An Overview of Genetic Changes and Risk of Pancreatic Ductal Adenocarcinoma

Abstract

The pancreatic carcinoma is a leading cause of death in cancer carriers worldwide. The early diagnostic is difficult due to late stage during diagnosis, lack of characteristic symptoms and also multifactor basis. In cancer development take part both, environmental and genetic factors, alone or in conjunction with each other. The nonspecific biomarkers of cancers are a reason for the search for more accurate factors which allow for fast and personalized diagnostics. Some of cancers have identified molecular (metabolic, biochemical or genetic) markers but in most cases the only clue is patient`s interview and abnormal levels of organ functions markers.Possible genetic basis of cancer suggests to widen studies on connection between environmental factors with both, nuclear and mitochondrial, genes changes.

Impact of genetic variants of ABCB1, APOB, CAV1, and NAMPT on susceptibility to pancreatic ductal adenocarcinoma in Chinese patients

“…Pancreatic cancer remains one of the most lethal malignancies, with poor prognoses and a mortality/incidence ratio of 94% (Bray et al, 2018). Due to its atypical clinical features, nonspecific, diagnostic tools which lack specificity and no definitive cures for patients with advanced‐stage pancreatic cancer, the 1‐year survival rate of pancreatic cancer has been significantly reduced from 25% to <5% (Sarnecka, Zagozda, & Durlik, 2016). Despite advances in our understanding of this disease and potential risk factors, and advances in diagnostic tools to improve early detection, the incidence is estimated to increase with a predicted 355,317 new cases globally in 2040 (Rawla et al, 2019).…”

Multi-omic molecular comparison of primary versus metastatic pancreatic tumours

“…4 A majority of these patients ultimately develop distant recurrence and outcomes for unresectable or advanced-stage disease remain poor. 5 For patients with metastatic pancreatic cancer, combination systemic therapies with gemcitabine/nabpaclitaxel or FOLFIRINOX have resulted only in modest improvements in outcome. 6,7 In pancreatic cancer, whole-genome sequencing reveals a complex mutational landscape.…”

“…8 Currently, the molecular biology that links genetic changes to the aggressive nature of pancreatic cancer remains poorly defined. 5 These mutations allow for a survival and growth advantage to pancreatic cancer, as demonstrated by invasive and metastatic phenotypes that are resistant to conventional treatment strategies. 5 In certain tumour types, such as breast, lung, prostate, renal cell, uterus, ovary and colorectal cancers, it has been well established that the genomic landscape of metastases is altered from that of the primary tumour.…”

“…5 These mutations allow for a survival and growth advantage to pancreatic cancer, as demonstrated by invasive and metastatic phenotypes that are resistant to conventional treatment strategies. 5 In certain tumour types, such as breast, lung, prostate, renal cell, uterus, ovary and colorectal cancers, it has been well established that the genomic landscape of metastases is altered from that of the primary tumour. [9][10][11] This is likely due to the development of certain molecular alterations that allow for a growth and invasion advantage to the metastatic cell.…”

Network analyses of circular RNAs expression profiles and their hub genes in pancreatic ductal adenocarcinoma

“…Beside the dietary habit and environmental factors, PDAC is also related with genetic basis. The family history of pancreatic carcinoma is predisposing to increased risk in direct relatives [3].…”