Chronic Inflammation Promotes Cancer Progression as a Second hit.

Kód výsledku v IS VaVaI

<a href="https://www.isvavai.cz/riv?ss=detail&h=RIV%2F68378050%3A_____%2F23%3A00578355" target="_blank" >RIV/68378050:_____/23:00578355 - isvavai.cz</a>

Nalezeny alternativní kódy

RIV/00216208:11130/23:10469708 RIV/00216208:11310/23:10469708

Výsledek na webu

<a href="https://www.sciencedirect.com/science/article/pii/S0301472X23017022?via%3Dihub" target="_blank" >https://www.sciencedirect.com/science/article/pii/S0301472X23017022?via%3Dihub</a>

DOI - Digital Object Identifier

<a href="http://dx.doi.org/10.1016/j.exphem.2023.09.002" target="_blank" >10.1016/j.exphem.2023.09.002</a>

Jazyk výsledku

angličtina

Název v původním jazyce

Chronic Inflammation Promotes Cancer Progression as a Second hit.

Popis výsledku v původním jazyce

Acute myeloid leukemia (AML) is a malignant neoplasia of the hematopoietic system characterized by the accumulation of immature and nonfunctional leukemic blasts in the bone marrow and peripheral tissues. Mechanistically, the development of AML is explained by the .two-hit. theory, which is based on the accumulation of driver mutations that will cooperate to induce transformation. However, a significant percentage of patients with AML exhibit only one driver mutation, and thus, how leukemic transformation occurs in these cases is unclear. Accumulating evidence suggests that nongenetic factors, such as chronic inflammation, might influence AML development, and accordingly, clinical data have reported that patients with chronic inflammatory disorders have an increased risk of developing hematological malignancies. Here, using a mouse model of chronic inflammation, we demonstrate that systemic elevated levels of cytokines and chemokines and hyperactivation of the Jak/Stat3 signaling pathway may substitute .second hit. mutations and accelerate tumorigenesis. Altogether, our data highlight chronic inflammation as an additional factor in the development of AML, providing additional understanding of the mechanisms of transformation and opening new avenues for the treatment of this disease.

Název v anglickém jazyce

Chronic Inflammation Promotes Cancer Progression as a Second hit.

Popis výsledku anglicky

Acute myeloid leukemia (AML) is a malignant neoplasia of the hematopoietic system characterized by the accumulation of immature and nonfunctional leukemic blasts in the bone marrow and peripheral tissues. Mechanistically, the development of AML is explained by the .two-hit. theory, which is based on the accumulation of driver mutations that will cooperate to induce transformation. However, a significant percentage of patients with AML exhibit only one driver mutation, and thus, how leukemic transformation occurs in these cases is unclear. Accumulating evidence suggests that nongenetic factors, such as chronic inflammation, might influence AML development, and accordingly, clinical data have reported that patients with chronic inflammatory disorders have an increased risk of developing hematological malignancies. Here, using a mouse model of chronic inflammation, we demonstrate that systemic elevated levels of cytokines and chemokines and hyperactivation of the Jak/Stat3 signaling pathway may substitute .second hit. mutations and accelerate tumorigenesis. Altogether, our data highlight chronic inflammation as an additional factor in the development of AML, providing additional understanding of the mechanisms of transformation and opening new avenues for the treatment of this disease.

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

I - Institucionalni podpora na dlouhodoby koncepcni rozvoj vyzkumne organizace

Rok uplatnění

2023

Kód důvěrnosti údajů

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

Název periodika

Experimental Hematology

ISSN

0301-472X

e-ISSN

1873-2399

Svazek periodika

128

Číslo periodika v rámci svazku

Dec 23

Stát vydavatele periodika

US - Spojené státy americké

Počet stran výsledku

8

Strana od-do

30-37

Kód UT WoS článku

001130092800001

EID výsledku v databázi Scopus

2-s2.0-85172769299