Objective To summarize the progress in related basic research of molecular targeted therapy in pancreatic cancer. Method The relevant literatures on oncogenes, epigenome, tumour microenvironment and immunotherapy in recent years at home and abroad were reviewed. ResultsIn basic research, molecularly targeted drugs had shown some efficacy in the treatment of progression of pancreatic cancer, however, in clinical trials, more satisfactory results were not achieved. Conclusion Molecularly targeted therapies for pancreatic cancer are still at a preliminary stage of exploration, and basic research has not yet been effectively translated clinically, which requires further exploration efforts in subsequent studies to provide a more solid and reliable basis for precise treatment of pancreatic cancer and achieve better clinical benefits.
Objective To summarize the advance in targeted therapy for radioactive iodine-refractory differentiated thyroid cancer (RAIR-DTC). Method The literatures relevant to the targeted therapy for RAIR-DTC were reviewed and summarized. Results Targeted therapy for RAIR-DTC mainly included multi-kinase inhibitors suppressing angiogenesis and mutation-specific kinase inhibitors targeting specific mutations. Representative multi-kinase inhibitors such as sorafenib and lenvatinib, which significantly prolonged progression-free survival, had been approved to put into clinical use, though there were shortcomings such as adverse effects and resistance. Mutation-specific kinase inhibitors acted on targets such as RET, mitogen-activated protein kinase pathway, phosphoinositide 3-kinase pathway respectively, with relatively small side effects, most of which had only been applied in clinical trials up to now. Conclusions Targeted therapy for RAIR-DTC has made rapid progress in recent years, filling the gap in treatment for RAIR-DTC. Further explorations and investigations are needed to establish a more effect and safer treatment mode.
ObjectiveTo summarize the research progress of KRAS mutation in pancreatic tumorigenesis and therapy.MethodThe research progress of KRAS mutation in pancreatic tumorigenesis and therapy were summarized by reading the domestic and international literatures published in recent years.ResultsPancreatic cancer had the title of " king of cancer”. More than 90% of pancreatic cancer patients had KRAS mutation. KRAS had a complex relationship with pancreatic cancer through downstream signaling pathways, including Raf (rapidly accelerated fibrosarcoma)-mitogen-activated protein kinase kinase (MEK)-extracellular signal-regulated kinase (ERK), phosphatidylinositol-4, 5-bisphosphate 3-kinase (PI3K)-protein kinase B (AKT), and RalGDS-Ral. Although basic research on pancreatic cancer was deepening, there was still a lack of effective molecular targeted drugs.ConclusionsKRASgene plays an important role in the occurrence of pancreatic cancer. The treatment associated with KRAS mutation provides a more effective prognostic possibility for pancreatic cancer patients.
ObjectiveThis study aims to systematically review the dynamic evolution mechanisms of the tumor microenvironment (TME) in colorectal cancer liver metastasis (CRLM), to provide a theoretical basis for developing early diagnostic biomarkers and novel therapeutic targets for CRLM. MethodsBy integrating existing research, this review focuses on the key multi-step processes involved in CRLM-TME formation. It elaborates on the complex interactions among tumor cells, stromal cells, immune components, and key signaling pathways during this process, with an emphasis on their multi-factorial interplay. ResultsThe formation of the CRLM-TME involves several key steps: remote regulation by the primary tumor, specific recruitment of immune cells, adaptive remodeling of the liver microenvironment, and final colonization of the metastatic sites. This process is collectively driven by various factors such as tumor-derived metabolites, specific immune cell subsets, stromal components, and neovascularization, ultimately acts on the entire cascade of colorectal cancer cell invasion, migration, and colonization into the liver. ConclusionsThe CRLM-TME plays a critical role in the development, progression, treatment and drug resistance of CRLM. In-depth exploration of its mechanisms can provide direction for the development of early diagnostic biomarkers and therapies targeting the CRLM-TME, thereby aiming to improve the prognosis of CRLM patients.
