Title:Kirsten Rat Sarcoma Viral Oncogene Homologue (KRAS) Mutations in the Occurrence and Treatment of Pancreatic Cancer
VOLUME: 19 ISSUE: 23
Author(s):Ziying Zhu, Saisong Xiao, Haojie Hao*, Qian Hou* and Xiaobing Fu*
Affiliation:Institute of Basic Medical Science, Wound Healing and Cell Biology Laboratory, Chinese PLA General Hospital, 100039 Beijing, Department of Anesthesia, Dongzhimen Hospital, Beijing University of Chinese Medicine, 100700 Beijing, Institute of Basic Medical Science, Wound Healing and Cell Biology Laboratory, Chinese PLA General Hospital, 100039 Beijing, Institute of Basic Medical Science, Wound Healing and Cell Biology Laboratory, Chinese PLA General Hospital, 100039 Beijing, Institute of Basic Medical Science, Wound Healing and Cell Biology Laboratory, Chinese PLA General Hospital, 100039 Beijing
Keywords:Pancreatic cancer, Drug screening, KRAS mutations, Chemistry drugs, Precision treatment, Malignant tumor.
Abstract:Pancreatic cancer is a highly malignant tumor with a 5-year survival rate of less than 6%, and
incidence increasing year by year globally. Pancreatic cancer has a poor prognosis and a high recurrence
rate, almost the same as the death rate. However, the available effective prevention and treatment measures
for pancreatic cancer are still limited. The genome variation is one of the main reasons for the development
of pancreatic cancer. In recent years, with the development of gene sequencing technology,
in-depth research on pancreatic cancer gene mutation presents that a growing number of genetic mutations
are confirmed to be in a close relationship with invasion and metastasis of pancreatic cancer.
Among them, KRAS mutation is a special one. Therefore, it is particularly important to understand the
mechanism of the KRAS mutation in the occurrence and development of pancreatic cancer, and to explore
the method of its transformation into clinical tumor molecular targeted treatment sites, to further
improve the therapeutic effect on pancreatic cancer. Therefore, to better design chemical drugs, this review
based on the biological functions of KRAS, summarized the types of KRAS mutations and their
relationship with pancreatic cancer and included the downstream signaling pathway Raf-MEK-ERK,
PI3K-AKT, RalGDS-Ral of KRAS and the current medicinal treatment methods for KRAS mutations.
Moreover, drug screening and clinical treatment for KRAS mutated cell and animal models of pancreatic
cancer are also reviewed along with the prospect of targeted medicinal chemistry therapy for precision
treatment of pancreatic cancer in the future.