The Intricate Metabolism of Pancreatic Cancers

  • Felipe Camelo
  • Anne LeEmail author
Part of the Advances in Experimental Medicine and Biology book series (AEMB, volume 1063)


Currently, approximately 95% of pancreatic cancers are pancreatic ductal adenocarcinoma (PDAC), which is the most aggressive form and the fourth leading cause of cancer death with extremely poor prognosis [1]. Poor prognosis is primarily attributed to the late diagnosis of the disease when patients are no longer candidates for surgical resection [2]. Cancer cells are dependent on the oncogenes that allow them to proliferate limitlessly. Thus, targeting the expression of known oncogenes in pancreatic cancer has been shown to lead to more effective treatment [3]. This chapter will discuss the complexity of metabolic features in pancreatic cancers. To be able to fully comprehend the heterogeneous nature of cancer metabolism, we need to take into account the close relationship between cancer metabolism and genetics. Gene expression varies tremendously, not only among different types of cancers, but also within the same type of cancer among different patients. Cancer metabolism heterogeneity is often prompted and perpetuated not only by genetic mutations in oncogenes and tumor suppressor genes but also by the innate diversity of the tumor microenvironment. Much effort has been focused on elucidating the genetic alterations that correlate with disease progression and treatment response [4]. However, the precise mechanism by which tumor metabolism contributes to cancer growth, survival, mobility, and aggressiveness represents a functional readout of tumor progression.


Pancreatic ductal adenocarcinoma KRAS mutation Glucose metabolism Glutamine metabolism Combined therapy 





Epidermal growth factor receptor




Glutamate dehydrogenase 1


Glucose transporter


Glutamic-oxaloacetic transaminase 1


Hypoxia-inducible factor 1-alpha


Hexokinase 2


Kirsten rat sarcoma viral oncogene homolog


Lactate dehydrogenase


Monocarboxylate transporter




Pancreatic ductal adenocarcinoma


Phosphofructokinase 1


Tricarboxylic acid cycle


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Copyright information

© Springer International Publishing AG, part of Springer Nature 2018

Authors and Affiliations

  1. 1.Department of PathologyJohns Hopkins University School of MedicineBaltimoreUSA
  2. 2.Department of Pathology and OncologyJohns Hopkins University School of MedicineBaltimoreUSA

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