An anti-tumor necrosis factor-alpha antibody inhibits the development of experimental skin tumors

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Transfer of Manipulated Tumor-associated Neutrophils into Tumor-Bearing Mice to Study their Angiogenic Potential In Vivo
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Transfer of Manipulated Tumor-associated Neutrophils into Tumor-Bearing Mice to Study their Angiogenic Potential In Vivo

Published on: July 20, 2019

Kate A Scott1, Robert J Moore, Caroline H Arnott

  • 1Cancer Research UK Translational Oncology Laboratory, John Vane Science Centre, Barts & The London, Queen Mary's School of Medicine and Dentistry, London EC1M 6BQ, United Kingdom. kate.scott@cancer.org.uk

Molecular Cancer Therapeutics
|May 16, 2003
PubMed

Insights

Tumor necrosis factor-alpha (TNF-alpha) promotes skin tumor development. Blocking TNF-alpha with cV1q significantly reduced tumor growth, suggesting its role in cancer promotion and potential for antagonist therapies.

Area of Science:

  • Oncology
  • Immunology
  • Dermatology

Background:

  • Tumor necrosis factor-alpha (TNF-alpha) was initially recognized for anti-cancer properties.
  • Emerging evidence suggests TNF-alpha may paradoxically promote tumor growth.
  • This study investigates the dual role of TNF-alpha in skin carcinogenesis.

Purpose of the Study:

  • To elucidate the role of TNF-alpha in skin tumor development.
  • To determine if TNF-alpha acts as an endogenous tumor promoter.
  • To evaluate the efficacy of TNF-alpha neutralization in preventing and treating skin tumors.

Main Methods:

  • Mice genetically deficient in TNF-alpha (TNF-alpha(-/-)) and wild-type (wt) mice were used.
  • Skin tumors were induced using 9,10-dimethyl-1,2-benzanthracene and 12-O-tetradecanoylphorbol-13-acetate (TPA).
  • TNF-alpha was neutralized in vivo using a cV1q antibody; keratinocyte and skin homogenate analyses were performed.

Main Results:

  • TNF-alpha(-/-) mice exhibited resistance to papilloma development compared to wt mice.
  • TPA treatment stimulated TNF-alpha expression in keratinocytes and epidermis.
  • cV1q neutralization significantly decreased skin tumor incidence and growth, even when administered early.
  • cV1q also reduced TPA-induced matrix metalloproteinase 9 and granulocyte macrophage colony-stimulating factor expression.
  • cV1q treatment inhibited the growth of a transplantable breast carcinoma.

Conclusions:

  • Early induction of TNF-alpha is critical for skin tumor promotion.
  • TNF-alpha exhibits pro-cancer effects, acting as an endogenous tumor promoter.
  • Neutralization of TNF-alpha offers a potential therapeutic strategy for cancer prevention and treatment.

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