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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...

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[VEGF in neoplastic angiogenesis].

V P Chekhonin, S A Shein, A A Korchagina

Vestnik Rossiiskoi Akademii Meditsinskikh Nauk

|May 31, 2012

Summary

Vascular Endothelium Growth Factor (VEGF) drives tumor growth. Inhibiting VEGF restricts tumor vascularization and progression, but resistance limits complete recovery in cancer patients.

Area of Science:

Oncology
Molecular Biology
Cancer Research

Context:

Solid tumor progression is critically dependent on tumor vascularization and angiogenesis.
Vascular Endothelium Growth Factor (VEGF) is a key regulator of angiogenesis.
Antiangiogenic therapies targeting VEGF have shown promise in various cancers.

Purpose:

To review the role of VEGF in tumor progression and the efficacy of antiangiogenic therapies.
To discuss the mechanisms of resistance to antiangiogenic treatment.

Summary:

VEGF is essential for the development of new blood vessels in tumors, supporting their growth and metastasis.
Inhibition of VEGF, exemplified by bevacizumab, can lead to regression of tumor vessels and restrict tumor growth.
Clinical applications include breast cancer, colorectal cancer, and gliomas.

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Impact:

Antiangiogenic therapy provides a valuable strategy for cancer treatment, primarily by restricting tumor growth.
Understanding resistance mechanisms is crucial for improving the long-term effectiveness of antiangiogenic therapies.
Further research into overcoming resistance pathways is necessary for achieving complete tumor eradication.