Jove
Visualize
Contact Us
JoVE
x logofacebook logolinkedin logoyoutube logo
ABOUT JoVE
OverviewLeadershipBlogJoVE Help Center
AUTHORS
Publishing ProcessEditorial BoardScope & PoliciesPeer ReviewFAQSubmit
LIBRARIANS
TestimonialsSubscriptionsAccessResourcesLibrary Advisory BoardFAQ
RESEARCH
JoVE JournalMethods CollectionsJoVE Encyclopedia of ExperimentsArchive
EDUCATION
JoVE CoreJoVE BusinessJoVE Science EducationJoVE Lab ManualFaculty Resource CenterFaculty Site
Terms & Conditions of Use
Privacy Policy
Policies

Related Concept Videos

Targeted Cancer Therapies02:57

Targeted Cancer Therapies

The targeted cancer therapies, also known as “molecular targeted therapies,” take advantage of the molecular and genetic differences between the cancer cells and the normal cells. It needs a thorough understanding of the cancer cells to develop drugs that can target specific molecular aspects that drive the growth, progression, and spread of cancer cells without affecting the growth and survival of other normal cells in the body.
There are several types of targeted therapies against specific...
Targeted Cancer Therapies02:57

Targeted Cancer Therapies

The targeted cancer therapies, also known as “molecular targeted therapies,” take advantage of the molecular and genetic differences between the cancer cells and the normal cells. It needs a thorough understanding of the cancer cells to develop drugs that can target specific molecular aspects that drive the growth, progression, and spread of cancer cells without affecting the growth and survival of other normal cells in the body.
There are several types of targeted therapies against specific...
Regulation of Angiogenesis and Blood Supply01:24

Regulation 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...
Mechanism of Angiogenesis01:10

Mechanism 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...
The Tumor Microenvironment02:17

The Tumor Microenvironment

Every normal cell or tissue is embedded in a complex local environment called stroma, consisting of different cell types, a basal membrane, and blood vessels. As normal cells mutate and develop into cancer cells, their local environment also changes to allow cancer progression. The tumor microenvironment (TME) consists of a complex cellular matrix of stromal cells and the developing tumor. The cross-talk between cancer cells and surrounding stromal cells is critical to disrupt normal tissue...
Tumor Immunotherapy01:27

Tumor Immunotherapy

Immunotherapy is a treatment that boosts or manipulates the immune system to fight diseases, including cancer. For instance, by stimulating an immune response through vaccinations against viruses that cause cancers, like hepatitis B virus and human papillomavirus, these diseases can be prevented. Nonetheless, some cancer cells can avoid the immune system due to their rapid mutation and division. The immune response to many cancers involves three phases: elimination, equilibrium, and escape.

You might also read

Related Articles

Articles linked to this work by shared authors, journal, and citation graph.

Sort by
Same author

Promoting Reasonable Career Expectations and Maximizing Professional Fulfillment for Academic Oncologists: ASCO Recommendations for Academic Medical Centers.

Journal of clinical oncology : official journal of the American Society of Clinical Oncology·2025
Same author

Enhancing efficacy of the MEK inhibitor trametinib with paclitaxel in <i>KRAS</i>-mutated colorectal cancer.

Therapeutic advances in medical oncology·2024
Same author

Leucine-Rich Alpha-2-Glycoprotein 1 Promotes Metastatic Colorectal Cancer Growth Through Human Epidermal Growth Factor Receptor 3 Signaling.

Gastroenterology·2024
Same author

Enhancing efficacy of the MEK inhibitor trametinib with paclitaxel in <i>KRAS</i> -mutated colorectal cancer.

bioRxiv : the preprint server for biology·2024
Same author

Vincristine Enhances the Efficacy of MEK Inhibitors in Preclinical Models of KRAS-mutant Colorectal Cancer.

Molecular cancer therapeutics·2023
Same author

Combining MEK and SRC inhibitors for treatment of colorectal cancer demonstrate increased efficacy in vitro but not in vivo.

