| Literature DB >> 31092057 |
Seyed Mostafa Parizadeh1, Seyed Alireza Parizadeh1, Mohadese Alizade-Noghani1, Reza Jafarzadeh-Esfehani2, Maryam Ghandehari1,3, Ali Mottaghi-Moghaddam1, Fatemeh Goldani1, Majid Khazaei1, Majid Ghayour-Mobarhan1,4, Gordon A Ferns5, Seyed Mahdi Hassanian1, Amir Avan1,4,6.
Abstract
Introduction: Colorectal cancer (CRC) is a common malignancy, ranking fourth among the causes of cancer-related deaths globally. Its incidence has increased in recent decades, and now more than one million CRC patients are diagnosed and thousands die annually. The 5-year survival rate varies with the stage at diagnosis, are approximately 90% in the early stages of disease, and less than 10% in advanced disease. Non-alcoholic fatty liver disease (NAFLD), which is a major cause of chronic liver disease, and characterized by the accumulation of fat in hepatocytes, has also emerged as a risk factor for CRC, and to be related with the development of colorectal polyps. Areas covered: The purpose of this current review is to summarize the main findings of studies that have investigated the role of NAFLD in development of CRC. Expert opinion: Various molecular pathways are altered during the development of NAFLD, which are also important in CRC tumorigenesis. There is growing body of evidence showing the potential role of activation of pro-inflammatory, disruption of anti-inflammatory pathways, increasing the activity of pathways involved in cell proliferation/survival. Thus targeting these dysregulated pathways via novel inhibitors can be a potential therapy for CRC prevention in cases with NAFLD.Entities:
Keywords: Non-alcoholic fatty liver disease; colorectal cancer; diabetes; dyslipidemia; metabolic syndrome; polyp
Mesh:
Year: 2019 PMID: 31092057 DOI: 10.1080/17474124.2019.1617696
Source DB: PubMed Journal: Expert Rev Gastroenterol Hepatol ISSN: 1747-4124 Impact factor: 3.869