Pancreatic cancer is a common malignant disease with a poor prognosis and low survival rate. This is primarily due to the late detection of the disease which becomes rapidly aggressive to an advanced stage in addition to having high recurrence and resistance to therapeutic approaches and treatment. Pancreatic ductal adenocarcinomas (PDACs) harbor mutated genes that aggregate into many various pathways including KRAS, TGF-ß, WNT, NOTCH, ROBO/SLIT signalling, G1/S transition, SWI-SNF, chromatin modification, DNA repair and RNA processing.
Pancreatic cancers are hypothesized to arise from a small population of abnormal cancer stem cells (CSCs) that promote tumorigenesis, metastasis and therapeutic resistance. The molecular markers CD133, CXCR4, DCLK1, c-MET, ABCG2 and Lgr5 are routinely used to detect and observe pathologic behaviours of pancreatic cancer stem cells (PCSCs). CSCs increase in number by undergoing symmetric cell division which generates two identical pluripotent daughter cells. CSCs can self-renew through asymmetric cell division, which produces a tumor progenitor cell (TPC) and a daughter cell possessing stem-cell properties. The delicate balance between symmetric and asymmetric cellular division is tightly controlled by various oncogenes that employ the Hedgehog, Notch and Wnt signalling mediators. A complex network of oncogenes, tumour suppressor genes and related molecules cooperate to initiate and promote pancreatic cancer development and progression. In particularly, cancer stem cell formation and function will be crucial for multi-drug resistance, early relapse and recurrence, local invasion and distant metastasis, which jointly leads to dismal prognosis of pancreatic cancer (with the lowest 5-year survival rate among all malignancies). The network is regulated in response to selective pressure under stress and treatment (including surgery, chemotherapy, radiotherapy, molecular targeted therapy and immunotherapy).
The aim of this Research Topic is to discuss how stem cells impact pancreatic cancer and whether they provide a potential therapeutic approach towards treatment for patients. We welcome Original Research, Review Articles, Systematic Reviews and Mini-Reviews.
Please note: manuscripts consisting solely of bioinformatics or computational analysis of public genomic or transcriptomic databases which are not accompanied by validation (independent cohort or biological validation in vitro or in vivo) are out of scope for this section and will not be accepted as part of this Research Topic.
Pancreatic cancer is a common malignant disease with a poor prognosis and low survival rate. This is primarily due to the late detection of the disease which becomes rapidly aggressive to an advanced stage in addition to having high recurrence and resistance to therapeutic approaches and treatment. Pancreatic ductal adenocarcinomas (PDACs) harbor mutated genes that aggregate into many various pathways including KRAS, TGF-ß, WNT, NOTCH, ROBO/SLIT signalling, G1/S transition, SWI-SNF, chromatin modification, DNA repair and RNA processing.
Pancreatic cancers are hypothesized to arise from a small population of abnormal cancer stem cells (CSCs) that promote tumorigenesis, metastasis and therapeutic resistance. The molecular markers CD133, CXCR4, DCLK1, c-MET, ABCG2 and Lgr5 are routinely used to detect and observe pathologic behaviours of pancreatic cancer stem cells (PCSCs). CSCs increase in number by undergoing symmetric cell division which generates two identical pluripotent daughter cells. CSCs can self-renew through asymmetric cell division, which produces a tumor progenitor cell (TPC) and a daughter cell possessing stem-cell properties. The delicate balance between symmetric and asymmetric cellular division is tightly controlled by various oncogenes that employ the Hedgehog, Notch and Wnt signalling mediators. A complex network of oncogenes, tumour suppressor genes and related molecules cooperate to initiate and promote pancreatic cancer development and progression. In particularly, cancer stem cell formation and function will be crucial for multi-drug resistance, early relapse and recurrence, local invasion and distant metastasis, which jointly leads to dismal prognosis of pancreatic cancer (with the lowest 5-year survival rate among all malignancies). The network is regulated in response to selective pressure under stress and treatment (including surgery, chemotherapy, radiotherapy, molecular targeted therapy and immunotherapy).
The aim of this Research Topic is to discuss how stem cells impact pancreatic cancer and whether they provide a potential therapeutic approach towards treatment for patients. We welcome Original Research, Review Articles, Systematic Reviews and Mini-Reviews.
Please note: manuscripts consisting solely of bioinformatics or computational analysis of public genomic or transcriptomic databases which are not accompanied by validation (independent cohort or biological validation in vitro or in vivo) are out of scope for this section and will not be accepted as part of this Research Topic.