Zavoral M, Minarikova P, Zavada F, Salek C, Minarik M. Molecular biology of pancreatic cancer. World J Gastroenterol 2011; 17(24): 2897-2908 [PMID: 21734801 DOI: 10.3748/wjg.v17.i24.2897]
Corresponding Author of This Article
Marek Minarik, PhD, Head, CEGES and Laboratory for Molecular Genetics and Oncology, Genomac International., Bavorska 856, 155 41 Prague 5, Czech Republic. mminarik@email.com
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World J Gastroenterol. Jun 28, 2011; 17(24): 2897-2908 Published online Jun 28, 2011. doi: 10.3748/wjg.v17.i24.2897
Molecular biology of pancreatic cancer
Miroslav Zavoral, Petra Minarikova, Filip Zavada, Cyril Salek, Marek Minarik
Miroslav Zavoral, Petra Minarikova, Filip Zavada, Charles University, 1st Medical Faculty, Internal Clinic, 128 00 Prague 2, Czech Republic
Miroslav Zavoral, Petra Minarikova, Filip Zavada, Central Military Hospital, 162 00 Prague 6, Czech Republic
Miroslav Zavoral, Petra Minarikova, Filip Zavada, Institute for postgraduate medical education, 141 00 Prague 4, Czech Republic
Cyril Salek, Institute of hematology and blood transfusion, 128 00 Prague 2, Czech Republic
Marek Minarik, Center for Applied Genomics of Solid Tumors (CEGES), Genomac International, 155 41 Prague 6, Czech Republic
Marek Minarik, Laboratory for Molecular Genetics and Oncology, Genomac International, 155 41 Prague 5, Czech Republic
Author contributions: Zavoral M performed the data analysis and literature search for the chronic pancreatitis, diabetes mellitus and molecular diagnostics sections; Minarikova P performed the data analysis and literature search for the risk factors and genetic susceptibility sections; Zavada F performed the data analysis and literature search for the molecular diagnostics section; Salek C performed the data analysis and literature search for the epidemiology and chronic pancreatitis sections; Minarik M contributed to the genetic susceptibility section, and performed the data analysis and literature search for the molecular mechanisms section; Zavoral M and Minarik M wrote the paper; Zavoral M, Minarikova P, Zavada F, Salek C and Minarik M revised and approved the final draft of the paper.
Supported by the Czech Ministry of Health Project 9809. It is a contribution No. 3 from CEGES (OPPK CZ.2.16/3.1.00/22213)
Correspondence to: Marek Minarik, PhD, Head, CEGES and Laboratory for Molecular Genetics and Oncology, Genomac International., Bavorska 856, 155 41 Prague 5, Czech Republic. mminarik@email.com
Telephone: +42-224-458048 Fax: +42-224-458021
Received: January 6, 2011 Revised: February 19, 2011 Accepted: February 26, 2011 Published online: June 28, 2011
Abstract
In spite of continuous research efforts directed at early detection and treatment of pancreatic cancer, the outlook for patients affected by the disease remains dismal. With most cases still being diagnosed at advanced stages, no improvement in survival prognosis is achieved with current diagnostic imaging approaches. In the absence of a dominant precancerous condition, several risk factors have been identified including family history, chronic pancreatitis, smoking, diabetes mellitus, as well as certain genetic disorders such as hereditary pancreatitis, cystic fibrosis, familial atypical multiple mole melanoma, and Peutz–Jeghers and Lynch syndromes. Most pancreatic carcinomas, however, remain sporadic. Current progress in experimental molecular techniques has enabled detailed understanding of the molecular processes of pancreatic cancer development. According to the latest information, malignant pancreatic transformation involves multiple oncogenes and tumor-suppressor genes that are involved in a variety of signaling pathways. The most characteristic aberrations (somatic point mutations and allelic losses) affect oncogenes and tumor-suppressor genes within RAS, AKT and Wnt signaling, and have a key role in transcription and proliferation, as well as systems that regulate the cell cycle (SMAD/DPC, CDKN2A/p16) and apoptosis (TP53). Understanding of the underlying molecular mechanisms should promote development of new methodology for early diagnosis and facilitate improvement in current approaches for pancreatic cancer treatment.
