Lactic acidosis in patients with solid cancer

Kód výsledku v IS VaVaI

<a href="https://www.isvavai.cz/riv?ss=detail&h=RIV%2F00216208%3A11120%2F22%3A43923230" target="_blank" >RIV/00216208:11120/22:43923230 - isvavai.cz</a>

Výsledek na webu

<a href="https://doi.org/10.1089/ars.2021.0267" target="_blank" >https://doi.org/10.1089/ars.2021.0267</a>

DOI - Digital Object Identifier

<a href="http://dx.doi.org/10.1089/ars.2021.0267" target="_blank" >10.1089/ars.2021.0267</a>

Jazyk výsledku

angličtina

Název v původním jazyce

Lactic acidosis in patients with solid cancer

Popis výsledku v původním jazyce

Significance Tissue-specific lactic acidosis in cancer stimulates and mediates tumor invasion and metastasis and is druggable. Rarely, malignancy causes systemic lactic acidosis, the role of which is poorly understood. Recent advances The understanding of the role of lactate has shifted dramatically since its discovery. Long recognized as only a waste product, lactate has become known as an alternative metabolism substrate and secreted nutrient that is exchanged between the tumor and the microenvironment. Tissue-specific lactic acidosis is targeted to improve the host body&apos;s anticancer defense and serves as a tool that allows the targeting of anticancer compounds. Systemic lactic acidosis is associated with poor survival. In patients with solid cancer, systemic lactic acidosis is associated with an extremely poor prognosis, as revealed by the analysis of 57 published cases in this study. Although it is considered a pathology worth treating, targeting systemic lactic acidosis in patients with solid cancer is usually inefficient. Critical issues Research gaps include simple questions, such as the unknown nuclear pH of the cancer cells and its effects on chemotherapy outcomes, pH sensitivity of glycosylation in cancer cells, in vivo mechanisms of response to acidosis in the absence of lactate, and overinterpretation of in vitro results that were obtained using cells that were not preadapted to acidic environments. Future directions Numerous metabolism-targeting anticancer compounds induce lactatemia, lactic acidosis or other types of acidosis. Their potential to induce acidic environments is largely overlooked, although these compounds might contribute to a substantial portion of the observed clinical effects.

Název v anglickém jazyce

Lactic acidosis in patients with solid cancer

Popis výsledku anglicky

Significance Tissue-specific lactic acidosis in cancer stimulates and mediates tumor invasion and metastasis and is druggable. Rarely, malignancy causes systemic lactic acidosis, the role of which is poorly understood. Recent advances The understanding of the role of lactate has shifted dramatically since its discovery. Long recognized as only a waste product, lactate has become known as an alternative metabolism substrate and secreted nutrient that is exchanged between the tumor and the microenvironment. Tissue-specific lactic acidosis is targeted to improve the host body&apos;s anticancer defense and serves as a tool that allows the targeting of anticancer compounds. Systemic lactic acidosis is associated with poor survival. In patients with solid cancer, systemic lactic acidosis is associated with an extremely poor prognosis, as revealed by the analysis of 57 published cases in this study. Although it is considered a pathology worth treating, targeting systemic lactic acidosis in patients with solid cancer is usually inefficient. Critical issues Research gaps include simple questions, such as the unknown nuclear pH of the cancer cells and its effects on chemotherapy outcomes, pH sensitivity of glycosylation in cancer cells, in vivo mechanisms of response to acidosis in the absence of lactate, and overinterpretation of in vitro results that were obtained using cells that were not preadapted to acidic environments. Future directions Numerous metabolism-targeting anticancer compounds induce lactatemia, lactic acidosis or other types of acidosis. Their potential to induce acidic environments is largely overlooked, although these compounds might contribute to a substantial portion of the observed clinical effects.

Druh

J_imp - Článek v periodiku v databázi Web of Science

CEP obor

—

OECD FORD obor

30204 - Oncology

Projekt

—

Návaznosti

I - Institucionalni podpora na dlouhodoby koncepcni rozvoj vyzkumne organizace

Rok uplatnění

2022

Kód důvěrnosti údajů

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

Název periodika

Antioxidants &amp; Redox Signaling

ISSN

1523-0864

e-ISSN

1557-7716

Svazek periodika

37

Číslo periodika v rámci svazku

16-18

Stát vydavatele periodika

US - Spojené státy americké

Počet stran výsledku

23

Strana od-do

1130-1152

Kód UT WoS článku

000810230000001

EID výsledku v databázi Scopus

2-s2.0-85138702256