<abstract xmlns="http://www.w3.org/1999/xhtml"><p> The progressive growth and spread of tumour cells in the form of metastases requires an interaction of healthy host cells, such as endothelial cells, fibroblasts, and other cells of mesenchymal origin with immune cells taking part in innate and adaptive responses within the tumour lesion and entire body. The host cells interact with tumour cells to create a dynamic tumour microenvironment, in which healthy cells can both positively and negatively influence the growth and spread of the tumour. The balance of cellular homeostasis and the effect of substances they secrete on the tumour microenvironment determine whether the tumour has a tendency to grow or disappear, and whether the cells remain within the lesion or are capable of metastasis to other regions of the body. Intercellular interactions also determine the tumour’s susceptibility to radiation or other types of cancer treatment. They may also be a rational explanation for differences in treatment outcomes, in which some metastases regress and others progress in response to the same treatment method.</p></abstract>

The progressive growth and spread of tumour cells in the form of metastases requires an interaction of healthy host cells, such as endothelial cells, fibroblasts, and other cells of mesenchymal origin with immune cells taking part in innate and adaptive responses within the tumour lesion and entire body. The host cells interact with tumour cells to create a dynamic tumour microenvironment, in which healthy cells can both positively and negatively influence the growth and spread of the tumour. The balance of cellular homeostasis and the effect of substances they secrete on the tumour microenvironment determine whether the tumour has a tendency to grow or disappear, and whether the cells remain within the lesion or are capable of metastasis to other regions of the body. Intercellular interactions also determine the tumour’s susceptibility to radiation or other types of cancer treatment. They may also be a rational explanation for differences in treatment outcomes, in which some metastases regress and others progress in response to the same treatment method.

Mechanisms of tumour escape from immune surveillance

Department of Epizootiology and Clinic of Infectious Diseases, Faculty of Veterinary Medicine University of Life Sciences, 20-950 Lublin,

Journal of Veterinary Research

This work is licensed under the Creative Commons Attribution-NonCommercial-NoDerivatives 4.0 License.

{"article-title":"Mechanisms of tumour escape from immune surveillance"}

The progressive growth and spread of tumour cells in the form of metastases requires an interaction of healthy host cells, such as endothelial cells,...

Mechanisms of tumour escape from immune surveillance

Online veröffentlicht: 17. Dez. 2016

Seitenbereich: 453 - 460

Eingereicht: 13. Apr. 2016

Akzeptiert: 07. Nov. 2016

DOI: https://doi.org/10.1515/jvetres-2016-0068

Schlüsselwörter
cancer immunology, immune surveillance, immunosuppression, tumour escape, regulatory T lymphocytes

© 2016

This work is licensed under the Creative Commons Attribution-NonCommercial-NoDerivatives 4.0 License.

Mechanisms of tumour escape from immune surveillance

Online veröffentlicht: 17. Dez. 2016

Seitenbereich: 453 - 460

Eingereicht: 13. Apr. 2016

Akzeptiert: 07. Nov. 2016

DOI: https://doi.org/10.1515/jvetres-2016-0068

Schlüsselwörtercancer immunology, immune surveillance, immunosuppression, tumour escape, regulatory T lymphocytes

© 2016

This work is licensed under the Creative Commons Attribution-NonCommercial-NoDerivatives 4.0 License.

Schlüsselwörter
cancer immunology, immune surveillance, immunosuppression, tumour escape, regulatory T lymphocytes