Related Experiment Video
Updated: Aug 5, 2026
09:03
Monitoring Functionality and Morphology of Vasculature Recruited by Factors Secreted by Fast-growing Tumor-generating Cells
Published on: November 23, 2014
Diffusion with evolving sources and competing sinks: development of angiogenesis
M Scalerandi1, B Capogrosso Sansone, C A Condat
1INFM, Dipartimento di Fisica, Politecnico di Torino, Torino, Italy.
Physical Review. E, Statistical, Nonlinear, and Soft Matter Physics
|January 22, 2002
Summary
Tumors promote growth via angiogenesis, a process of blood vessel enlargement. This study models angiogenesis, predicting tumor growth, blood flow, and potential therapeutic strategies.
Area of Science:
- Oncology
- Biophysics
- Mathematical Biology
Background:
- Tumor growth relies on angiogenesis, the formation of new blood vessels.
- Angiogenesis is regulated by nutrient diffusion, molecular messengers, and cellular interactions.
- The dynamic nature of nutrient sources and cellular traps influences angiogenic processes.
Purpose of the Study:
- To develop a mathematical model of angiogenesis.
- To predict tumor-driven vascular system enlargement and blood flow.
- To explore directed growth and therapeutic synergy in angiogenesis.
Main Methods:
- Formulating a mathematical model based on cellular-level assumptions.
- Simulating the model to analyze angiogenesis dynamics.
- Investigating the impact of key parameters on tumor vascularization.
Main Results:
- The model predicts the evolution of angiogenesis and increased tumor blood flow.
- Simulations indicate the emergence of directed tumor growth.
- The model suggests potential for therapeutical synergy in anti-angiogenic strategies.
Conclusions:
- Mathematical modeling provides insights into the complex mechanisms of angiogenesis.
- The developed model can predict tumor vascularization and aid in therapeutic development.
- Understanding angiogenesis dynamics is crucial for effective cancer treatment strategies.
Related Concept Videos
02:07Tumor Progression
Tumor progression is a phenomenon where the pre-formed tumor acquires successive mutations to become clinically more aggressive and malignant. In the 1950s, Foulds first described the stepwise progression of cancer cells through successive stages.
Colon cancer is one of the best-documented examples of tumor progression. Early mutation in the APC gene in colon cells causes a small growth on the colon wall called a polyp. With time, this polyp grows into a benign, pre-cancerous tumor. Further...
Colon cancer is one of the best-documented examples of tumor progression. Early mutation in the APC gene in colon cells causes a small growth on the colon wall called a polyp. With time, this polyp grows into a benign, pre-cancerous tumor. Further...
02:53Adaptive Mechanisms in Cancer Cells
Cancer cells accumulate genetic changes at an abnormally rapid rate due to the defects in the DNA repair mechanisms. From an evolutionary perspective, such genetic instability is advantageous for cancer development. Mutant cell lines accumulate a series of beneficial mutations that contribute to their progression into cancer.
Some of the advantages that cancer cells have on normal cells include - enhanced ability to divide without terminally differentiating, induce new blood vessel formation,...
Some of the advantages that cancer cells have on normal cells include - enhanced ability to divide without terminally differentiating, induce new blood vessel formation,...
02:30Metastasis
Metastasis is the spread of cancer cells from the original site to distant locations in the body. Cancer cells can spread via blood vessels (hematogenous) as well as lymph vessels in the body.
Epithelial-to-Mesenchymal Transition
The epithelial-to-mesenchymal transition or EMT is a developmental process commonly observed in wound healing, embryogenesis, and cancer metastasis. EMT is induced by transforming growth factor-beta (TGF-β) or receptor tyrosine kinase (RTK) ligands, which further...
Epithelial-to-Mesenchymal Transition
The epithelial-to-mesenchymal transition or EMT is a developmental process commonly observed in wound healing, embryogenesis, and cancer metastasis. EMT is induced by transforming growth factor-beta (TGF-β) or receptor tyrosine kinase (RTK) ligands, which further...
01:10Mechanism of Angiogenesis
Blood vessel formation starts early during embryonic development, around day 7. In the extraembryonic yolk sac, mesodermal precursor cells called hemangioblast proliferate and differentiate into angioblast. Angioblasts express vascular endothelial growth factor receptor 2 or VEGFR2, which binds VEGF-A, a proangiogenic factor, guiding blood vessel formation. VEGF signaling promotes angioblasts to form a blood island in the developing embryo. Angioblasts further differentiate, giving rise to...
01:24Regulation of Angiogenesis and Blood Supply
Rapidly dividing tumors, embryos, and wounded tissues require more oxygen than usual, lowering the oxygen concentration in the blood. At low oxygen or hypoxic conditions, an oxygen-sensitive transcription factor called the hypoxia-inducible factor 1 or HIF1 is activated. HIF1 is a dimeric protein of alpha (ɑ) and beta (β) subunits. Under optimal oxygen conditions, HIF1β is present in the nucleus while HIF1ɑ remains in the cytosol. HIF1ɑ is hydroxylated by prolyl hydroxylase and factor...
01:07Development of Blood Vessels
The development of the vascular system in a fetus is a complex and intricate process that begins as early as 15 to 16 days post-conception. This process starts outside the embryo, specifically in the mesoderm of the yolk sac, chorion, and connecting stalk. Approximately two days later, the formation of blood vessels occurs within the embryo itself.
The initial formation of this system is facilitated by the small amount of yolk present in the ovum and yolk sac. Blood vessels originate from...
The initial formation of this system is facilitated by the small amount of yolk present in the ovum and yolk sac. Blood vessels originate from...