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

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...
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...
Targets for Drug Action: Overview01:26

Targets for Drug Action: Overview

Drugs target macromolecules to modify ongoing cellular processes. Primary drug targets include receptors, ion channels, transporters, and enzymes.
Receptors are either membrane-spanning or intracellular proteins, which upon binding a ligand, get activated and transmit the signal downstream to elicit a response. Drugs bind receptors, either mimicking the action of endogenous ligands or blocking the receptor activity to bring about a modified response. Nearly 35% of approved drugs target the G...
Cancer Therapies02:49

Cancer Therapies

Cancer therapies are various modes of treatment, such as surgery, radiation therapy, and chemotherapy that are administered to cancer patients.
However, cancer treatments can pose several challenges, as therapies used to kill cancer cells are generally also toxic to normal cells. Moreover, cancer cells mutate rapidly and can develop resistance to chemical agents or radiation therapy. Besides, all types of cancer cells may not respond to the same therapy. Some cancer cells respond to one...

You might also read

Related Articles

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

Sort by
Same author

PRECLINICAL ACTIVITY OF THE B7-H3- TARGETING ANTIBODY-DRUG CONJUGATE (ADC) VOBRAMITAMAB DUOCARMAZINE (VOBRA DUO) IN PEDIATRIC SOLID TUMORS.

Clinical cancer research : an official journal of the American Association for Cancer Research·2026
Same author

Endosialin (CD248) Cancer Role and Therapeutics: 33 Years on.

Molecular cancer therapeutics·2026
Same author

Lamin A/C loss promotes R-loop-mediated genomic instability and poor survival in small-cell lung cancer.

Proceedings of the National Academy of Sciences of the United States of America·2025
Same author

High-throughput combination screening of Pidnarulex and other G-quadruplex ligands in multi-cell type tumor spheroids.

SLAS discovery : advancing life sciences R & D·2025
Same author

Lamin A/C Deficiency Drives Genomic Instability and Poor Survival in Small-Cell Lung Cancer through Increased R-loop Accumulation.

bioRxiv : the preprint server for biology·2025
Same author

RAS Pathway Inhibitors Combined with Targeted Agents Are Active in Patient-Derived Spheroids with Oncogenic KRAS Variants from Multiple Cancer Types.

Cancer research communications·2025

Related Experiment Video

Updated: Jun 8, 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

Antiangiogenic agents and targets: A perspective.

Beverly A Teicher1

  • 1Genzyme Corporation, 49 New York Avenue, Framingham, MA 01701-9322, USA. Beverly.Teicher@Genzyme.com

Biochemical Pharmacology
|October 6, 2010
PubMed
Summary
This summary is machine-generated.

New antiangiogenic therapies are expanding beyond the VEGF pathway to overcome tumor resistance. These next-generation agents target diverse pathways, offering hope for refractory cancers.

More Related Videos

Modified In Vivo Matrix Gel Plug Assay for Angiogenesis Studies
09:03

Modified In Vivo Matrix Gel Plug Assay for Angiogenesis Studies

Published on: June 30, 2023

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

Related Experiment Videos

Last Updated: Jun 8, 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

Modified In Vivo Matrix Gel Plug Assay for Angiogenesis Studies
09:03

Modified In Vivo Matrix Gel Plug Assay for Angiogenesis Studies

Published on: June 30, 2023

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

Area of Science:

  • Oncology
  • Molecular Biology
  • Drug Discovery

Background:

  • First-generation antiangiogenic agents primarily targeted the Vascular Endothelial Growth Factor (VEGF) pathway.
  • Limitations include de novo resistance and acquired resistance through alternative angiogenic pathways.
  • Understanding these limitations necessitates exploring novel therapeutic targets.

Purpose of the Study:

  • To review the limitations of current VEGF-targeted antiangiogenic therapies.
  • To explore next-generation antiangiogenic agents targeting pathways beyond VEGF.
  • To discuss the potential for combination regimens and agents for refractory diseases.

Main Methods:

  • Review of current and emerging antiangiogenic targets and agents in clinical trials.
  • Analysis of alternative angiogenic pathways utilized by tumors.
  • Examination of novel therapeutic strategies including peptibodies and multi-targeted inhibitors.

Main Results:

  • Tumors can evade VEGF-targeted therapy by activating alternative angiogenic pathways like Placental Growth Factor (PlGF), Angiopoietins, HGF/c-Met, CXCL12/CXCR4, CXCR2, Notch, and Sphingosine-1-phosphate (S-1-P).
  • Several novel agents targeting these pathways, including peptibodies and multi-targeted kinase inhibitors, are in clinical trials.
  • These next-generation agents show promise for treating tumors resistant to VEGF-directed therapies.

Conclusions:

  • The field of antiangiogenesis is evolving beyond VEGF to address therapeutic resistance.
  • Expanding targets to include PlGF, Angiopoietins, HGF/c-Met, chemokine axes, Notch, and S-1-P is crucial.
  • Future strategies will likely involve combination regimens and single agents for refractory cancers, improving patient outcomes.