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Related Concept Videos

Tumor Progression02:07

Tumor 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...
Adaptive Mechanisms in Cancer Cells02:53

Adaptive 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.
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Mechanism of Angiogenesis01:10

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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...
Regulation of Angiogenesis and Blood Supply01:24

Regulation of Angiogenesis and Blood Supply

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TGF - β Signaling Pathway01:16

TGF - β Signaling Pathway

The TGF-β signaling pathway regulates cell growth, differentiation, adhesion, motility, and development. TGF-β ligands that induce TGF-β signaling are synthesized in their latent form. Several proteases or cell surface receptors such as integrins act upon the latent form, releasing the active ligand. There are three types of mammalian TGF-βs: (TGF-β1, TGF-β2, and TGF-β3) that bind as homodimers or heterodimers to TGF-β receptors. The TGF-β receptors are of three kinds RI, RII, and RIII. The RI...

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Tumorigenesis and the angiogenic switch.

Gabriele Bergers1, Laura E Benjamin

  • 1University of California San Francisco, Department of Neurological Surgery, Brain Tumor Research Center and Comprehensive Cancer Center, HSE 722, 513 Parnassus Avenue, San Francisco, California 94143-0520, USA. bergers@cgl.ucsf.edu

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Tumour growth depends on the tumor microenvironment, including vasculature. Understanding tumor-vasculature interactions can improve anti-angiogenic cancer therapies and prevent recurrence.

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Published on: April 12, 2018

Area of Science:

  • Oncology
  • Cancer Biology
  • Tumor Microenvironment Research

Background:

  • Tumor growth is intricately linked to the stromal microenvironment, particularly the vasculature.
  • The tumor phenotype dictates the characteristics of the developing tumor vasculature.
  • Angiogenesis and its reciprocal influence on the microvasculature are critical areas of cancer research.

Purpose of the Study:

  • To elucidate the complex interplay between tumor and vascular compartments.
  • To enhance the understanding of how tumor-stroma interactions influence cancer progression.
  • To inform the development of improved anti-angiogenic therapeutic strategies.

Main Methods:

  • This study synthesizes current research on tumor-vasculature interactions.
  • It involves analyzing the impact of angiogenesis on tumor development.
  • It examines the reciprocal influences of tumor products on the microvasculature.

Main Results:

  • Tumor growth cannot be fully understood without considering the stromal microenvironment, especially vasculature.
  • Tumor phenotype significantly influences the nature of tumor-associated vasculature.
  • Reciprocal interactions between tumor and vascular compartments are crucial for tumor progression.

Conclusions:

  • A comprehensive understanding of tumor-vascular interactions is essential for advancing cancer treatment.
  • Improved knowledge of these interactions can lead to more effective anti-angiogenic therapies.
  • This understanding is key to preventing cancer recurrence.