Cellular mechanisms and signal pathways transduction in pancreatic cancer

01/2018

As. RNDr. Ing. Libor Staněk, PCTM^1,2,3; prof. MUDr. Robert Gurlich, DrSc.³; doc. MUDr. Petra Tesařová, CSc.²; Mgr. Zdeněk Musil⁴; prof. MUDr. Luboš Petruželka, CSc.²

1) Ústav patologie FN Královské Vinohrady, Praha

2) Onkologická klinika 1. LF UK a VFN, Praha

3) Chirurgická klinika 3. LF UK a FN Královské Vinohrady, Praha

4) Ústav biologie a lékařské genetiky 1. LF UK a VFN, Praha

SUMMARY

Pancreatic cancer is one of the most severe types of human tumors. It is the second most common cause of cancer deaths in the world. Worldwide, more than 300,000 new diseases are diagnosed annually and approximately the same number of patients die of this disease. In 2015, the incidence of 20/100,000 inhabitants in the Czech Republic was the second highest in the world. Despite all the advances in modern oncology treatment, the long-term survival of people with this type of malignant growth is rather exceptional. Therefore, attention is focused on the genetic causes of this cancer. Essentially, this is a genetic disease where the exact sequence of somatic DNA mutations with a multistage process is known, with the cumulative effect of mutations obtained in both coding and regulatory genes, changes in ploidy, gene amplification, structural rearrangement, deletion or loss of heterozygosity. The most frequent mutations occur in the protooncogenes of K-ras and tumor suppressor genes p16, p53, BRCA2 and DPC4/SMAD4, leading to malignant change of the epithelium of leads.

KEY WORDS

pancreatic carcinoma, mutation, KRAS, HER2/neu, tumor-suppressor gene