A Comprehensive Review on MAPK: A Promising Therapeutic Target in Cancer
Identifikátory výsledku
Kód výsledku v IS VaVaI
<a href="https://www.isvavai.cz/riv?ss=detail&h=RIV%2F00209805%3A_____%2F19%3A00078347" target="_blank" >RIV/00209805:_____/19:00078347 - isvavai.cz</a>
Nalezeny alternativní kódy
RIV/00216224:14740/19:00112969
Výsledek na webu
<a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6827047/" target="_blank" >https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6827047/</a>
DOI - Digital Object Identifier
<a href="http://dx.doi.org/10.3390/cancers11101618" target="_blank" >10.3390/cancers11101618</a>
Alternativní jazyky
Jazyk výsledku
angličtina
Název v původním jazyce
A Comprehensive Review on MAPK: A Promising Therapeutic Target in Cancer
Popis výsledku v původním jazyce
The mitogen-activated protein kinase (MAPK) pathway is an important bridge in the switch from extracellular signals to intracellular responses. Alterations of signaling cascades are found in various diseases, including cancer, as a result of genetic and epigenetic changes. Numerous studies focused on both the homeostatic and the pathologic conduct of MAPK signaling; however, there is still much to be deciphered in terms of regulation and action models in both preclinical and clinical research. MAPK has implications in the response to cancer therapy, particularly the activation of the compensatory pathways in response to experimental MAPK inhibition. The present paper discusses new insights into MAPK as a complex cell signaling pathway with roles in the sustenance of cellular normal conduit, response to cancer therapy, and activation of compensatory pathways. Unfortunately, most MAPK inhibitors trigger resistance due to the activation of compensatory feed-back loops in tumor cells and tumor microenvironment components. Therefore, novel combinatorial therapies have to be implemented for cancer management in order to restrict the possibility of alternative pathway activation, as a perspective for developing novel therapies based on integration in translational studies.
Název v anglickém jazyce
A Comprehensive Review on MAPK: A Promising Therapeutic Target in Cancer
Popis výsledku anglicky
The mitogen-activated protein kinase (MAPK) pathway is an important bridge in the switch from extracellular signals to intracellular responses. Alterations of signaling cascades are found in various diseases, including cancer, as a result of genetic and epigenetic changes. Numerous studies focused on both the homeostatic and the pathologic conduct of MAPK signaling; however, there is still much to be deciphered in terms of regulation and action models in both preclinical and clinical research. MAPK has implications in the response to cancer therapy, particularly the activation of the compensatory pathways in response to experimental MAPK inhibition. The present paper discusses new insights into MAPK as a complex cell signaling pathway with roles in the sustenance of cellular normal conduit, response to cancer therapy, and activation of compensatory pathways. Unfortunately, most MAPK inhibitors trigger resistance due to the activation of compensatory feed-back loops in tumor cells and tumor microenvironment components. Therefore, novel combinatorial therapies have to be implemented for cancer management in order to restrict the possibility of alternative pathway activation, as a perspective for developing novel therapies based on integration in translational studies.
Klasifikace
Druh
J<sub>imp</sub> - Článek v periodiku v databázi Web of Science
CEP obor
—
OECD FORD obor
30204 - Oncology
Návaznosti výsledku
Projekt
—
Návaznosti
I - Institucionalni podpora na dlouhodoby koncepcni rozvoj vyzkumne organizace
Ostatní
Rok uplatnění
2019
Kód důvěrnosti údajů
S - Úplné a pravdivé údaje o projektu nepodléhají ochraně podle zvláštních právních předpisů
Údaje specifické pro druh výsledku
Název periodika
Cancers (Basel)
ISSN
2072-6694
e-ISSN
—
Svazek periodika
11
Číslo periodika v rámci svazku
10
Stát vydavatele periodika
CH - Švýcarská konfederace
Počet stran výsledku
25
Strana od-do
1618
Kód UT WoS článku
000498826000215
EID výsledku v databázi Scopus
2-s2.0-85074947906