ABSRACT The development of hepatocellular car-cinoma(HCC)is closely related to the formation of tumour blood vessels.VEGF-mediated angiogenesis is a major driver of the immune escape response in tumours.VEGF binds to vascular endothelial growth factor receptor2(VEGFR2)on endothelial cells,promoting endothelial cell proliferation and migration,inducing vascular changes in HCC,and thus promote the growth of hepatocellular carcino-ma cells.Anti-VEGF and its receptor-targeted mo-lecular drugs are currently effective new treat-ments for HCC.Monoclonal antibodies against VEGF and small-molecule tyrosine kinase inhibitors targeting VEGF have been shown to block its angio-genic activity,alleviate the inhibitory effect of the tumour microenvironment,and ultimately achieve tumour regression.This article provides a review of the research progress of VEGF/VEGFR inhibitors in HCC treatment.

ABSRACT The development of hepatocellular car-cinoma(HCC)is closely related to the formation of tumour blood vessels.VEGF-mediated angiogenesis is a major driver of the immune escape response in tumours.VEGF binds to vascular endothelial growth factor receptor2(VEGFR2)on endothelial cells,promoting endothelial cell proliferation and migration,inducing vascular changes in HCC,and thus promote the growth of hepatocellular carcino-ma cells.Anti-VEGF and its receptor-targeted mo-lecular drugs are currently effective new treat-ments for HCC.Monoclonal antibodies against VEGF and small-molecule tyrosine kinase inhibitors targeting VEGF have been shown to block its angio-genic activity,alleviate the inhibitory effect of the tumour microenvironment,and ultimately achieve tumour regression.This article provides a review of the research progress of VEGF/VEGFR inhibitors in HCC treatment.

ABSRACT The development of hepatocellular car-cinoma(HCC)is closely related to the formation of tumour blood vessels.VEGF-mediated angiogenesis is a major driver of the immune escape response in tumours.VEGF binds to vascular endothelial growth factor receptor2(VEGFR2)on endothelial cells,promoting endothelial cell proliferation and migration,inducing vascular changes in HCC,and thus promote the growth of hepatocellular carcino-ma cells.Anti-VEGF and its receptor-targeted mo-lecular drugs are currently effective new treat-ments for HCC.Monoclonal antibodies against VEGF and small-molecule tyrosine kinase inhibitors targeting VEGF have been shown to block its angio-genic activity,alleviate the inhibitory effect of the tumour microenvironment,and ultimately achieve tumour regression.This article provides a review of the research progress of VEGF/VEGFR inhibitors in HCC treatment.

ABSRACT The development of hepatocellular car-cinoma(HCC)is closely related to the formation of tumour blood vessels.VEGF-mediated angiogenesis is a major driver of the immune escape response in tumours.VEGF binds to vascular endothelial growth factor receptor2(VEGFR2)on endothelial cells,promoting endothelial cell proliferation and migration,inducing vascular changes in HCC,and thus promote the growth of hepatocellular carcino-ma cells.Anti-VEGF and its receptor-targeted mo-lecular drugs are currently effective new treat-ments for HCC.Monoclonal antibodies against VEGF and small-molecule tyrosine kinase inhibitors targeting VEGF have been shown to block its angio-genic activity,alleviate the inhibitory effect of the tumour microenvironment,and ultimately achieve tumour regression.This article provides a review of the research progress of VEGF/VEGFR inhibitors in HCC treatment.

ABSRACT The development of hepatocellular car-cinoma(HCC)is closely related to the formation of tumour blood vessels.VEGF-mediated angiogenesis is a major driver of the immune escape response in tumours.VEGF binds to vascular endothelial growth factor receptor2(VEGFR2)on endothelial cells,promoting endothelial cell proliferation and migration,inducing vascular changes in HCC,and thus promote the growth of hepatocellular carcino-ma cells.Anti-VEGF and its receptor-targeted mo-lecular drugs are currently effective new treat-ments for HCC.Monoclonal antibodies against VEGF and small-molecule tyrosine kinase inhibitors targeting VEGF have been shown to block its angio-genic activity,alleviate the inhibitory effect of the tumour microenvironment,and ultimately achieve tumour regression.This article provides a review of the research progress of VEGF/VEGFR inhibitors in HCC treatment.

ABSRACT The development of hepatocellular car-cinoma(HCC)is closely related to the formation of tumour blood vessels.VEGF-mediated angiogenesis is a major driver of the immune escape response in tumours.VEGF binds to vascular endothelial growth factor receptor2(VEGFR2)on endothelial cells,promoting endothelial cell proliferation and migration,inducing vascular changes in HCC,and thus promote the growth of hepatocellular carcino-ma cells.Anti-VEGF and its receptor-targeted mo-lecular drugs are currently effective new treat-ments for HCC.Monoclonal antibodies against VEGF and small-molecule tyrosine kinase inhibitors targeting VEGF have been shown to block its angio-genic activity,alleviate the inhibitory effect of the tumour microenvironment,and ultimately achieve tumour regression.This article provides a review of the research progress of VEGF/VEGFR inhibitors in HCC treatment.

