Pancreatic cancer: molecular targets for therapy (EC, 2015)



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Encyclopedia of cancer (2015)


Pancreatic cancer, synonym pancreas cancer, is a virulent disease with no effective therapy besides surgical resection. The possibility for surgical tumor removal is limited by early metastatic spread of tumor to sites outside the pancreas. The survival for patients with metastatic pancreatic cancer is less than 1 year following diagnosis. Clinicians must translate the available knowledge of the molecular basis of this disease into rationale and effective therapeutic strategies for treatment.

Pancreas cancer is one of the tumors with the highest number of genetic mutations of any solid malignancy. These include oncogenes, tumor suppressor genes, and DNA-stability genes. The stability genes include mismatch repair (MMR) and base excision repair (BER) genes, which control the mutation rate of other genes. A number of genetic alterations have been, and still are being, tested as molecular target for antipancreatic cancer therapy. It is clear that novel molecular targets and strategies need to be developed for the treatment of pancreatic cancer.


Pancreatic cancer ranks 13th in incidence but eighth as a cause of cancer death worldwide. In the United States and Europe, pancreatic cancer is the fourth leading cause of cancer death in both men and women. Chemotherapy and radiation therapy have had little impact on survival, prompting the National Cancer Institute to declare that survival for pancreatic cancer has remained unchanged for three decades and its treatment has consistently been identified as an area of unmet medical need.


K-Ras Oncogene

The KRas proto-oncogene is the most commonly mutated gene in pancreatic cancer. K-Ras is a member of the RAS family GTP-binding proteins and has intrinsic GTPase activity. The Ras proteins mediate a wide variety of cellular functions including proliferation, differentiation, and survival by transduction of growth-promoting signals from the cell-surface tyrosine kinase receptors to intracellular pathways. Activating K-Ras point mutations at codon 12 result in substitution of amino acids and are early genetic alterations, occurring in 30 % of early pancreatic neoplasms and with a frequency approaching 100 % in advanced pancreatic adenocarcinoma.

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