Pancreatic cancer triggers diabetes through TGF-β-mediated selective depletion of islet β-cells.
Animals
Antibodies, Neutralizing
/ pharmacology
Apoptosis
/ drug effects
Carcinoma, Pancreatic Ductal
/ complications
Cells, Cultured
Diabetes Mellitus
/ etiology
Disease Models, Animal
Disease Progression
Gene Deletion
Insulin-Secreting Cells
/ metabolism
Mice
Mice, Inbred C57BL
Mice, Transgenic
Pancreatic Neoplasms
/ complications
Prognosis
Receptor, Transforming Growth Factor-beta Type II
/ genetics
Signal Transduction
/ drug effects
Smad4 Protein
/ genetics
Transforming Growth Factor beta1
/ immunology
Journal
Life science alliance
ISSN: 2575-1077
Titre abrégé: Life Sci Alliance
Pays: United States
ID NLM: 101728869
Informations de publication
Date de publication:
06 2020
06 2020
Historique:
received:
07
10
2019
revised:
21
04
2020
accepted:
23
04
2020
entrez:
7
5
2020
pubmed:
7
5
2020
medline:
8
7
2021
Statut:
epublish
Résumé
Pancreatic ductal adenocarcinoma (PDAC) is a lethal disease that remains incurable because of late diagnosis, which renders any therapeutic intervention challenging. Most PDAC patients develop de novo diabetes, which exacerbates their morbidity and mortality. How PDAC triggers diabetes is still unfolding. Using a mouse model of Kras
Identifiants
pubmed: 32371554
pii: 3/6/e201900573
doi: 10.26508/lsa.201900573
pmc: PMC7211975
pii:
doi:
Substances chimiques
Antibodies, Neutralizing
0
Smad4 Protein
0
Smad4 protein, mouse
0
Tgfb1 protein, mouse
0
Transforming Growth Factor beta1
0
Receptor, Transforming Growth Factor-beta Type II
EC 2.7.11.30
Tgfbr2 protein, mouse
EC 2.7.11.30
Types de publication
Journal Article
Research Support, N.I.H., Extramural
Research Support, Non-U.S. Gov't
Research Support, U.S. Gov't, Non-P.H.S.
Langues
eng
Sous-ensembles de citation
IM
Subventions
Organisme : NIGMS NIH HHS
ID : P20 GM121334
Pays : United States
Organisme : NIAMS NIH HHS
ID : R01 AR059070
Pays : United States
Organisme : NCI NIH HHS
ID : R01 CA210911
Pays : United States
Informations de copyright
© 2020 Parajuli et al.
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