PloS one·2023

Related Experiment Video

Updated: Jun 23, 2026

Preparation Of Neovascular Tissues from Human Glioma Tissues for Quantitative Proteomics Analysis of Tumor Angiogenesis
09:33

Preparation Of Neovascular Tissues from Human Glioma Tissues for Quantitative Proteomics Analysis of Tumor Angiogenesis

Published on: March 20, 2026

Targeting tumor angiogenesis.

Puja Gaur1, Debashish Bose, Shaija Samuel

  • 1Department of Surgical Oncology, The University of Texas M.D. Anderson Cancer Center, Houston, TX, USA.

Seminars in Oncology
|April 28, 2009
PubMed
Summary
This summary is machine-generated.

Vascular endothelial growth factor (VEGF) therapies improve cancer survival but are short-lived. Understanding complementary pathways is key to overcoming resistance and improving anti-VEGF treatment efficacy.

More Related Videos

Monitoring Functionality and Morphology of Vasculature Recruited by Factors Secreted by Fast-growing Tumor-generating Cells
09:03

Monitoring Functionality and Morphology of Vasculature Recruited by Factors Secreted by Fast-growing Tumor-generating Cells

Published on: November 23, 2014

Intravital Microscopy of Tumor-associated Vasculature Using Advanced Dorsal Skinfold Window Chambers on Transgenic Fluorescent Mice
08:52

Intravital Microscopy of Tumor-associated Vasculature Using Advanced Dorsal Skinfold Window Chambers on Transgenic Fluorescent Mice

Published on: January 19, 2018

Related Experiment Videos

Last Updated: Jun 23, 2026

Preparation Of Neovascular Tissues from Human Glioma Tissues for Quantitative Proteomics Analysis of Tumor Angiogenesis
09:33

Preparation Of Neovascular Tissues from Human Glioma Tissues for Quantitative Proteomics Analysis of Tumor Angiogenesis

Published on: March 20, 2026

Monitoring Functionality and Morphology of Vasculature Recruited by Factors Secreted by Fast-growing Tumor-generating Cells
09:03

Monitoring Functionality and Morphology of Vasculature Recruited by Factors Secreted by Fast-growing Tumor-generating Cells

Published on: November 23, 2014

Intravital Microscopy of Tumor-associated Vasculature Using Advanced Dorsal Skinfold Window Chambers on Transgenic Fluorescent Mice
08:52

Intravital Microscopy of Tumor-associated Vasculature Using Advanced Dorsal Skinfold Window Chambers on Transgenic Fluorescent Mice

Published on: January 19, 2018

Area of Science:

  • Oncology
  • Molecular Biology
  • Biochemistry

Background:

  • Tumor angiogenesis, crucial for cancer growth, is primarily mediated by vascular endothelial growth factor (VEGF).
  • Significant advancements in understanding VEGF and related pathways have occurred since the 1970s.
  • Anti-VEGF therapies have shown clinical benefits in advanced malignancies, improving progression-free and overall survival.

Purpose of the Study:

  • To review the evolving understanding of tumor angiogenesis and the role of VEGF.
  • To discuss the clinical efficacy and limitations of anti-VEGF therapies.
  • To highlight the importance of complementary pathways in mediating resistance to anti-VEGF therapy.

Main Methods:

  • Literature review of studies on tumor angiogenesis, VEGF, and anti-angiogenic agents.
  • Analysis of clinical trial data regarding anti-VEGF therapy outcomes.
  • Exploration of molecular mechanisms underlying VEGF-mediated angiogenesis and resistance pathways.

Main Results:

  • VEGF inhibition offers survival benefits but is often transient due to tumor adaptation.
  • Redundant and complementary pathways, such as the angiopoietin/Tie-2 axis, contribute to tumor vascular maintenance and resistance.
  • Current anti-VEGF therapies do not fully address the complexity of tumor angiogenesis regulation.

Conclusions:

  • A deeper understanding of VEGF biology and complementary pathways is essential for improving anti-VEGF therapy.
  • Identifying predictive biomarkers for treatment efficacy and resistance is a critical clinical challenge.
  • Future strategies must target multiple pathways to overcome resistance and enhance long-term patient outcomes.