Sammanfattning

The most common form of pancreatic cancer, pancreatic ductal adenocarcinoma (PDAC), has a dismal 5-year survival rate of less than 5%. Radical surgical resection, in combination with adjuvant chemotherapy, provides the best option for long-term patient survival. However, only approximately 20% of patients are resectable at the time of diagnosis, due to locally advanced or metastatic disease. There is an urgent need for the identification of new, specific, and more sensitive biomarkers for diagnosis, prognosis, and prediction to improve the treatment options for pancreatic cancer patients. Dysregulation of proteostasis is linked to many pathophysiological conditions, including various types of cancer. In this review, we report on findings relating to the main cellular protein degradation systems, the ubiquitin-proteasome system (UPS) and autophagy, in pancreatic cancer. The expression of several components of the proteolytic network, including E3 ubiquitinligases and deubiquitinating enzymes, are dysregulated in PDAC, which accounts for approximately 90% of all pancreatic malignancies. In the future, a deeper understanding of the emerging role of proteostasis in pancreatic cancer has the potential to provide clinically relevant biomarkers and new strategies for combinatorial therapeutic options to better help treat the patients.

Originalspråkengelska
Titel på gästpublikationPROTEOSTASIS AND DISEASE: FROM BASIC MECHANISMS TO CLINICS : From basic Mechanisms to Clinics
RedaktörerRosa Barrio, James D. Sutherland, Manuel S. Rodriguez
Antal sidor15
UtgivningsortCham
FörlagSpringer
Utgivningsdatum2020
Sidor101-115
ISBN (tryckt)978-3-030-38265-0
ISBN (elektroniskt)978-3-030-38266-7
DOI
StatusPublicerad - 2020
MoE-publikationstypA3 Del av bok eller annan forskningsbok

Publikationsserier

NamnAdvances in Experimental Medicine and Biology
FörlagSPRINGER INTERNATIONAL PUBLISHING AG
Volym1233
ISSN (tryckt)0065-2598

Vetenskapsgrenar

  • 3111 Biomedicinska vetenskaper
  • 1182 Biokemi, cell- och molekylärbiologi

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