Journal Basic Info

  • Impact Factor: 2.709**
  • H-Index: 11 
  • ISSN: 2474-1663
  • DOI: 10.25107/2474-1663
**Impact Factor calculated based on Google Scholar Citations. Please contact us for any more details.

Major Scope

  •  Sarcomas
  •  Carcinomas
  •  Cervical Cancer
  •  Gastrointestinal Cancer
  •  Blood Cancer
  •  Targeted Therapy
  •  Thoracic Oncology
  •  Urological Cancers

Abstract

Citation: Clin Oncol. 2016;1(1):1123.DOI: 10.25107/2474-1663.1123

Diabetes Mellitus and Reprogrammed Glucose Metabolism in Pancreatic Cancer: Features for Clinical Translation

Daniela Basso, Andrea Padoan, Paola Fogar, Carlo-Federico Zambon and Mario Plebani


Department of Medicine–DIMED, University of Padova, Italy

*Correspondance to: Daniela Basso 

 PDF  Full Text Review Article | Open Access

Abstract:

The reprogrammed metabolism of cancer cells underlies the shift of glucose energetics from the highly efficient oxidative phosphorylation to the less efficient aerobic glycolysis, the Warburg effect. This phenomenon, with the activation of the glutamine pathway, advantages survival and proliferation of pancreatic ductal adenocarcinoma (PDAC) cells, which live in an adverse hypoxic and nutrient restricted microenvironment. In PDAC, glucose metabolic alterations occur also at the whole organism, Diabetes Mellitus (DM) being diagnosed in approximately 60% to 80% of patients. The association between PDAC and DM is a dual face phenomenon, DM being both a risk factor for and a consequence of this tumor type. Data from epidemiology indicate that longstanding DM increases PDAC risk 1.5 to 2.0 fold, probably because of the pro-proliferative effects of hyperinsulinemia. By contrast early onset DM, i.e. diabetes diagnosed no more than two years prior to cancer diagnosis, is considered a consequence of PDAC. Secondary DM is due to complex interactions between tumor cells, tumor microenvironment and pancreatic endocrine cells. In this scenario the role of the inflammatory S100A8 calcium binding protein, matrix metalloproteinases, Vanin1 or amylin has been experimentally demonstrated. However, the efforts made to translate in the clinical practice any individual new poteantial biomarker failed, because none reached enough sensitivity and specificity to be considered a reliable biomarker to diagnose PDAC even in high risk subjects as those with new onset DM. Therefore the identification and clinical validation of new biomarkers remains a challenge for future studies.

Keywords:

Cite the Article:

Basso D, Padoan A, Fogar P, Zambon C-F, Plebani M. Diabetes Mellitus and Reprogrammed Glucose Metabolism in Pancreatic Cancer: Features for Clinical Translation. Clin Oncol. 2016; 1: 1123.

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