PPM1D as a driver and pharmacological target in clonal hematopoiesis

Kód výsledku v IS VaVaI

<a href="https://www.isvavai.cz/riv?ss=detail&h=RIV%2F68378050%3A_____%2F19%3A00502886" target="_blank" >RIV/68378050:_____/19:00502886 - isvavai.cz</a>

Výsledek na webu

—

DOI - Digital Object Identifier

—

Jazyk výsledku

angličtina

Název v původním jazyce

PPM1D as a driver and pharmacological target in clonal hematopoiesis

Popis výsledku v původním jazyce

Chemotherapy or radiotherapy cause genotoxic stress that kills cancer cells and ideally only tolerable DNA damage to the neighboring healthy tissues. Cell fate after exposure to genotoxic stress is determined by the tumor suppressor p53 that controls transcription of both pro-survival and pro-apoptotic genes. Depending on the DNA damage load, cells activate the cell cycle checkpoint arrest or die through programmed cell death. Protein phosphatase 2C delta (referred to as WIP1) is a negative regulator of p53 and has been proposed as potential pharmaceutical target. Recently, mutations in PPM1D were observed in patients that developed secondary cancer after receiving a chemotherapy. This review will discuss the role of PPM1D in development of the secondary cancers as well as potential use of small-molecule inhibitors as prevention to causing these adverse effects of chemotherapy.

Název v anglickém jazyce

PPM1D as a driver and pharmacological target in clonal hematopoiesis

Popis výsledku anglicky

Chemotherapy or radiotherapy cause genotoxic stress that kills cancer cells and ideally only tolerable DNA damage to the neighboring healthy tissues. Cell fate after exposure to genotoxic stress is determined by the tumor suppressor p53 that controls transcription of both pro-survival and pro-apoptotic genes. Depending on the DNA damage load, cells activate the cell cycle checkpoint arrest or die through programmed cell death. Protein phosphatase 2C delta (referred to as WIP1) is a negative regulator of p53 and has been proposed as potential pharmaceutical target. Recently, mutations in PPM1D were observed in patients that developed secondary cancer after receiving a chemotherapy. This review will discuss the role of PPM1D in development of the secondary cancers as well as potential use of small-molecule inhibitors as prevention to causing these adverse effects of chemotherapy.

Druh

C - Kapitola v odborné knize

CEP obor

—

OECD FORD obor

10601 - Cell biology

Projekt

<a href="/cs/project/LO1220" target="_blank" >LO1220: CZ-OPENSCREEN: Národní infrastruktura chemické biologie</a><br>

Návaznosti

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

Rok uplatnění

2019

Kód důvěrnosti údajů

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

Název knihy nebo sborníku

Advances in Chemical Biology

ISBN

978-80-88011-03-3

Počet stran výsledku

7

Strana od-do

32-39

Počet stran knihy

210

Název nakladatele

OPTIO CZ

Místo vydání

Praha

Kód UT WoS kapitoly

—