Genetics, Genomics and Emerging Molecular Therapies of Pancreatic Cancer
Author:
Liu Jakub1, Mroczek Magdalena2ORCID, Mach Anna34, Stępień Maria5ORCID, Aplas Angelika4, Pronobis-Szczylik Bartosz4, Bukowski Szymon4, Mielczarek Magda16ORCID, Gajewska Ewelina4, Topolski Piotr4, Król Zbigniew J.4ORCID, Szyda Joanna16ORCID, Dobosz Paula4
Affiliation:
1. Biostatistics Group, Wroclaw University of Environmental and Life Sciences, 51-631 Wroclaw, Poland 2. Centre for Cardiovascular Genetics and Gene Diagnostics, Foundation for People with Rare Diseases, Wagistrasse 25, 8952 Schlieren, Switzerland 3. Department of Psychiatry, Medical University of Warsaw, 00-665 Warsaw, Poland 4. Central Clinical Hospital of Ministry of the Interior and Administration in Warsaw, 02-507 Warsaw, Poland 5. Department of Infectious Diseases, Doctoral School, Medical University of Lublin, 20-059 Lublin, Poland 6. National Research Institute of Animal Production, Krakowska 1, 32-083 Balice, Poland
Abstract
The number of cases of pancreatic cancers in 2019 in Poland was 3852 (approx. 2% of all cancers). The course of the disease is very fast, and the average survival time from the diagnosis is 6 months. Only <2% of patients live for 5 years from the diagnosis, 8% live for 2 years, and almost half live for only about 3 months. A family predisposition to pancreatic cancer occurs in about 10% of cases. Several oncogenes in which somatic changes lead to the development of tumours, including genes BRCA1/2 and PALB2, TP53, CDKN2A, SMAD4, MLL3, TGFBR2, ARID1A and SF3B1, are involved in pancreatic cancer. Between 4% and 10% of individuals with pancreatic cancer will have a mutation in one of these genes. Six percent of patients with pancreatic cancer have NTRK pathogenic fusion. The pathogenesis of pancreatic cancer can in many cases be characterised by homologous recombination deficiency (HRD)—cell inability to effectively repair DNA. It is estimated that from 24% to as many as 44% of pancreatic cancers show HRD. The most common cause of HRD are inactivating mutations in the genes regulating this DNA repair system, mainly BRCA1 and BRCA2, but also PALB2, RAD51C and several dozen others.
Subject
Cancer Research,Oncology
Reference201 articles.
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