Since the relationship between angiogenesis and tumor growth was established by Folkman in 1971, scientists have made efforts exploring the possibilities in treating cancer by targeting angiogenesis. Inhibition of angiogenesis growth factors and administration of angiogenesis inhibitors are the basics of anti-angiogenesis therapy. Transfer of anti-angiogenesis genes has received attention recently not only because of the advancement of recombinant vectors, but also because of the localized and sustained expression of therapeutic gene product inside the tumor after gene transfer. This review provides the up-to-date information about the strategies and the vectors studied in the field of anti-angiogenesis cancer gene therapy.
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http://dx.doi.org/10.3748/wjg.v12.i43.6941 | DOI Listing |
JCI Insight
January 2025
Medical Oncology Department, Research Institute for Medical Innovation, Radboud University Medical Center, Nijmegen, Netherlands.
Background: Previously, we demonstrated that changes in circulating tumor DNA (ctDNA) are promising biomarkers for early response prediction (ERP) to immune checkpoint inhibitors (ICI) in metastatic urothelial cancer (mUC). In this study, we investigated the value of whole blood immunotranscriptomics for ERP-ICI and integrated both biomarkers into a multimodal model to boost accuracy.
Methods: Blood samples of 93 patients were collected at baseline and after 2-6 weeks of ICI for ctDNA (N=88) and immunotranscriptome (N=79) analyses.
J Clin Invest
January 2025
Division of Pediatric Hematology/Oncology, Department of Pediatrics, Pennsylvania State University College of Medicine, Hershey, United States of America.
Although nucleoporin 98 (NUP98) fusion oncogenes often drive aggressive pediatric leukemia by altering chromatin structure and expression of HOX genes, underlying mechanisms remain elusive. Here, we report that a Hoxb-associated lncRNA HoxBlinc was aberrantly activated in NUP98-PHF23 fusion-driven leukemias. HoxBlinc chromatin occupancies led to elevated MLL1 recruitment and aberrant homeotic topologically associated domains (TADs) that enhanced chromatin accessibilities and activated homeotic/hematopoietic oncogenes.
View Article and Find Full Text PDFGlycoconj J
January 2025
Department of Radiology, First Affiliated Hospital of Guangxi Medical University, No.6 Shuangyong Road, Nanning, Guangxi, 530021, China.
In this study, spatial and single-cell transcriptome techniques were used to investigate the role of beta-galactoside alpha-2,6-sialyltransferase 1 (ST6GAL1) in promoting peritoneal metastasis in ovarian cancer epithelial cells. We collected single-cell transcriptomic (GSE130000) and spatial transcriptomic datasets (GSE211956) from the Gene Expression Omnibus and RNA-sequencing data from The Cancer Genome Atlas. The Robust Cell Type Decomposition (RCTD) approach was implemented to integrate spatial and single-cell transcriptomic data.
View Article and Find Full Text PDFBiochem Genet
January 2025
Institute of Biological Sciences, Faculty of Science, Universiti Malaya, 50603, Kuala Lumpur, Malaysia.
Colorectal cancer (CRC) is the third most deadly cancer diagnosed in both men and women. 5-Fluorouracil (5-FU) treatment frequently causes the CRC cells to become chemoresistance, which has a negative impact on prognosis. Using bioinformatic techniques, this work describes important genes and biological pathways linked to 5-FU resistance in CRC cells.
View Article and Find Full Text PDFAdv Biotechnol (Singap)
July 2024
MOE Key Laboratory of Gene Function and Regulation, State Key Laboratory of Biocontrol, School of Life Sciences, Sun Yat-sen University, Guangzhou, 510275, Guangdong, China.
Cellular plasticity, the remarkable adaptability of cancer cells to survive under various stress conditions, is a fundamental hallmark that significantly contributes to treatment resistance, tumor metastasis, and disease recurrence. Oncogenes, the driver genes that promote uncontrolled cell proliferation, have long been recognized as key drivers of cellular transformation and tumorigenesis. Paradoxically, accumulating evidence demonstrates that targeting certain oncogenes to inhibit tumor cell proliferation can unexpectedly induce processes like epithelial-to-mesenchymal transition (EMT), conferring enhanced invasive and metastatic capabilities.
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