Selected Aspects of Chemoresistance Mechanisms in Colorectal CarcinomaA Focus on Epithelial-to-Mesenchymal Transition, Autophagy, and Apoptosis
Identifikátory výsledku
Kód výsledku v IS VaVaI
<a href="https://www.isvavai.cz/riv?ss=detail&h=RIV%2F00216208%3A11150%2F19%3A10400210" target="_blank" >RIV/00216208:11150/19:10400210 - isvavai.cz</a>
Výsledek na webu
<a href="https://verso.is.cuni.cz/pub/verso.fpl?fname=obd_publikace_handle&handle=9aE0QPj5sp" target="_blank" >https://verso.is.cuni.cz/pub/verso.fpl?fname=obd_publikace_handle&handle=9aE0QPj5sp</a>
DOI - Digital Object Identifier
<a href="http://dx.doi.org/10.3390/cells8030234" target="_blank" >10.3390/cells8030234</a>
Alternativní jazyky
Jazyk výsledku
angličtina
Název v původním jazyce
Selected Aspects of Chemoresistance Mechanisms in Colorectal CarcinomaA Focus on Epithelial-to-Mesenchymal Transition, Autophagy, and Apoptosis
Popis výsledku v původním jazyce
Chemoresistance has been found in all malignant tumors including colorectal carcinoma (CRC). Nowadays chemoresistance is understood as a major reason for therapy failure, with consequent tumor growth and spreading leading ultimately to the patient's premature death. The chemotherapy-related resistance of malignant colonocytes may be manifested in diverse mechanisms that may exist both prior to the onset of the therapy or after it. The ultimate function of this chemoresistance is to ensure the survival of malignant cells through continuing adaptation within an organism, therefore, the nature and spectrum of cell-survival strategies in CRC represent a highly significant target of scientific inquiry. Among these survival strategies employed by CRC cells, three unique but significantly linked phenomena stand outepithelial-to-mesenchymal transition (EMT), autophagy, and cell death. In this mini-review, current knowledge concerning all three mechanisms including their emergence, timeline, regulation, and mutual relationships will be presented and discussed.
Název v anglickém jazyce
Selected Aspects of Chemoresistance Mechanisms in Colorectal CarcinomaA Focus on Epithelial-to-Mesenchymal Transition, Autophagy, and Apoptosis
Popis výsledku anglicky
Chemoresistance has been found in all malignant tumors including colorectal carcinoma (CRC). Nowadays chemoresistance is understood as a major reason for therapy failure, with consequent tumor growth and spreading leading ultimately to the patient's premature death. The chemotherapy-related resistance of malignant colonocytes may be manifested in diverse mechanisms that may exist both prior to the onset of the therapy or after it. The ultimate function of this chemoresistance is to ensure the survival of malignant cells through continuing adaptation within an organism, therefore, the nature and spectrum of cell-survival strategies in CRC represent a highly significant target of scientific inquiry. Among these survival strategies employed by CRC cells, three unique but significantly linked phenomena stand outepithelial-to-mesenchymal transition (EMT), autophagy, and cell death. In this mini-review, current knowledge concerning all three mechanisms including their emergence, timeline, regulation, and mutual relationships will be presented and discussed.
Klasifikace
Druh
J<sub>imp</sub> - Článek v periodiku v databázi Web of Science
CEP obor
—
OECD FORD obor
10601 - Cell biology
Návaznosti výsledku
Projekt
<a href="/cs/project/GA17-10331S" target="_blank" >GA17-10331S: Objasnění role kadherinů a EMT v rozvoji chemoterapeutické rezistence u metastatického kolorektálního karcinomu</a><br>
Návaznosti
P - Projekt vyzkumu a vyvoje financovany z verejnych zdroju (s odkazem do CEP)
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
Cells [online]
ISSN
2073-4409
e-ISSN
—
Svazek periodika
8
Číslo periodika v rámci svazku
3
Stát vydavatele periodika
CH - Švýcarská konfederace
Počet stran výsledku
17
Strana od-do
234
Kód UT WoS článku
000465640400002
EID výsledku v databázi Scopus
—