Progress in molecularly targeted therapies for acute myeloid leukemia

Research output: Contribution to journalArticle

1 Citation (Scopus)

Abstract

Genetic abnormalities including specific point mutations have recently been confirmed by applying comprehensive genome sequencing analyses. Molecular targeting therapies, which focus on the mutated proteins and over-expressed proteins in acute myeloid leukemia (AML) cells, are now being developed in clinical studies and/or based on in vitro analyses. This manuscript summarizes the genetic abnormalities in AML cells and some of the current molecular targeting therapies including FLT3 inhibitors (e.g. AC220; Quizartinib), Polo like kinase 1 (PLK1) inhibitors (e.g. BI-6727; Volasertib), IDH2 inhibitors (e.g. AG-221), and XPO1 inhibitors (e.g. KPT-330; Selinexor).

Original languageEnglish
Pages (from-to)130-138
Number of pages9
Journal[Rinshō ketsueki] The Japanese journal of clinical hematology
Volume56
Issue number2
DOIs
Publication statusPublished - 01-02-2015
Externally publishedYes

Fingerprint

Myeloid Cells
Acute Myeloid Leukemia
Point Mutation
Proteins
Genome
Therapeutics
BI 6727
KPT-330
AG-221
polo-like kinase 1
In Vitro Techniques
Clinical Studies
quizartinib

All Science Journal Classification (ASJC) codes

  • Medicine(all)

Cite this

@article{21b513b795c64aa9a3f5b0aa8ff04996,
title = "Progress in molecularly targeted therapies for acute myeloid leukemia",
abstract = "Genetic abnormalities including specific point mutations have recently been confirmed by applying comprehensive genome sequencing analyses. Molecular targeting therapies, which focus on the mutated proteins and over-expressed proteins in acute myeloid leukemia (AML) cells, are now being developed in clinical studies and/or based on in vitro analyses. This manuscript summarizes the genetic abnormalities in AML cells and some of the current molecular targeting therapies including FLT3 inhibitors (e.g. AC220; Quizartinib), Polo like kinase 1 (PLK1) inhibitors (e.g. BI-6727; Volasertib), IDH2 inhibitors (e.g. AG-221), and XPO1 inhibitors (e.g. KPT-330; Selinexor).",
author = "Akihiro Tomita",
year = "2015",
month = "2",
day = "1",
doi = "10.11406/rinketsu.56.130",
language = "English",
volume = "56",
pages = "130--138",
journal = "[Rinsho ketsueki] The Japanese journal of clinical hematology",
issn = "0485-1439",
publisher = "Nihon Rinsho Ketsueki Gakkai/Japan Society of Clinical Hematology",
number = "2",

}

Progress in molecularly targeted therapies for acute myeloid leukemia. / Tomita, Akihiro.

In: [Rinshō ketsueki] The Japanese journal of clinical hematology, Vol. 56, No. 2, 01.02.2015, p. 130-138.

Research output: Contribution to journalArticle

TY - JOUR

T1 - Progress in molecularly targeted therapies for acute myeloid leukemia

AU - Tomita, Akihiro

PY - 2015/2/1

Y1 - 2015/2/1

N2 - Genetic abnormalities including specific point mutations have recently been confirmed by applying comprehensive genome sequencing analyses. Molecular targeting therapies, which focus on the mutated proteins and over-expressed proteins in acute myeloid leukemia (AML) cells, are now being developed in clinical studies and/or based on in vitro analyses. This manuscript summarizes the genetic abnormalities in AML cells and some of the current molecular targeting therapies including FLT3 inhibitors (e.g. AC220; Quizartinib), Polo like kinase 1 (PLK1) inhibitors (e.g. BI-6727; Volasertib), IDH2 inhibitors (e.g. AG-221), and XPO1 inhibitors (e.g. KPT-330; Selinexor).

AB - Genetic abnormalities including specific point mutations have recently been confirmed by applying comprehensive genome sequencing analyses. Molecular targeting therapies, which focus on the mutated proteins and over-expressed proteins in acute myeloid leukemia (AML) cells, are now being developed in clinical studies and/or based on in vitro analyses. This manuscript summarizes the genetic abnormalities in AML cells and some of the current molecular targeting therapies including FLT3 inhibitors (e.g. AC220; Quizartinib), Polo like kinase 1 (PLK1) inhibitors (e.g. BI-6727; Volasertib), IDH2 inhibitors (e.g. AG-221), and XPO1 inhibitors (e.g. KPT-330; Selinexor).

UR - http://www.scopus.com/inward/record.url?scp=84942508664&partnerID=8YFLogxK

UR - http://www.scopus.com/inward/citedby.url?scp=84942508664&partnerID=8YFLogxK

U2 - 10.11406/rinketsu.56.130

DO - 10.11406/rinketsu.56.130

M3 - Article

VL - 56

SP - 130

EP - 138

JO - [Rinsho ketsueki] The Japanese journal of clinical hematology

JF - [Rinsho ketsueki] The Japanese journal of clinical hematology

SN - 0485-1439

IS - 2

ER -