_keys_str_mv | AT negoteicristina areviewofflt3kinaseinhibitorsinaml AT colitaandrei areviewofflt3kinaseinhibitorsinaml AT mituiuliana areviewofflt3kinaseinhibitorsinaml AT lupuancaroxana areviewofflt3kinaseinhibitorsinaml AT lapadatmihaiemilian areviewofflt3kinaseinhibitorsinaml AT popoviciconstantaelena areviewofflt3kinaseinhibitorsinaml AT crainicumadalina areviewofflt3kinaseinhibitorsinaml AT stancaoana areviewofflt3kinaseinhibitorsinaml AT berbecnicoletamariana areviewofflt3kinaseinhibitorsinaml AT negoteicristina reviewofflt3kinaseinhibitorsinaml AT colitaandrei reviewofflt3kinaseinhibitorsinaml AT mituiuliana reviewofflt3kinaseinhibitorsinaml AT lupuancaroxana reviewofflt3kinaseinhibitorsinaml AT lapadatmihaiemilian reviewofflt3kinaseinhibitorsinaml AT popoviciconstantaelena reviewofflt3kinaseinhibitorsinaml AT crainicumadalina reviewofflt3kinaseinhibitorsinaml AT stancaoana reviewofflt3kinaseinhibitorsinaml AT berbecnicoletamariana reviewofflt3kinaseinhibitorsinaml |