ABSRACT The development of hepatocellular car-cinoma(HCC)is closely related to the formation of tumour blood vessels.VEGF-mediated angiogenesis is a major driver of the immune escape response in tumours.VEGF binds to vascular endothelial growth factor receptor2(VEGFR2)on endothelial cells,promoting endothelial cell proliferation and migration,inducing vascular changes in HCC,and thus promote the growth of hepatocellular carcino-ma cells.Anti-VEGF and its receptor-targeted mo-lecular drugs are currently effective new treat-ments for HCC.Monoclonal antibodies against VEGF and small-molecule tyrosine kinase inhibitors targeting VEGF have been shown to block its angio-genic activity,alleviate the inhibitory effect of the tumour microenvironment,and ultimately achieve tumour regression.This article provides a review of the research progress of VEGF/VEGFR inhibitors in HCC treatment.

ABSRACT The development of hepatocellular car-cinoma(HCC)is closely related to the formation of tumour blood vessels.VEGF-mediated angiogenesis is a major driver of the immune escape response in tumours.VEGF binds to vascular endothelial growth factor receptor2(VEGFR2)on endothelial cells,promoting endothelial cell proliferation and migration,inducing vascular changes in HCC,and thus promote the growth of hepatocellular carcino-ma cells.Anti-VEGF and its receptor-targeted mo-lecular drugs are currently effective new treat-ments for HCC.Monoclonal antibodies against VEGF and small-molecule tyrosine kinase inhibitors targeting VEGF have been shown to block its angio-genic activity,alleviate the inhibitory effect of the tumour microenvironment,and ultimately achieve tumour regression.This article provides a review of the research progress of VEGF/VEGFR inhibitors in HCC treatment.

Background::The conversion of adenosine (A) to inosine (I) through deamination is the prevailing form of RNA editing, impacting numerous nuclear and cytoplasmic transcripts across various eukaryotic species. Millions of high-confidence RNA editing sites have been identified and integrated into various RNA databases, providing a convenient platform for the rapid identification of key drivers of cancer and potential therapeutic targets. However, the available database for integration of RNA editing in hematopoietic cells and hematopoietic malignancies is still lacking.Methods::We downloaded RNA sequencing (RNA-seq) data of 29 leukemia patients and 19 healthy donors from National Center for Biotechnology Information (NCBI) Gene Expression Omnibus (GEO) database, and RNA-seq data of 12 mouse hematopoietic cell populations obtained from our previous research were also used. We performed sequence alignment, identified RNA editing sites, and obtained characteristic editing sites related to normal hematopoietic development and abnormal editing sites associated with hematologic diseases.Results::We established a new database, "REDH", represents RNA editome in hematopoietic differentiation and malignancy. REDH is a curated database of associations between RNA editome and hematopoiesis. REDH integrates 30,796 editing sites from 12 murine adult hematopoietic cell populations and systematically characterizes more than 400,000 edited events in malignant hematopoietic samples from 48 cohorts (human). Through the Differentiation, Disease, Enrichment, and knowledge modules, each A-to-I editing site is systematically integrated, including its distribution throughout the genome, its clinical information (human sample), and functional editing sites under physiological and pathological conditions. Furthermore, REDH compares the similarities and differences of editing sites between different hematologic malignancies and healthy control.Conclusions::REDH is accessible at http://www.redhdatabase.com/. This user-friendly database would aid in understanding the mechanisms of RNA editing in hematopoietic differentiation and malignancies. It provides a set of data related to the maintenance of hematopoietic homeostasis and identifying potential therapeutic targets in malignancies.

Epitranscriptomics focuses on the RNA-modification-mediated post-transcriptional regulation of gene expression. The past decade has witnessed tremendous progress in our understanding of the landscapes and biological functions of RNA modifications, as prompted by the emergence of potent analytical approaches. The hematopoietic system provides a lifelong supply of blood cells, and gene expression is tightly controlled during the differentiation of hematopoietic stem cells (HSCs). The dysregulation of gene expression during hematopoiesis may lead to severe disorders, including acute myeloid leukemia (AML). Emerging evidence supports the involvement of the mRNA modification system in normal hematopoiesis and AML pathogenesis, which has led to the development of small-molecule inhibitors that target N6-methyladenosine (m 6A) modification machinery as treatments. Here, we summarize the latest findings and our most up-to-date information on the roles of m 6A and N7-methylguanine in both physiological and pathological conditions in the hematopoietic system. Furthermore, we will discuss the therapeutic potential and limitations of cancer treatments targeting m 6A.