Disease Prediction and Drug Development
Arvind Kumar Bansal, Javed Iqbal Khan, S. Kaisar Alam in Introduction to Computational Health Informatics, 2019
Programmed cell-death is the automated death of an inactive cell. There are two types of cell-death: apoptosis and autophagy. Apoptosis occurs due to the lack of survival-factors. Autophagy is a natural degradation that disassembles dysfunctional components. Cytoskeleton gives a cell its shape and facilitates its movement using protein fibers. Extracellular matrix pathways are involved in cell-binding, cell-migration, proliferation and differentiation. The extracellular matrix is made of proteoglycans, water, minerals and fibrous proteins. Proteoglycans have a protein core surrounded by long chains of glycosaminoglycans – a starch like molecule. Angiogenesis is the formation of new blood-vessels. Epigenetic is the heritable changes caused by gene-expression variations with no change in genome sequence.
Chemopreventive Agents
David E. Thurston, Ilona Pysz in Chemistry and Pharmacology of Anticancer Drugs, 2021
Angiogenesis is the process underlying the formation and development of new blood vessels vital for the growth and development of new cells, as in wound healing. However, it also plays an important role in tumor growth, development, and metastasis, as it facilitates the transport of oxygen and nutrients to a growing tumor and the removal of waste products through the formation of a supporting vascular network. Angiogenesis is controlled by growth factors such as VEGF, TGF-α, TGF-β, TNF-α, angiogenin, IL-8, and the angiopoietins. One of the primary regulators of tumor angiogenesis is the pro-angiogenic factor VEGF, a potent endothelial cell-specific mitogen which stimulates endothelial cell growth originating in arteries, veins, and lymph drainage vessels (Figure 12.5).
Tissue injury and repair
C. Simon Herrington in Muir's Textbook of Pathology, 2020
The process of angiogenesis involves the formation of new capillary buds (sprouts) from pre-existing vessels. It follows a sequence of events that includes: (1) breakdown of the basement membrane of the pre-existing vessel, (2) migration of endothelial cells, (3) proliferation of endothelial cells behind the migrating cells, (4) maturation of endothelial cells with the formation of capillary tubes, and (5) recruitment of supporting cells (pericytes) to surround the endothelial cells. New vessel formation is thought to be critical in healing because it supplies oxygen and nutrients to the injured tissue and ensures the delivery of both humoral and cell-mediated arms of the immune system (see Chapter 4) to help prevent infection. Several growth factors have been found to stimulate angiogenesis, but the principal factor involved in the formation of new vessels in granulation tissue is a peptide known as vascular endothelial growth factor (VEGF). Matricellular proteins such as tenascin are also thought to have an important role in the formation and maintenance of new vessels, and there are also factors in the extracellular compartment (e.g. endostatin) that regulate angiogenesis, acting through inhibition of endothelial proliferation.
The role of PIGF blockade in the treatment of colorectal cancer: overcoming the pitfalls
Published in Expert Opinion on Biological Therapy, 2020
Teresa Macarulla, Clara Montagut, Francisco Javier Sánchez-Martin, Mónica Granja, Helena Verdaguer, Javier Sastre, Josep Tabernero
Angiogenesis is a crucial process for the formation of new blood vessels. It occurs under physiological conditions as well as during pathological processes such as tumor growth [5–7]. Under normal conditions, angiogenesis is well regulated through a balanced equilibrium between pro- and antiangiogenic factors [6]. Although the initial step of tumor angiogenesis is not well defined, it seems that recruitment of perivascular supporting cells is necessary for blood vessel formation. Different tissue-specific tumor-associated stromal stem cell types contribute to the formation of the tumor niche. Such cell types include carcinoma-associated fibroblasts, tumor-associated macrophages, lymphocytes, pericyte cells, inflammatory cells, normal epithelial cells, and mesenchymal stem cells [8].
Knockdown of CXCR4 Inhibits CXCL12-Induced Angiogenesis in HUVECs through Downregulation of the MAPK/ERK and PI3K/AKT and the Wnt/β-Catenin Pathways
Published in Cancer Investigation, 2018
Zhi-Yu Song, Feng Wang, Shu-Xiang Cui, Xian-Jun Qu
Angiogenesis is a physiological process of new blood vessel formation in organ tissues. It is also a fundamental and a rate-limiting step in solid cancer expansion dependent on the formation of angiogenesis to supply nutrients and oxygen (1). Angiogenesis is also an essential step for cancer invasion and metastasis in new environmental tissues (2). Angiogenesis might initiate by degradation of the vascular basement membrane in local to response various angiogenic factors, such as VEGF and bFGF, etc(3). Vasculature cells in cancer tissues might produce various enzymes that degrade basement membrane components, such as matrix metalloproteases, type IV collagenases, and aminopeptidases, leading to facilitate vascular cells migration into surrounding tissues (4). Anti-angiogenesis has thus been considered to be crucial in the treatment of cancers.
Inhibition of metastasis and angiogenesis in Hep-2 cells by wheatgrass extract – an in vitro and in silico approach
Published in Toxicology Mechanisms and Methods, 2018
Garima Shakya, Sangeetha Balasubramanian, Muddasarul Hoda, Rukkumani Rajagopalan
Angiogenesis is an important process in various physio-pathological conditions like embryonic development, chronic inflammation, wound healing, metastasis and cancer growth (Hseu et al. 2011). Generally a tumor cannot grow beyond the size of 1–2 mm, they require the formation of new vasculature from the preexisting ones to provide oxygen, nutrient and path for the exit (Weng and Yen 2012). Vascular endothelial growth factor (VEGF) is a mitogenic signal essential for angiogenesis. Most of the tumor cells can themselves secrete this angiogenic factor and initiate tumor angiogenesis. VEGF activates the endothelial cells receptors present on preexisting blood vessels. Activated receptors in turn, stimulates the endothelial cells sprouting, proliferation and migration toward the primary tumor, thus, ultimately leading to formation of new blood vessels. Various reports have documented the up regulation of VEGF expression in different cancers including head and neck squamous cell carcinoma (Sauter et al. 1999; Al- Dhaher et al. 2013). Similarly, in our study, in Hep-2 cells, VEGF was over expressed and this was reversed on treatment with MEWG as shown in Figures 2(A,B) (i). This result shows that WG has important role in inhibiting the VEGF, a key factor for angiogenesis and metastasis.
Related Knowledge Centers
- Mesoderm
- Wound Healing
- Embryo
- Endothelium
- Circulatory System
- Blood Vessel
- Granulation Tissue
- Vasculogenesis
- Coalescent Angiogenesis
- Neovascularization