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CancerQuest > Introduction to Patient Information > Introduction to Cancer by Type > Pancreatic Cancer: Introduction > Pancreatic Cancer: Tumor Biology

Pancreatic Cancer: Tumor Biology

More than 90% of pancreatic cancers are not known to be associated with an inherited defect. The cancer develops via the accumulation of mutations that occur over time. The genes thought to be involved in the development of pancreatic cancer include:⁽¹⁾

K-Ras
Ras is proto-oncogene. The protein product of the gene is involved in signal transduction. When mutated in a way that makes the protein constantly active, Ras can cause uncontrolled cell growth. 75-90% of pancreatic cancers involve a point mutation in this gene.

PTEN
The PTEN protein is a tumor suppressor that removes phosphate groups from targets (it is a phosphatase). Mutations which cause loss of function reduce the ability of cells to control cell division pathways.

HER2/neu
This is a growth factor receptor which lies on the external surface (plasma membrane) of cells. This is often mutated and overactive in breast cancer and has also been found to be altered in pancreatic cancer.

AKT2
AKT2 is a proto-oncogene that is amplified in 60% of pancreatic cancers. The protein product is an inhibitor of cell death (pro-apoptotic) proteins.

TP53
This tumor suppressor is is critical in the life:death decision in abnormal cells. More than 50% of pancreatic cancers have a loss-of-function in this key gene.

SHH
This gene produces a protein that regulates nervous system development and may play a role in the formation of pancreatic cancer.

There has also been recent discovery of pancreatic cancer stem cells (CSC) which may involved in the initiation and recurrence of cancer. Research is underway to target these CSCs.⁽²⁾

Learn more about cancer genes

References for this page:

1. Ghaneh P, Costello E, Neoptolemos JP. "Biology and Management of Pancreatic Cancer." Gut (2007); 56:1134-1152 [PUBMED]
2. Lee CJ, Dosch J, Simeone DM. "Pancreatic Cancer Stem Cells." Journal of Clinical Oncology (2008); 26(17):2806-12 [PUBMED]