Pancreatic cancer: branched-chain amino acids as putative key metabolic regulators?
The result's identifiers
Result code in IS VaVaI
<a href="https://www.isvavai.cz/riv?ss=detail&h=RIV%2F67985823%3A_____%2F21%3A00553167" target="_blank" >RIV/67985823:_____/21:00553167 - isvavai.cz</a>
Alternative codes found
RIV/00216208:11120/21:43922710
Result on the web
<a href="https://doi.org/10.1007/s10555-021-10016-0" target="_blank" >https://doi.org/10.1007/s10555-021-10016-0</a>
DOI - Digital Object Identifier
<a href="http://dx.doi.org/10.1007/s10555-021-10016-0" target="_blank" >10.1007/s10555-021-10016-0</a>
Alternative languages
Result language
angličtina
Original language name
Pancreatic cancer: branched-chain amino acids as putative key metabolic regulators?
Original language description
Branched-chain amino acids (BCAA) are essential amino acids utilized in anabolic and catabolic metabolism. While extensively studied in obesity and diabetes, recent evidence suggests an important role for BCAA metabolism in cancer. Elevated plasma levels of BCAA are associated with an increased risk of developing pancreatic cancer, namely pancreatic ductal adenocarcinoma (PDAC), a tumor with one of the highest 1-year mortality rates. The dreadful prognosis for PDAC patients could be attributable also to the early and frequent development of cancer cachexia, a fatal host metabolic reprogramming leading to muscle and adipose wasting. We propose that BCAA dysmetabolism is a unifying component of several pathological conditions, i.e., obesity, insulin resistance, and PDAC. These conditions are mutually dependent since PDAC ranks among cancers tightly associated with obesity and insulin resistance. It is also well-established that PDAC itself can trigger insulin resistance and new-onset diabetes. However, the exact link between BCAA metabolism, development of PDAC, and tissue wasting is still unclear. Although tissue-specific intracellular and systemic metabolism of BCAA is being intensively studied, unresolved questions related to PDAC and cancer cachexia remain, namely, whether elevated circulating BCAA contribute to PDAC etiology, what is the biological background of BCAA elevation, and what is the role of adipose tissue relative to BCAA metabolism during cancer cachexia. To cover those issues, we provide our view on BCAA metabolism at the intracellular, tissue, and whole-body level, with special emphasis on different metabolic links to BCAA intermediates and the role of insulin in substrate handling.
Czech name
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Czech description
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Classification
Type
J<sub>imp</sub> - Article in a specialist periodical, which is included in the Web of Science database
CEP classification
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OECD FORD branch
30202 - Endocrinology and metabolism (including diabetes, hormones)
Result continuities
Project
<a href="/en/project/NV19-01-00101" target="_blank" >NV19-01-00101: Pancreatic cancer: metabolic derangements assiocated with insulin resistance</a><br>
Continuities
P - Projekt vyzkumu a vyvoje financovany z verejnych zdroju (s odkazem do CEP)
Others
Publication year
2021
Confidentiality
S - Úplné a pravdivé údaje o projektu nepodléhají ochraně podle zvláštních právních předpisů
Data specific for result type
Name of the periodical
Cancer and Metastasis Reviews
ISSN
0167-7659
e-ISSN
1573-7233
Volume of the periodical
40
Issue of the periodical within the volume
4
Country of publishing house
NL - THE KINGDOM OF THE NETHERLANDS
Number of pages
25
Pages from-to
1115-1139
UT code for WoS article
000735340900001
EID of the result in the Scopus database
2-s2.0-85121865652