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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

  • Czech description

Classification

  • Type

    J<sub>imp</sub> - Article in a specialist periodical, which is included in the Web of Science database

  • CEP classification

  • 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