Much more than you expected: The non-DHFR-mediated effects of methotrexate

Kód výsledku v IS VaVaI

<a href="https://www.isvavai.cz/riv?ss=detail&h=RIV%2F00159816%3A_____%2F17%3A00066062" target="_blank" >RIV/00159816:_____/17:00066062 - isvavai.cz</a>

Výsledek na webu

<a href="http://dx.doi.org/10.1016/j.bbagen.2016.12.014" target="_blank" >http://dx.doi.org/10.1016/j.bbagen.2016.12.014</a>

DOI - Digital Object Identifier

<a href="http://dx.doi.org/10.1016/j.bbagen.2016.12.014" target="_blank" >10.1016/j.bbagen.2016.12.014</a>

Jazyk výsledku

angličtina

Název v původním jazyce

Much more than you expected: The non-DHFR-mediated effects of methotrexate

Popis výsledku v původním jazyce

ACKGROUND: For decades, methotrexate (MTX; amethopterin) has been known as an antifolate inhibitor of dihydrofolate reductase (DHFR), and it is widely used for the treatment of various malignancies and autoimmune diseases. Although the inclusion of MTX in various therapeutic regimens is based on its ability to inhibit DHFR and consequently to suppress the synthesis of pyrimidine and purine precursors, recent studies have shown that MTX is also able to target other intracellular pathways that are independent of folate metabolism. SCOPE OF REVIEW: The main aim of this review is to summarize the most important, up-to-date findings of studies regarding the non-DHFR-mediated mechanisms of MTX action. MAJOR CONCLUSIONS: The effectiveness of MTX is undoubtedly caused by its capability to affect various intracellular pathways at many levels. Although the most important therapeutic mechanism of MTX is strongly based on the inhibition of DHFR, many other effects of this compound have been described and new studies bring new insights into the pharmacology of MTX every year. GENERAL SIGNIFICANCE: Identification of these new targets for MTX is especially important for a better understanding of MTX action in new protocols of combination therapy.

Název v anglickém jazyce

Much more than you expected: The non-DHFR-mediated effects of methotrexate

Popis výsledku anglicky

ACKGROUND: For decades, methotrexate (MTX; amethopterin) has been known as an antifolate inhibitor of dihydrofolate reductase (DHFR), and it is widely used for the treatment of various malignancies and autoimmune diseases. Although the inclusion of MTX in various therapeutic regimens is based on its ability to inhibit DHFR and consequently to suppress the synthesis of pyrimidine and purine precursors, recent studies have shown that MTX is also able to target other intracellular pathways that are independent of folate metabolism. SCOPE OF REVIEW: The main aim of this review is to summarize the most important, up-to-date findings of studies regarding the non-DHFR-mediated mechanisms of MTX action. MAJOR CONCLUSIONS: The effectiveness of MTX is undoubtedly caused by its capability to affect various intracellular pathways at many levels. Although the most important therapeutic mechanism of MTX is strongly based on the inhibition of DHFR, many other effects of this compound have been described and new studies bring new insights into the pharmacology of MTX every year. GENERAL SIGNIFICANCE: Identification of these new targets for MTX is especially important for a better understanding of MTX action in new protocols of combination therapy.

Druh

J_imp - Článek v periodiku v databázi Web of Science

CEP obor

—

OECD FORD obor

10608 - Biochemistry and molecular biology

Projekt

Výsledek vznikl pri realizaci vícero projektů. Více informací v záložce Projekty.

Návaznosti

P - Projekt vyzkumu a vyvoje financovany z verejnych zdroju (s odkazem do CEP)

Rok uplatnění

2017

Kód důvěrnosti údajů

S - Úplné a pravdivé údaje o projektu nepodléhají ochraně podle zvláštních právních předpisů

Název periodika

Biochimica et Biophysica Acta - General Subjects

ISSN

0304-4165

e-ISSN

—

Svazek periodika

1861

Číslo periodika v rámci svazku

3

Stát vydavatele periodika

NL - Nizozemsko

Počet stran výsledku

5

Strana od-do

499-5035

Kód UT WoS článku

000394076400001

EID výsledku v databázi Scopus

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